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J Knox

Publications and source records attributed to J Knox.

At least 55 records · Page 3Linked to original sources
PubMed1994

An in vitro study of the effects of different crystal growth solutions on the topography of the enamel surface.

This study evaluated the effect on the topography of the enamel surface of applying various solutions based on polyacrylic acid. This base solution consisted of 50 per cent aqueous polyacrylic acid (molecular weight 5000) and concentrated sulphuric acid (98 per cent). Previously, similar solutions have been found to initiate a crystal growth on the enamel surface and have been proposed as being suitable for the attachment of orthodontic brackets via a composite resin interface. The base solution was modified by the addition of various ionic salts: the sulphates of lithium, magnesium and potassium, respectively. Human premolar teeth were then treated to a standard format and the effect on the enamel surface was examined by the use of a scanning electron microscope at x 500 and x 1500 magnification. The resultant micrographs of the specimens were presented to three independent observers who assessed the length, quality, and degree of coverage of the crystals. The solution containing potassium sulphate gave the longest crystals, whilst the greatest degree of coverage was obtained with the magnesium sulphate solution. Each solution was found to produce a consistent and recognizable morphology.

Acid Etching, Dental↗
PubMed1994

Blood amino acids in the pregnant mare and fetus: the effects of maternal fasting and intrafetal insulin.

Blood amino acids were measured in twelve chronically catheterized mares and fetuses between 250 and 310 days gestation. The concentrations of the majority of individual amino acids were similar in maternal and fetal arterial blood and no gestational changes were detected. Only methionine, phosphoserine, 3-methyl-histidine and glutamine were consistently higher in the fetus than the mare, whilst certain other amino acids were higher in the maternal blood. Fasting the mares for 36 h led to significant falls in plasma glucose and rises in urea and maternal free fatty acids (FFA). Small but significant decreases in a few amino acids were seen in both fetus and mother, with an overall amino acid fall of 15% in the fetus and 13% in the mare. Virtually all amino acids had risen to basal values by 6 h after feeding. Intrafetal insulin (1 i.u./kg I.V.) as a bolus caused a more dramatic fall in fetal glucose than fasting, with no change in the mare. There were also rapid decreases in many amino acids by 30 min post-insulin and by 2 h all but five amino acids had fallen significantly. There was a drop in total fetal blood amino acids of 29%. These findings show that, in contrast to most other species studied, there is no overall feto-maternal gradient in blood amino acids in the mare, and that fasting leads to small falls in amino acid concentration, whereas intrafetal insulin induces a severe hypoglycaemia with dramatic decreases in almost all amino acids and no change in urea, suggesting a direct anabolic effect of insulin on fetal tissues.

Amino Acids↗
PubMed1993

Relationship between liver oxidant stress and antioxidant activity after zymosan peritonitis in the rat.

OBJECTIVE: To determine the effect of a severe nonbacterial-dependent peritonitis on the degree and time course of liver oxidant stress and antioxidant activity. DESIGN: Prospective, randomized, controlled study. SETTING: Animal laboratory. SUBJECTS: Thirty-eight male Sprague-Dawley rats were injected with zymosan 0.75 mg/g body weight, mixed in mineral oil, and fluid resuscitated. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Oxygen consumption (VO2), base deficit, and blood gases were determined. Liver tissue oxidized and reduced glutathione, malondialdehyde catalase, xanthine oxidase, and xanthine dehydrogenase were measured and data were compared with both a pair-fed and an ad libitum fed group over a 24-hr period. We noted a 30% mortality rate with animals dying between 20 and 24 hrs. Peak decrease in VO2 occurred at 12 hrs, corresponding with a metabolic acidosis. Marked liver oxidant stress was seen at 4 hrs with oxidized glutathione increased from a control value of 0.2 +/- 0.1 to 1.1 +/- 0.2 mg/g of tissue, while reduced glutathione decreased from a control value of 1.8 +/- 0.1 to 0.3 +/- 0.1 mg/g. By 24 hrs, oxidized glutathione activity was no longer increased, but reduced glutathione concentrations were still markedly decreased. Tissue catalase was also significantly decreased at the 24-hr period. Liver malondialdehyde was increased at 24 hrs when the peak decrease in antioxidants was evident. Liver xanthine oxidase activity increased significantly from 15 +/- 3 to 45 +/- 8 mumol uric acid/min/g by 4 hrs and remained increased, with the initial increase predating evidence of impaired perfusion. Pair-fed animals demonstrated no changes in oxidant or antioxidant activity. CONCLUSIONS: We conclude that a marked increase in liver oxidant stress and decrease in antioxidant activity occurs in the first several hours after the onset of nonbacterial peritonitis. An early increase in liver xanthine oxidase activity may be a source of the oxidants. Decreased liver antioxidant activity persists well after the oxidant stress resolves.

Acidosis, Lactic↗
PubMed1993

Quantitative elemental mapping of biomedical specimens using the nuclear microprobe.

Quantitative and structural elemental information is available from the nuclear microprobe through a time consuming fit of the (X-ray) spectrum at each point. An alternative technique is proposed which greatly shortens the analysis procedure and allows an increased number of samples to be processed. The method discussed here is to create elemental maps which, when they are divided by the charge/pixel and multiplied by a scaling factor, will form quantitative maps. The scaling factors are obtained from a calibration procedure comparing a large number of fitted X-ray spectra with the corresponding contents of selected energy windows. The technique also allows the reduction of artefacts due to spectral overlap, assuming that a simple background model can be used.

Animals↗
PubMed1993

The effect of acute nonbacterial dependent peritonitis on lung and liver oxidant stress and antioxidant activity.

BACKGROUND: The role of oxidant release and tissue antioxidant defenses on inflammation-induced organ injury is not clearly defined. METHODS: We determined the effect of acute zymosan peritonitis in rats on lung and liver tissue oxidant stress and antioxidant defenses during a 5-day period. Oxidant activity was measured as tissue malondialdehyde and oxidized glutathione (GSSG). Antioxidant activity was measured as tissue-reduced glutathione (GSH) and catalase activity. Rats were maintained hydrated with subcutaneous crystalloid. Animals were killed at 4, 12, and 24 hours and 5 days. RESULTS: Acute peritonitis was evident at 12 and 24 hours but was resolving at 5 days. Peritoneal fluid cultures were negative after 24 hours. A 50% mortality rate was noted between 20 and 30 hours, with no deaths after 30 hours. We noted a significant increase in lung GSSG and malondialdehyde at 4 hours that persisted for the 5 days, as did histologic evidence of a progressing severe lung inflammation. No increased conversion of lung xanthine dehydrogenase to xanthine oxidase was noted. Lung GSH and catalase activity were maintained at control despite negligible food intake. In contrast, liver GSSG was increased significantly only at the 4-hour period, corresponding with a transient conversion of xanthine dehydrogenase to xanthine oxidase from 10% to 31%. Tissue malondialdehyde did not increase despite the initial oxidant stress. However, tissue GSH and catalase values decreased by more than 50% after 24 hours and remained decreased at 5 days. CONCLUSIONS: We conclude that early lung and liver oxidant stress is initiated by acute peritonitis. Lung oxidant changes persist and lung dysfunction progresses, even though antioxidant activity is maintained and acute peritonitis is resolving. Liver lipid peroxidation did not develop despite oxidant release, probably because of a large antioxidant reserve. However, a severe and sustained decrease in liver antioxidants results, increasing the potential damage from a subsequent oxidant insult.

Animals↗
PubMed1993

Pentoxifylline does not prevent endotoxin induced lung and liver lipid peroxidation in the adult sheep.

Our purpose was to determine the effect of pentoxifylline pretreatment on endotoxin-induced (5 microgram/kg) lung and systemic oxidant activity, measured as lipid peroxidation. We used the awake adult sheep with lung and soft tissue lymph fistulae to monitor microvascular changes as well as to monitor oxygen delivery and consumption. Oxidant activity was monitored using the level of plasma conjugated dienes, a measure of circulating lipid peroxides, and lung and liver malondialdehyde content, a measure of tissue lipid peroxidation. Sixteen sheep were given endotoxin, eight of which were pretreated with pentoxifylline (20 mg/kg bolus) followed by a 6 mg/kg/hr infusion. We found that the degree of early endotoxin-induced pulmonary hypertension and hypoxia and later increased pulmonary microvascular permeability was not attenuated with pentoxifylline. In addition, a comparable increase in circulating conjugated dienes, lung neutrophil sequestration, and a three-fold increase in lung malondialdehyde was seen in both groups. Soft tissue QL also increased to the same degree in both groups. Liver MDA increased from a control of 110 +/- 20 nM/g tissue to 165 +/- 32 nM/g with endotoxin alone and to 260 +/- 55 nM/g with pentoxifylline pretreatment, a significant increase over both control and endotoxin alone groups. Pentoxifylline, however, did improve hemodynamic stability, required significantly less fluid, and prevented the hyperdynamic state seen at 4-5 hr post endotoxin. We conclude that pentoxifylline attenuates the initial endotoxin-induced hemodynamic instability, and later hyperdynamic state. However, pentoxifylline pretreatment does not appear to prevent endotoxin-induced oxygen radical release in the unanesthetized sheep.

Animals↗
PubMed1992

Relationship between hepatic blood flow and tissue lipid peroxidation in the early postburn period.

OBJECTIVES: To determine the effect of a body burn on effective or nutrient liver blood flow and the relationship between blood flow and oxidant-induced lipid peroxidation. DESIGN: Anesthetized sheep were given a 40% of total body surface, third-degree burn, after which animals were fluid resuscitated to return ventricular filling pressures and cardiac output to baseline values. Animals, for the 6-hr study period, were resuscitated with lactated Ringer's solution alone or lactated Ringer's solution plus 1500 mL of 5% hydroxyethyl starch or lactated Ringer's solution plus hydroxyethyl starch on which was complexed the iron chelator deferoxamine to prevent oxidant release. Effective liver blood flow was measured using the galactose infusion technique. Liver tissue lipid peroxidation was monitored using malondialdehyde content. RESULTS: We found that effective liver blood flow was decreased by 50% in the 4- to 5-hr postburn period, even when animals were resuscitated to baseline cardiac output values with lactated Ringer's solution. Tissue malondialdehyde content increased in the group treated with lactated Ringer's solution from a control value of 110 +/- 7 to 202 +/- 59 nmol/g of tissue. Resuscitation with hydroxyethyl starch restored postburn effective liver blood flow to control values, but malondialdehyde content was still increased two-fold. Resuscitation with hydroxyethyl starch and deferoxamine resulted in an increase in effective liver blood flow postburn to a value 80% above controls. In addition, lipid peroxidation was prevented. CONCLUSIONS: Effective liver blood flow is markedly decreased after burn injury, even with apparently adequate volume resuscitation, when using lactated Ringer's solution. Liver lipid peroxidation persists even when effective liver blood flow is maintained, indicating that the oxidant process is not solely related to blood flow. Infusion of the antioxidant deferoxamine during resuscitation not only prevents the lipid peroxidation, most likely by a nonblood-flow-related process, but also results in an increase in blood flow above normal rates, suggesting that postburn liver oxygen needs exceed normal values.

Animals↗
PubMed1992

Oxygen consumption early postburn becomes oxygen delivery dependent with the addition of smoke inhalation injury.

We determined the relationship between oxygen delivery, DO2, and oxygen consumption, VO2, in sheep after a moderate smoke inhalation injury and 15% TBSA third-degree burn compared with burn alone and controls. Comparison was made beginning three hours after injury when carboxyhemoglobin levels were back to baseline values. We decreased DO2 between three and eight hours by 25% by either removing blood (controls) or decreasing the resuscitation fluid infusion rate. Lung oxidant, measured as tissue malondialdehyde (MDA) levels, and histologic changes were also assessed. Animals were killed at 24 hours. We found that in controls and animals with a burn alone, a 25% decrease in DO2 was compensated for by an increase in O2 extraction, maintaining VO2 constant. Correlation of DO2 to VO2 was r2 = 0.3, indicating independence of VO2 from DO2. With the combined injury, VO2 decreased in proportion to DO2, since O2 extraction did not increase. The correlation of DO2 to VO2 was r2 = 0.9, indicating delivery-dependent consumption, a pathologic process most likely caused by increased inflammatory mediators from the combined injury. Lung lipid peroxidation was markedly increased in the combined injury, 148 +/- 18 nmol MDA/gram of tissue compared with burn alone, 64 +/- 5 nmol/g, or controls, 45 +/- 4 nmol/g. However, no decrease in arterial O2 tension or increase in lung water was noted, i.e., the sheep did not have ARDS, which is known to impair O2 extraction. We conclude that a pathologic O2 delivery-dependent consumption develops with the combination of burn and inhalation injury, increasing the potential for tissue hypoxemia. This change corresponds with increased lung tissue oxidant change.

Animals↗
PubMed1992

Lung oxidant changes after zymosan peritonitis: relationship between physiologic and biochemical changes.

Our purpose was to determine the effect of non-bacteria-dependent systemic inflammation on the degree and time course of lung oxidant activity and antioxidant defenses, comparing these changes with lung, physiologic, and histologic alterations. Adult male rats were given intraperitoneal zymosan (0.7 mg/g body weight) and were fluid resuscitated. Oxidant changes were measured as lung tissue oxidized glutathione (GSSG) and malondialdehyde (MDA) content, antioxidant defenses as tissue reduced glutathione (GSH), and catalase. Animals were killed at 4, 12, and 24 h, and at 5, 10, and 30 days. Lung data were compared with that found in liver. We noted a 45% mortality in the first 18 to 36 h with all remaining animals surviving. In the first 24 h, we noted a doubling of lung MDA and an 80% conversion of tissue GSH to GSSG compared with less than 5% in control animals, indicating a severe oxidant stress. These findings corresponded with marked increase in lung neutrophils. Arterial pressure (PaO2) was significantly decreased from a control of 95 +/- 4 mm Hg to 80 +/- 5 mm Hg and 75 +/- 4 mm Hg at Days 5 and 10, respectively, but returned toward control by 30 days. Lung GSSG and MDA remained significantly increased for the 30-day period, whereas amounts of the antioxidants, catalase, and GSH returned to control after 24 h. The ongoing oxidant stress corresponded with marked mononuclear cell infiltration and interstitial thickening, which persisted over the 30-day period even after peritonitis had completely resolved.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Burn edema is accentuated by a moderate smoke inhalation injury in sheep.

We determined the lung and systemic response of a moderate smoke inhalation injury combined with a 15% total body surface third-degree burn compared with a burn alone and inhalation alone. Adult sheep were prepared with chronic lung and bilateral prefemoral soft tissue lymph fistula. The burn was confined to one side. Physiologic parameters, lymph flow (QL), and lymph/plasma protein ratio were monitored. Oxidant changes were measured as lipid peroxidation by circulating and lymph-conjugated dienes and lung tissue malondialdehyde. Animals were resuscitated with lactated Ringer's solution during the 24-hour study period to restore and maintain vascular filling pressures and cardiac index. We found net 24-hour fluid balance for burn-inhalation injuries to be 4.1 +/- 1.2 L compared with burn alone of 2.9 +/- 0.9 L and inhalation alone of 2.4 +/- 0.5 L, a significant difference. Protein-rich burn tissue QL increased by fivefold to sixfold with burn alone compared with more than tenfold with burn-inhalation injury. A twofold increase in both lung and nonburn soft tissue QL was also seen in the combined injury not seen with burn alone. Arterial blood gases decreased only at 12 hours. Plasma conjugated dienes were increased in all groups, whereas burn lymph values were increased only in combined insult. In addition, lung malondialdehyde content at 24 hours was 155 +/- 11 nmol/gm with burn-inhalation injury compared with 62 +/- 8 nmol/L for burn alone, 55 +/- 9 nmol/L in inhalation alone, and 45 +/- 4 nmol/L for controls. However, no alveolar flooding was noted in any group. We conclude that a modest smoke inhalation (carboxyhemoglobin of 25%) added to a 15% total body surface burn markedly increases the degree of burn edema, as well as nonburn soft tissue and lung QL, compared with burn alone, indicating increased plasma to interstitial fluid transport in these tissues as well. Increased burn tissue lipid peroxidation products corresponded with the increased burn fluid losses. The increased lung lipid peroxidation also indicates further lung oxidant activity as well.

Animals↗
PubMed1992

Effect of dobutamine infusion on endotoxin-induced lipid peroxidation in awake sheep.

beta-agonists are known to not only increase oxygen delivery, but also attenuate the inflammatory response. We studied the effect of infusing the beta-agonist, dobutamine, on the oxidant-induced lung and liver tissue lipid peroxidation seen after endotoxemia. Twelve unanesthetized adult sheep with lung and soft tissue (prefemoral) lymph fistulae were given 5 micrograms/kg of Escherichia coli endotoxin intravenously. In six sheep, dobutamine 10 to 15 micrograms/kg/min was infused beginning 3 hours after endotoxin to increase oxygen delivery by 75% above baseline. Animals were killed at 6 hours, and lung and liver lipid peroxidation, measured as malondialdehyde, was obtained. Data were compared to six control sheep. Endotoxin alone produced increased lung and soft tissue vascular permeability as evidenced by a twofold increase in protein-rich lymph flow. Lung and liver malondialdehyde increased to 116 +/- 40 nmol/gm and 202 +/- 64 nmol/gm, respectively, compared to control values of 42 +/- 7 nmol/gm and 110 +/- 20 nmol/gm, respectively. Dobutamine infusion after endotoxin increased oxygen delivery by 75%, although changes in total oxygen consumption were not different from those seen with endotoxin alone. Lung and soft tissue lymph flow did not change with dobutamine. However, lung malondialdehyde was 41 +/- 17 nmol/gm, not different from controls. Liver malondialdehyde remained elevated at 164 +/- 26 nmol/gm. We conclude that dobutamine infusion prevents further oxidant-induced lung tissue lipid peroxidation but does not reverse the increased permeability already present. Liver lipid peroxidation was not decreased, suggesting the liver oxidant process may not be caused by the same mechanism as the lung lipid peroxidation.

Animals↗
PubMed1991

Effect of dobutamine on oxygen consumption and fluid and protein losses after endotoxemia.

OBJECTIVE: To determine the effect of a dobutamine infusion on the relationship between oxygen consumption (VO2) and oxygen delivery (DO2) after endotoxin administration, as well as the rate of fluid and protein loss from permeability-injured tissue. METHODS: Unanesthetized adult sheep with lung and soft-tissue lymph fistulas were given 5 micrograms/kg Escherichia coli endotoxin alone, or E. coli endotoxin plus a continuous infusion of dobutamine (10 to 15 micrograms/kg.min) beginning at 3 hrs. Lymph flow reflected the vascular permeability and surface area perfused. Data were compared with dobutamine alone and with controls. Filling pressures were maintained at baseline. RESULTS: Dobutamine alone produced a 75% increase in DO2, a transient 10 +/- 4% increase in VO2, but no increase in lung or soft-tissue lymph flow. Beginning at 3 hrs after endotoxin alone, a significant increase in protein-rich lung and soft-tissue lymph flow was noted, but only a transient 14 +/- 5% increase in VO2. Plasma proteins were slightly decreased. With the addition of dobutamine at 3 hrs postendotoxin, DO2 increased by greater than 50% for the 3-hr infusion period, while VO2 increased for a 30-min period by 25 +/- 8%, which was not different than endotoxin alone. Lung and soft-tissue lymph flow did not increase further, but plasma proteins did decrease significantly compared with controls and with endotoxin alone. CONCLUSION: Increasing DO2 with dobutamine postendotoxin does not increase the surface area perfused or the edema process, at least in lung and soft tissue. Therefore, no microvessels in these tissues are reopened with dobutamine when normal filling pressures are present. Dobutamine administration does not increase VO2 more than the increase seen with endotoxin alone.

Animals↗
PubMed1991

Fluid resuscitation with deferoxamine prevents systemic burn-induced oxidant injury.

We studied the effect of deferoxamine (DFO) infused after burns on hemodynamic stability as well as local and systemic inflammation and oxidant-induced lipid peroxidation. Eighteen anesthetized sheep were given a 40% of total body surface burn and fluid resuscitated to restore oxygen delivery (DO2) and filling pressures to baseline values. Animals were resuscitated with lactated Ringer's (LR) alone or LR plus 1,500 ml of a 5% hetastarch complexed with DFO (8 mg/ml). Animals were killed 6 hours postburn. The sheep resuscitated with LR and LR plus hetastarch demonstrated significant lung inflammation and significant increases in lung and liver malondialdehyde (MDA) from controls of 47 +/- 6 and 110 +/- 7 nMol/gm to 63 +/- 13 and 202 +/- 59 for LR and 67 +/- 4 and 211 +/- 9 for LR + hetastarch, respectively. The group resuscitated with hetastarch alone required 15% less fluid. VO2 returned to baseline values in both groups by 2 hours. Resuscitation with the 5% hetastarch-DFO decreased total fluids by 30% over LR and prevented the increase in lung and liver MDA. In addition, postburn VO2 increased by 25% above baseline values. Burn tissue edema, measured as protein-rich lymph flow, was significantly increased with the administration of DFO compared with the other groups. We conclude that DFO used for burn resuscitation prevents systemic lipid peroxidation and decreases the vascular leak in nonburn tissues while also increasing O2 utilization. Resuscitation with hetastarch-DFO may accentuate burn tissue edema, possibly by increased perfusion of burn tissue.

Animals↗
PubMed1991

The effect of caffeine on postprandial blood pressure in the frail elderly.

In a double-blind, random-order, cross-over study the effects of placebo and 100 mg of caffeine on postprandial sitting and erect blood pressure and heart rate were studied in 20 frail elderly subjects (mean age 84, range 75-93 years) after a standardized 400 K-calorie glucose drink. Maximal postprandial reduction in sitting systolic blood pressure occurred, at 60 minutes post-placebo, of - 11 mmHg (95% confidence interval -5 to -17 mmHg, P less than 0.01), and was attenuated by caffeine (P less than 0.05) with changes in systolic blood pressure, at 60 minutes post-drink, of 1 mmHg (95% CI -6 to 7 mmHg, not significant). Four subjects developed symptomatic postprandial hypotension after placebo which was prevented by caffeine. There were no significant changes in erect systolic blood pressure, postural systolic blood pressure change, sitting and erect, diastolic blood pressure and heart rate between treatment phases. Caffeine attenuates the postprandial fall in sitting blood pressure in frail elderly subjects and in particular prevented symptomatic blood pressure reductions in subjects with postprandial hypotension.

Aged↗
PubMed1991

Relationship between circulating tri-iodothyronine and cortisol in the perinatal period in the foal.

Pre- and post partum changes in plasma T3 have been examined in relation to plasma cortisol in 23 newborn foals (12 full term, 6 premature and 5 'twilight'), and in 5 fetuses catheterized in late gestation. Blood samples were collected daily from the fetuses and from the neonates at 30-min intervals for 2 h after birth; the plasma was assayed for T3 and cortisol by standard radioimmunoassay methods. In the full-term foals, plasma cortisol and T3 concentrations were high at birth (67.4 +/- 6.1 and 4.3 +/- 0.3 ng/ml respectively) and rose to a maximum during the following 2-h period to 141.0 +/- 8.8 ng/ml and 8.4 +/- 0.5 ng/ml. The corresponding changes in the premature foals over the same period were significantly lower (P less than 0.01; 17.2 +/- 2.2 to 27.0 +/- 4.3 ng cortisol/ml and 2.9 +/- 0.5 to 5.4 +/- 0.6 ng T3/ml). In the 'twilight' group, intermediate increases in both cortisol and T3 were observed. In the 5 chronically catheterized fetuses, both plasma cortisol and T3 were low in the last few weeks of gestation (7.0 +/- 1.1 ng/ml and 1.2 +/- 0.2 ng/ml respectively). In 2 fetuses there was little or no increase in plasma cortisol or T3 before induction of labour at about 320 days; one foal was premature and the other 'twilight'. Infusion of adrenocorticotrophic hormone for 4.5 days into the third fetus from 309 days led to an increase in both cortisol and T3 and the birth of a viable, full term foal. The 2 remaining fetuses were delivered spontaneously, one at term and one at 300 days (well before term). The latter was viable but dysmature; it showed a slight prenatal rise in plasma cortisol with little change in T3. When all the data were combined from both fetuses and neonates a significant positive correlation between plasma T3 and cortisol was found (P less than 0.001). These results demonstrate a relationship between circulating cortisol and T3 in the perinatal period and show that prematurity is associated with low concentrations of both hormones.

Adrenocorticotropic Hormone↗