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PubMed2000

Intracerebral administration of interleukin-1beta and induction of inflammation, apoptosis, and vasogenic edema.

OBJECT: The proinflammatory cytokines interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha (TNFalpha) are produced intracerebrally in brain disorders such as trauma, ischemia, meningitis, and multiple sclerosis. This investigation was undertaken to analyze the effect of intracerebral administration of IL-1beta and TNFalpha on inflammatory response, cell death, and edema development. METHODS: Intracerebral microinjections of these cytokines were administered to rats. The animals were killed 24 or 72 hours after the injections, and their brains were analyzed by using deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling (TUNEL) with digoxigenin-labeled deoxyuridine triphosphate, immunohistochemical studies, and brain-specific gravity measurement. The IL-1beta induced a transient inflammatory response (p < 0.001) and TUNEL staining (p < 0.001), indicating cell death, in intrinsic central nervous system (CNS) cells and infiltrating inflammatory cells. In 73.8+/-6.77% of the TUNEL-positive cells, small, fragmented nuclei were found. All TUNEL-positive cells expressed the proapoptotic gene Bax, and 69.6+/-4.6% of the TUNEL-positive cells expressed the antiapoptotic gene Bcl-2; the Bax expression was stronger than the Bcl-2 expression. Taken together, the data indicate that cell death occurred via the apoptotic pathway. The TNFalpha did not induce inflammation or DNA fragmentation within the analyzed time period. Both IL-1beta (p < 0.001) and TNFalpha (p < 0.01) caused vasogenic edema, as measured by specific gravity and albumin staining. The edematous effect of TNFalpha persisted 72 hours after injection (p < 0.01), whereas the IL-1beta-treated animals had normalized by that time. CONCLUSIONS: Intracerebral inflammation, death of intrinsic CNS cells, and vasogenic edema can be mediated by IL-1beta, and TNFalpha can cause vasogenic edema. Suppression of these cytokines in the clinical setting may improve outcome.

Animals↗
PubMedDate not supplied

[Capacities of examination of renal function at excretory urography].

The study was undertaken to enhance the diagnostic capacities of excretory urography in evaluating renal function, by determining the renal clearance of a contrast medium. The main task of the study was to develop bloodless and rather reliable ways of estimating the volume of the body's distributed contrast medium and its urinary concentration in the patient at urography. Excretory urography was performed in 248 patients aged 12 to 75 years. The specific gravity of excreted urine was determined with a standard laboratory urometer to 0.001 g/cm3. Absoption spectrophotometry was used to determine the serum concentration of contrast medium in 67 patients. The values of concentrations were plotted in the semilogarithmic ordinate system, followed by extrapolation of the initial segment of the plot to the so-called zero point determining the value of the concentration of contrast medium at the moment of its complete distribution in the intercellular space. The derived value was compared with the medium's dose coming into the body, which made it possible to determine the degree of dilution of the substance, i.e. the volume of its distribution in the organism. There was a linear relationship between the concentrations of renally eliminated contrast medium and the specific gravity of excreted urine. The numerical value of the constant reflecting this relationship is equal to 6. There was evidence for that such studies could be made by routine urometry. A high correlation was found between the body mass and the volume of distribution of contrast medium in the intercellular space. The discovery of the above regularities permitted the procedure for measuring the values of two most important physiological renal process (glomerular filtration and trabecular water reabsorption) to be simplified and widely available. The paper outlines the great promises for using excretory urography as a scanning functional test during a primary study and a follow-up of the patient's status.

Adolescent↗
PubMed1990

Time course of postischemic intracellular alkalosis reflects the duration of ischemia.

We investigated the long-term (up to 1 week) relationships between the duration of cerebral ischemia and postischemic energy metabolic profile, pH, and tissue edema in the rat. Ten rats each were subjected to 8 or 12 min of forebrain ischemia induced by bicarotid occlusion concurrent with systemic hypotension, and the results were compared with those of 10 sham-operated rat controls. In vivo 31P nuclear magnetic resonance spectroscopy was performed prior to ischemia and at intervals up to 168 h after ischemia. Cerebral edema (measured by specific gravity) was assessed prior to ischemia and at 24, 72, and 168 h after ischemia. The data revealed significant differences in the brain tissue pH profile over time between the ischemic groups (p less than 0.03). The 12-min ischemic animals exhibited brain tissue alkalosis (pH = 7.27 +/- 0.12) at 24 h compared with both sham (pH = 7.09 +/- 0.08) at 24 h and preischemic (pH = 7.06 +/- 0.04) pH values. The pH remained alkalotic (pH = 7.23 +/- 0.15) through the 48-h time period. In contrast, in the 8-min group, the onset of alkalosis was delayed until 48 h after ischemia (pH = 7.24 +/- 0.15), and pH remained alkalotic for only 24 h. No difference in high-energy phosphate metabolism was detected between groups. A different time dependence of tissue pH and specific gravity changes after 12 min of ischemia was detected. The present study suggests that the duration of an ischemic event marks the time of onset of brain tissue alkalosis and its duration and that cerebral edema alone cannot explain the pH changes.

Alkalosis↗
PubMed1994

Quantitative effects of low-dose dopamine on urine output in oliguric surgical intensive care unit patients.

OBJECTIVE: To quantify the magnitude and time course of the effect of low-dose dopamine (2.5 micrograms/kg/min) infusions on urine output in oliguric patients. DESIGN: A prospective, clinical study. SETTING: A surgical intensive care unit (ICU) at a university hospital. PATIENTS: A total of 19 surgical ICU patients with oliguria (< 0.5 mL/kg/hr) after resuscitation to pulmonary artery occlusion pressures > 10 mm Hg, mean arterial pressures > 65 mm Hg, and cardiac index > 2 L/min/m2. Patients with acute renal failure and those patients receiving diuretics were excluded. MEASUREMENTS AND MAIN RESULTS: Urine output was monitored hourly before and after dopamine was instituted for the treatment of oliguria. Spot urine electrolyte determinations and urine specific gravity measurements were obtained. Patients with urine output improvement (> 50% increase) had dopamine stopped after 4 hrs. If urine output decreased to < 0.5 mL/kg/hr, dopamine was resumed. There were no dopamine-induced changes in heart rate, pulmonary artery occlusion pressure, mean arterial pressure, or cardiac index. Mean urine output increased from 0.29 to 1.04 mL/kg/hr (p < .001) while patients were receiving dopamine. Time-to-peak response to dopamine was 7 hrs. Urine output increased to > 0.5 mL/kg/hr in 95% of patients, doubled in 89% of patients, and exceeded 1.0 mL/kg/hr in 84% of patients. After dopamine was stopped, urine output decreased to < 0.5 mL/kg/hr in 79% of patients and responded to resumption of dopamine in 100% of patients. There were no significant changes in urine sodium concentration or specific gravity. CONCLUSIONS: Low-dose dopamine infusion alone produces a drug-dependent increase in urine output in oliguric, euvolemic ICU patients. Maximal effect is temporally variable.

Adult↗
PubMed1997

The influence of acute and chronic alcohol treatment on brain edema, cerebral infarct volume and neurological outcome following experimental head trauma in rats.

The aim of this study was to determine the influence of acute and chronic ethanol treatment on neurological outcome following head trauma in rats. Eight-two Sprague-Dawley rats were divided into 10 groups. Four groups received sham head trauma (surgical incision of the scalp but no trauma) and were treated with (A) nothing, (B) chronic ethanol (6% ethanol in drinking water for 40 days), (C) acute ethanol 1.5 g/kg, intraperitoneally (IP) and (D) acute ethanol 3 g/kg IP. Four groups (E-H) received the same treatment; in addition, head trauma was delivered using a weight-drop device to the left cranium (2 h after ethanol treatment in the acute ethanol groups). To assess the influence of acute plus chronic alcohol and whether the glutamate antagonist ketamine can modify the neurologic outcome following head trauma, two additional head trauma groups were studied: group I received both acute and chronic ethanol treatment and group J received acute ethanol (1.5 g/kg) IP plus ketamine (180 mg/kg). Neurologic assessment was performed at 1, 2, 4, 8, 10, and 24 hours after head trauma or sham trauma in all animals who survived the treatment (omitted in group J animals while still under the anesthetic influence of ketamine). At the end of 24 hours, or at the time of death, the animals were decapitated. Specific gravity was determined from brain tissues adjacent to the injury and the contralateral hemispheres and the volume of hemorrhagic necrosis was quantified. None of the rats in the sham trauma groups died or had neurologic deficits. Of the head trauma groups, the mortality in animals that received 3 g/kg of ethanol and the animals that received acute plus chronic ethanol treatment was 100% before the end of 24 hours. Fifty percent of the animals receiving low-dose acute ethanol treatment (1.5 g/kg) died before 24 hours. In contrast, the mortality in the other groups was only 30% (p < 0.05). The neurologic severity score was significantly higher (greater neurological deficit) in the surviving animals that received acute ethanol treatment at 10 and 24 hours than in rats receiving no ethanol or chronic ethanol treatment. Specific gravity was also lower in the acute ethanol-treated groups compared with no ethanol, chronic ethanol, and acute ethanol plus ketamine groups (p < 0.03). Based on these observations, we conclude that in this rat head trauma model acute ethanol treatment increases mortality, neurological deficit, hemorrhagic necrosis volume, and brain edema. On the other hand, chronic ethanol treatment has no apparent effect and ketamine treatment does not counteract the effect of acute ethanol treatment.

Administration, Oral↗
PubMed1996

[A 4-week oral toxicity study of prulifloxacin (NM441) in rats followed by a 4-week recovery test].

A repeated dose toxicity study of prulifloxacin, a new antibacterial agent, was conducted in Sprague-Dawley rats. Male and female rats were given the test material orally for 4 weeks at doses of 0 (control), 30, 300 and 3000 mg/kg. After discontinuation of the treatment, a 4-week recovery test was also conducted. There was one case of death in the 3000 mg/kg group. Grayish green and soft feces, unkempt fur, transient deep respiration and decreased body weight gain were observed in the 3000 mg/kg group. Decreased food consumption and increased water intake were seen in the 300 and 3000 mg/kg groups. Ophthalmoscopic examination failed to show any abnormalities related to the treatment. In urinalysis, crystalline substance in the urinary sediments, cloudy urine and decreased Na+ excretion were observed in the 300 and 3000 mg/kg groups. Increased urine volume, lowered urine specific gravity and decreased K+ and Cl- excretions were seen in the 3000 mg/kg group. Hematologic examination showed decreased Hb, Ht, MCV and MCH and increased WBC in the 3000 mg/kg group. Blood chemical examination revealed increased BUN and decreased K+ and Cl- in the 3000 mg/kg group, and decreased K+ and gamma-globulin in the 300 mg/kg group. Pathological changes caused by the treatment were as follows. Cecal weight was increased in all dose groups. Cecal distention and swelling of its absorptive cells were seen in the 300 and 3000 mg/kg groups. In kidney, tubular nephrosis with crystalline substance was observed in the 300 and 3000 mg/kg groups, and its organ weight was increased in the 3000 mg/kg group. The above-mentioned changes were reversible except for decreased gamma-globulin, increased BUN and urine volume, and lowered urine specific gravity. Ulcer and small cavities associated with proliferation of fibrous tissue in the femoral articular cartilage were observed in the 3000 mg/kg group at the end of recovery period of 4 weeks. Plasma levels and urinary concentrations of active metabolite of the test material were increased in all dose groups with dose-related manner, whereby no sex difference was observed. No effects caused by the repeated dosing were seen in the plasma concentrations. Increased cecal weight in the 30 mg/kg group was considered to be attributable to the pharmacological effect of the test material. The results show that the NOAEL of prulifloxacin is 30 mg/kg for 4-week repeated dose toxicity in rats.

Administration, Oral↗
PubMed1992

Effect of sodium fluoride on bone density in chickens.

In addition to increasing bone volume, fluoride has been demonstrated to increase ash weight and mineral density. To determine whether newly formed or older bone is most affected by fluoride treatment, bone from chickens receiving fluoridated water was fractionated into lower density (recently formed) and higher density (more mature) specific gravity fractions. Fluoride was administered to the chickens for different lengths of time (4 or 13 weeks) or at varying doses for a 4-week period (0, 4.2, 16.8 mmol/liter drinking water). Fluoride treatment caused a shift in the mineral density profile, showing an increased proportion of mineral distribution in the more mature, higher density fractions. To determine whether this density gradient shift was due to increased maturation rate of bone or decreased resorption and mineralization rates, [3H]proline and 45Ca were injected 5 days and 24 hours prior to sacrifice, respectively. The distributions of both 3H or 45Ca, as percentages of total counts incorporated, were shifted by fluoride treatment into more mature, higher density fractions. Expressing the number of counts as a percent of the bone in each fraction (total hydroxyproline or Ca) revealed an increased incorporation of both 3H and 45Ca into the higher specific gravity fractions 2.0-2.2. These results suggest that fluoride treatment increases bone maturation and the rate of secondary mineralization in the cortical bone. Such changes in the quality of more mature, well-mineralized bone, in humans as well as animals, may have a significant influence on brittleness and strength.

Animals↗
PubMed2004

Carbohydrate-electrolyte (E-Lyte) solution enhances bowel preparation with oral fleet phospho-soda.

PURPOSE: Bowel preparation with oral sodium phosphate can cause symptomatic dehydration and electrolyte disturbances. This randomized, controlled trial was designed to evaluate whether carbohydrate-electrolyte (E-Lyte) solution enhanced bowel preparation and improved patient acceptance with oral sodium phosphate. METHODS: A total of 187 consecutive adults undergoing colonoscopy by two endoscopists were randomized to receive two packets of oral sodium phosphate (Fleet Phospho-soda) with or without additional supplement of a carbohydrate-electrolyte (E-Lyte) solution. All patients and endoscopists completed a standardized questionnaire. Urine-specific gravity and serum biochemistry were randomly performed in 150 and 50 patients, respectively. RESULTS: Ninety patients were randomized to have oral sodium phosphate with E-Lyte supplements (Group 1) and 94 patients to sodium phosphate without E-Lyte supplements (Group 2). The groups were similar in age and gender, indication for colonoscopy, and previous colonic surgery. Patients taking E-Lyte supplement had significantly less dizziness (none, 80 vs. 56 percent; P < 0.001) and a trend toward less nausea (none, 70 vs. 56 percent; P = 0.05). All patients in Group 1 completed the bowel preparation as opposed to 3 percent of Group 2 being unable to complete the preparation. Hypokalemia was significantly more frequent ( P = 0.008) in Group 2 patients without E-Lyte supplements. More patients in Group 2 needed intravenous rehydration (11 vs. 4 percent). Differences in serum creatinine and urine-specific gravity suggested possibly a lesser degree of hypovolemia in patients taking E-Lyte supplements. The quality of bowel cleansing in patients taking E-Lyte supplements was considered better by both the endoscopists and patients. CONCLUSIONS: Carbohydrate-electrolyte (E-Lyte) solution protects against hypokalemia, improves patient tolerability, and may enhance use of oral sodium phosphate as a bowel-preparation agent.

Administration, Oral↗
PubMed2002

Comparison of nasogastric and intravenous methods of rehydration in pediatric patients with acute dehydration.

OBJECTIVE: To assess the safety, efficacy, and cost-effectiveness of rapid nasogastric hydration (RNG) and rapid intravenous hydration (RIV) administered in the emergency department (ED) to young children suffering with uncomplicated, acute moderate dehydration. METHODS: Ninety-six children aged 3 to 36 months, who presented with signs and symptoms of uncomplicated, acute moderate dehydration caused by vomiting and/or diarrhea, presumed to be caused by viral gastroenteritis, were randomly assigned to receive either RNG with a standard oral rehydration solution or RIV with normal saline. Each solution was administered at a rate of 50 mL/kg of body weight, delivered over a 3-hour period in our urban pediatric ED. All participants were weighed pretreatment and posttreatment and underwent initial and final measurements of their serum electrolytes, blood urea nitrogen, creatinine, and glucose levels, along with urine chemistry and urine specific gravity. Telephone follow-up by completion of a standardized questionnaire was obtained approximately 24 hours after discharge from the ED. RESULTS: Ninety-two of 96 enrolled patients completed the study. Three patients failed treatment (2 RIV and 1 RNG) and were excluded and hospitalized because of severe, intractable vomiting, and 1 patient was withdrawn secondary to an intussusception. Among 92 evaluable patients, 2 were found to be severely dehydrated (>10% change in body weight) and were excluded from analysis, leaving 90 patients (RNG: N = 46 and RIV: N = 44), who completed the study. Both RNG and RIV were found to be a safe and efficacious means of treating uncomplicated, acute moderate dehydration in the ED. Determinations of electrolytes, blood urea nitrogen, creatinine, or glucose were not found to be of value on an intent-to-treat basis in the care of these patients. The urine specific gravity and incidence of ketonuria declined from levels commensurate with moderate dehydration in the RNG group, but not as consistently so in the RIV group. Both RNG and RIV were substantially less expensive to administer than standard care with intravenous fluid deficit therapy in-hospital, and RNG was more cost-effective to administer over RIV in the outpatient setting. CONCLUSION: RNG and RIV administered in the ED are safe, efficacious, and cost-effective alternatives to the standard treatment for uncomplicated, acute moderate dehydration in young children. RNG is as efficacious as RIV, is no more labor intensive than RIV, and is associated with fewer complications. In addition, we found that most routine laboratory testing is of little value in these patients and should be avoided, except when clearly clinically indicated.

Child, Preschool↗
PubMed1991

Effects of hyperglycemia on ischemic brain damage, local cerebral blood flow and ischemic cerebral edema.

The effects of hyperglycemia on ischemic brain damage, local cerebral blood flow (LCBF), and ischemic cerebral edema were studied in a rat model of transient middle cerebral artery (MCA) occlusion with a microclip. Hyperglycemia was induced by intraperitoneal injection of 50% glucose, and same volume of 50% D-mannitol or physiological saline were injected in the controls. LCBF was measured by the quantitative autoradiogram using 14C-iodoantipyrine at 2 hours after MCA occlusion and 2 hours after reperfusion. Cerebrovascular permeability was measured by same technique using 14C-alpha-aminoisobutyric acid (AIB) at 2 hours after reperfusion following 2 hours ischemia. Specific gravity of the brain, determined by the gradient column, was used to study the topographic changes of brain water content at 2 hours after MCA occlusion and 2 hours after reperfusion. Some rats were prepared for neuropathological observation 72 hours after reperfusion. Histological study 72 hours after restoration of CBF following 2 hours MCA occlusion revealed ischemia neuronal cell damage to be more extensive in hyperglycemic rats than in normoglycemic rats. LCBF in the ischemic focus decreased significantly in hyperglycemic rats compared with the controls at 2 hours after MCA occlusion. Furthermore, the reduction of LCBF was observed also in the contralateral non-ischemic side. At 2 hours after reperfusion, in hyperglycemic rats, hyperemia up to 121-156% of the contralateral LCBF was observed within the previously ischemic area, along with a zone of reduced CBF in the surrounding area. At 2 hours after MCA occlusion, the decrease of specific gravity of the ischemic brain, in hyperglycemic rats, was significant compared with the control, and these decreases became more prominent in the entire territory of the MCA at 2 hours after reperfusion. Furthermore, 14C-AIB autoradiogram disclosed the prominent and wide leakage of the tracer within the previous ischemic focus of MCA occlusion. In contrast, in normoglycemic rats, ischemic brain edema showed a reducing trend after reperfusion, and no demonstrable changes of cerebrovascular permeability were disclosed on autoradiograms. These findings suggest that the enhancing mechanisms of hyperglycemia for ischemic brain damage are severely reduced CBF during ischemia and postischemic vasogenic edema.

Animals↗
PubMed1995

Experimental stroke and neuroprotection in the aging rat brain.

BACKGROUND AND PURPOSE: Experimental stroke research has for the most part incorporated the use of young animals despite the importance of aging in cerebrovascular disease in humans. We hypothesized that age-related reductions in the density and function of cortical N-methyl-D-aspartate (NMDA) receptors might limit neuroprotective potential in the elderly. In this study, a model of occlusive stroke in the aging rat brain has been developed and used to establish the effects of age on cerebral infarction and to evaluate the scope for protecting the aging brain during ischemia. METHODS: Focal cerebral ischemia was produced by thermocoagulation of the left middle cerebral artery in adult (11 to 17 months) and aged (28 to 36 months) male Wistar rats. Infarcts were assessed histologically with volumetric analysis of infarct size, hemodynamically by serial cerebral blood flow measurement using the hydrogen clearance technique, and by analysis of specific gravity as an index of brain edema. Neuroprotective potential was assessed using the competitive NMDA receptor antagonist 3-(2-carboxy piperazin-4-yl)propyl-1-phosphonate (D-CPPene). RESULTS: Aging was associated with a significant increase in infarct size, with a mean infarct volume of 40.5 +/- 2.6% of the hemisphere volume in aged rats compared with 30.9 +/- 0.7% in adult rats (P < .01). D-CPPene reduced the mean infarct volume to 33 +/- 1.8% and 20.7 +/- 3.2% in aged and adult rats, respectively (P < .05). Cerebral blood flow fell markedly after infarction, but thereafter D-CPPene-pretreated rats maintained higher cerebral blood flow than untreated animals throughout the duration of the experiment (22.8 +/- 3.2 and 30.1 +/- 5.5 mL.100 g-1.min-1 in treated aged and adult rats, respectively, compared with 11.3 +/- 2.7 and 16.5 +/- 3.2 mL.100 g-1.min-1 in untreated aged and adult groups, 90 minutes after infarction [P < .05]). Pretreatment also reduced cortical edema; mean cortical specific gravity 4 hours after infarction was 1.0381 +/- 0.0013 in untreated aged rats and 1.0391 +/- 0.0014 in untreated adults compared with 1.0458 +/- 0.0031 in treated aged rats and 1.0442 +/- 0.0014 in treated adult rats (P < .05). CONCLUSIONS: Under similar experimental conditions, there was an age-related increase in cerebral infarct size. However, NMDA receptor antagonism was neuroprotective in the aging brain and resulted in a significant reduction in cerebral ischemic damage, less cortical edema, and preservation of cerebral blood flow.

Aging↗
PubMed1986

Influence of hatcher holding times on several physiological parameters associated with the immune system of chickens.

Two experiments were conducted with broiler chicks to study the effects of posthatch holding time in the incubator on physiological and disease parameters. In each experiment, half of the chicks were removed shortly after hatching and half of the chicks were allowed to remain in the hatcher for an additional 30 hr. Bursa weights, hematocrits, total plasma protein, and blood glucose concentrations were measured at various times up to 35 and 28 days of age in Experiments 1 and 2, respectively. In addition, chicks hatched from eggs with one of two specific gravities (less than or equal to 1.065 and greater than or equal to 1.075) were tested in the second experiment. Spleen weights, heterophil:lymphocyte ratios and the influence of an aerosol Newcastle disease-Mycoplasma gallisepticum vaccine challenge were also measured in the second experiment. In Experiment 1, when chicks were held in the hatcher for an additional 30 hr, bursa weights were reduced through 8 days of age; however, they were significantly heavier by 21 days of age. In Experiment 2, both bursa and spleen weights were significantly reduced through 14 days of age when chicks were held in the incubator. Total plasma protein and glucose concentrations, hematocrits, and heterophil:lymphocyte ratios were all significantly higher for chicks held in the incubator. Chicks held in the incubator and then exposed to an aerosol vaccine challenge at 1 day of age had a significantly greater percentage of air sac lesions and the lesions were more severe at 28 days of age. Egg specific gravity had no influence on any of the parameters measured.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Transient renal impairment in rats after oral exposure to diethylene glycol.

Volume, specific gravity, creatinine, lactate dehydrogenase (LDH), leucine aminopeptidase (LAP), beta-galactosidase (GAL), leucocytes, erythrocytes, nitrite, protein (albumin), glucose, ketone, urobilinogen, bilirubin and pH were estimated in urine of rats after single (by gavage) or repeated (via drinking water) oral administration of diethylene glycol (DEG). Following single or repetitive doses (daily over 90 days) of 0.2 g DEG kg-1 body weight, no change in renal function was observed (no effect level). In urine of rats treated once with 0.7 g DEG kg-1 body weight, LDH activity was significantly enhanced one day after treatment. A single dose of 2.0 g DEG kg-1 body weight resulted in an additional rise in urinary GAL activity two days after treatment, a significant rise of urinary volume and a decrease in creatinine concentration and pH on the first day. One day following a single dose of 8.0 g DEG kg-1 body weight, in addition to the changes mentioned before, LAP activity was significantly elevated and the specific gravity decreased. However, in all experiments the wet weight of the kidneys remained normal as compared to controls. The results thus show dose-dependent changes in several renal parameters, indicating a slight-to-moderate and reversible renal impairment.

Animals↗
PubMed1995

Chronic glucocorticoid excess and impaired osmoregulation of vasopressin release in dogs with hepatic encephalopathy.

Chronic liver disease may be accompanied by disturbed sodium and water homeostasis. There is usually sodium retention and ascites. However, spontaneous natriuresis has also been reported in humans and experimental animals with liver cirrhosis. Chronic hypercortisolism, which may occur in dogs with advanced liver disease, is known to induce the inhibition of the osmostimulation of vasopressin (AVP) release. We have therefore investigated the osmoregulation of AVP release in 11 dogs with chronic hypercortisolism associated with advanced liver dysfunction and hepatic encepahlopathy and in 10 control dogs. Basal pituitary-adrenocortical activity was investigated by measuring the concentration in multiple plasma samples of adrenocorticotropin (ACTH), alpha-melanocyte-stimulating hormone (MSH), and cortisol and the cortisol:creatinine ratio in 24-hr urine. Urine specific gravity was also measured. The feedback regulation of the system was investigated by measuring these hormones in plasma after an intravenous (iv) injection of 0.01 mg/kg of dexamethasone. The osmoregulation of the release of AVP was investigated by the intravenous infusion of a 20% NaCl solution at a flow rate of 0.03 ml/kg for 2 hr and the measurement of AVP in plasma sampled at 20-min intervals. The AVP release was analyzed in terms of the threshold osmolality at which it commenced and the sensitivity, which reflects the magnitude of the response. All dogs had highly increased urinary cortisol:creatinine ratios, ranging from 21 to 210 x 10(-6) (normally < 10 x 10(-6)). The mean basal plasma concentrations of the three pituitary-adrenocortical hormones were significantly increased. ACTH values were 35 to 146 ng/l (normally, 14 to 68), MSH values were 26 to 118 ng/l (normally, 10 to 36), and cortisol values were 88 to 194 nmol/l (normally, 23 to 112). The feedback inhibition of the secretion of ACTH and cortisol in response to dexamethasone was unaffected. Urine specific gravity was significantly decreased. The regulation of AVP release was found to be abnormal in all dogs with hepatic encephalopathy. The osmotic threshold at which the release of AVP was induced was abnormally high in seven of the dogs with liver disease and in the normal range in one. It could not be determined in three dogs. The sensitivity of AVP release in response to increasing plasma hypertonicity was normal in two dogs and decreased in nine. In three dogs, there was no increase in AVP release. None of the dogs had normal values for both the sensitivity and the threshold.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenocorticotropic Hormone↗
PubMed1999

Influence of mass and volume of ruminal contents on voluntary intake and digesta passage of a forage diet in steers.

To assess the influence of volume and mass of ruminal contents on voluntary intake and related variables, five ruminally cannulated steers (550 kg) were fed a low-quality forage diet (43.1% ADF, 8.1% CP) in a 5 x 5 Latin square experiment. Mass and volume of ruminal contents were altered by adding varying numbers and weights of filled tennis balls (6.7-cm diameter) to the rumen immediately before the initiation of each experimental period. Treatments consisted of 0 balls (control), 50 balls with a 1.1 specific gravity (SG), 100 balls with a 1.1 SG, 50 balls with a 1.3 SG, and 100 balls with a SG of 1.3. The total volume of balls was 7.25 and 14.5 L for 50 and 100 balls, respectively. The total weight of balls was 8.5 and 17 kg for 50 and 100 balls with a 1.1 SG and 10.75 and 21.5 kg for 50 and 100 balls with a 1.3 SG, respectively. Daily DMI was 8.3, 7.3, 7.0, 6.5, and 6.0 kg for control; 50, 1.1 SG; 50, 1.3 SG; 100, 1.1 SG; and 100, 1.3 SG, respectively. Addition of balls to the rumen reduced (P < .01) DMI. Increasing the number (P < .01) and SG (P <. 01) of the balls decreased DMI further. However, digestibilities of DM, NDF, ADF, and CP were not influenced by treatment. Increasing the number of balls in the rumen increased (P < .05) rate of passage of digesta from the rumen, but increasing SG of the balls did not alter rate of passage. There was a treatment x hour interaction (P < .05) in the proportion of ruminal digesta with a functional specific gravity (FSG) less than 1.1, which decreased with time after feeding for the control but increased with time after feeding for other treatments. Ruminal passage rate of inert particles added in the rumen of different SG (1.1 and 1.3) and length (1 and 3 mm) decreased (P < .05) as SG of the balls increased. Mean fecal particle size was greater for those treatments with the heavier balls. Both the number and SG of balls (P < .10) influenced total VFA, and total concentrations were greater for the control and for the 1.1 SG than for the 1.3 SG treatments.

Ammonia↗
PubMed2006

The vitamin D3 requirement of broiler breeders.

An experiment was conducted with 25- to 66-wk-old Ross broiler breeders in an environment excluding ultraviolet light to determine the cholecalciferol (D3) requirements for hen day egg production; hatchability; body weight of the progeny at 1 d; embryo mortality during the early (1 to 10 d of incubation), middle (11 to 15 d of incubation), and late stages (16 to 21 d of incubation) of development; egg weight; specific gravity; and body ash of the progeny at 1 d of age. Five levels of vitamin D3 (125, 250, 500, 1,000, and 2,000 IU/kg of diet) were fed to hens from 25 to 66 wk of age. One additional group was fed no supplemental D3 until 36 wk of age and was then changed to 4,000 IU/kg of diet. Separate regression analyses were performed for wk 27 to 36 (peak original design) and for wk 37 to 66 (postpeak production modified design). The D3 levels for the predicted maximum hen day egg production during peak and postpeak were 1,424 and 2,804 IU/kg, respectively. The D3 levels for the predicted maximum hatchability were 1,390 IU/ kg (peak) and 2,708 IU/kg (postpeak). The level of D3 that resulted in the minimum early embryo mortality was 1,288 IU/kg at peak; however, no significant effect was observed at postpeak. The D3 levels for minimum middle stage embryo mortality were 1,130 IU/kg (peak) and 2,568 IU/kg (postpeak) and for late stage embryo mortality were 1,393 IU/kg (peak) and 2,756 IU/kg (postpeak). The D3 level for maximum egg weight was 1,182 IU/kg (peak) and for specific gravity was 1,337 IU/kg (peak) and >2,000 IU/kg (postpeak). The D3 level for maximum body ash of progeny at d 1 was >2,000 IU/kg. Analysis of the data from the original design of the experiment (treatments providing 0, 125, 250, 500, 1,000, and 2,000 IU of vitamin D3/kg for the 27- to 36-wk-old birds) indicates a requirement of approximately 1,400 IU of D3/kg of feed for broiler breeder hens. When the data from the modified experiment (37 to 66 wk of age) include conversion of the treatment provided at 0 IU of D3/kg to a treatment providing 4,000 IU of D3/kg, the requirement may be approximately 2,800 IU of D3/kg.

Aging↗
PubMedDate not supplied

Elevated amniotic fluid nitric oxide metabolites and interleukin-6 in intra-amniotic infection.

OBJECTIVE: To compare amniotic fluid nitric oxide metabolites and interleukin-6 (IL-6) concentrations in patients with and without intra-amniotic infection. METHODS: Amniotic fluid nitric oxide metabolites, IL-6, Gram stains, glucose, leukocyte counts, leukocyte esterase activity, creatinine, pH, and specific gravity were determined in 14 patients with intra-amniotic infection and 26 patients without intra-amniotic infection. Intra-amniotic infection was defined as the presence of a positive amniotic fluid culture. The nitric oxide metabolites, nitrate and nitrite (NOx), were measured using Greiss reagent after reduction of nitrate to nitrite with aspergillus nitrate reductase. Interleukin-6 was measured by a two-site, enzyme-linked immunosorbent assay. Amniotic fluid nitric oxide metabolites and IL-6 concentrations were normalized by amniotic fluid creatinine levels. The Mann-Whitney U test, contingency table method, and Spearman's rank correlation test were used for statistical analyses. RESULTS: Amniotic fluid NOx and IL-6 levels were significantly higher in patients with intra-amniotic infection than in those without intra-amniotic infection (NOx: median = 2.06 mumol/mg creatinine, range = 0.74-6.81 versus 1.35 mumol/mg creatinine, range = 0.99-1.60, P = .01, IL-6: median = 2.00 micrograms/mg creatinine, range = 0.026-4.07 versus median = 0.04 micrograms/mg creatinine, range = 0.004-3.210, P = .0009, respectively). Patients with intra-amniotic infection had significantly elevated leukocyte counts, leukocyte esterase activity, Gram positive stains, and significantly lower amniotic fluid glucose levels compared with those without intra-amniotic infection. There were no differences in gestational age, maternal age, parity, race, pH, or specific gravity between the two groups. Amniotic fluid NOx was significantly correlated with IL-6 (r = .4, P = .02). Both amniotic fluid NOx and IL-6 were also positively correlated with amniotic fluid leukocyte counts, leukocyte esterase activity and Gram stains, and negatively correlated with glucose levels. CONCLUSIONS: Amniotic fluid NOx and IL-6 are significantly elevated and positively correlated during intra-amniotic infection. Both increased amniotic fluid IL-6 and nitric oxide may exert cytotoxic and cytostatic effects on the target cells. We suggest that measurements of amniotic fluid NOx and IL-6 may serve as useful clinical markers in patients with intra-amniotic infection.

Adolescent↗
PubMed1999

The effect of dietary wheat middlings and enzyme supplementation. 1. Late egg production efficiency, egg yields, and egg composition in two strains of Leghorn hens.

A study was conducted to test the effects of wheat middlings (WM) with and without enzyme (xylanase and protease) supplementation on late egg production (EP), egg yields, and egg composition in two strains of Leghorn hens (DeKalb Delta and Hisex White). Six diets were randomly assigned to 300 birds (150 birds per strain) from 42 to 60 wk of age. Diet 1 was a corn-soybean meal control, Diets 2 and 3 had 8 and 16% WM, respectively, Diet 4 had 8% WM with 0.1% enzyme, and Diets 5 and 6 had 16% WM with 0.1 and 0.2% enzyme, respectively. Each dietary treatment was replicated five times per strain. Egg production, feed consumption (FC), feed efficiency (FE), percentage dirty eggs, specific gravity (SP), egg weight (EW), and egg mass (EM) were measured on a weekly basis. Egg components (EC) were measured biweekly and birds were weighed every 4 wk. Egg production was not significantly affected by diet, with averages of 83.7, 85.7, 84.1, 84.2, 82.3, and 84.0% for Diets, 1, 2, 3, 4, 5, and 6, respectively. Strain had a marked effect on FC, with Hisex having higher FC than DeKalb hens. Feed consumption also showed a significant diet by strain effect, being lower for Hisex hens fed diets with enzyme compared to diets without enzyme. DeKalb hens had better FE than Hisex hens, and addition of enzyme to 16% WM improved it further. Strain and diet had a significant effect on EC with higher percentages of albumen and yolk for diets with enzyme and for DeKalb hens. Percentage shell was lower for DeKalb hens than for Hisex hens but was not affected by diet. There was also a significant increase in EW for Diets 4 (63.1 g), 5 (63.8 g), and 6 (63.2 g) compared to Diets 1 (62.1 g), 2 (62.4 g), and 3 (63.0 g), with DeKalb hens showing an increase with Diet 5 compared to Hisex hens. Egg mass improved with the higher rate of enzyme in 16% WM diet compared to the lower enzyme level. Specific gravity declined with enzyme supplementation in WM diets. Eggs from DeKalb hens had lower SP than those from Hisex hens for all diets. Percentage dirty eggs did not differ significantly among treatments but was higher for the Hisex strain than for the DeKalb strain. There were no differences in BW between the two strains of hens or among diets. Adding protease and xylanase to diets rich in fiber can improve the egg output without affecting production parameters.

Animal Husbandry↗