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PubMed1991

Physiological responses of sheep to two hours anaesthesia with diazepam-ketamine.

The cardiopulmonary effects of repeated intravenous injections of a combination of diazepam and ketamine for anaesthesia were evaluated in six domestic sheep. Induction doses of 0.375 mg/kg and 7.5 mg/kg were followed by maintenance doses of 0.188 mg/kg and 3.75 mg/kg every 15 minutes for 105 minutes. Although this dosing regimen produced the desired anaesthetic effects, it caused untoward cardiopulmonary effects. Salient features of multiple dosing with diazepam and ketamine were hypoventilation, respiratory acidosis and an increase in both systemic and pulmonary vascular resistance.

Anesthesia, Intravenous↗
PubMed1996

Clinical comparison of medetomidine with xylazine/l-methadone in dogs.

Seventy-two healthy dogs required sedation and analgesia for a variety of procedures causing discomfort or pain. They were treated either with the alpha 2-agonist medetomidine at 40 micrograms/kg (15 intravenously and 17 intramuscularly), or 80 micrograms/kg (15 intravenously and 15 intramuscularly) or with xylazine plus l-methadone (1.0 mg)(10 intravenously). The levels of sedation, analgesia and safety were compared clinically and by measurements of the effects on the electrocardiogram (ECG) and blood gases, body temperature, haematology and clinical chemistry. Sedation was achieved reliably with both medetomidine and xylazine plus l-methadone but its onset, depth and duration were influenced by the dose and route of administration. In the medetomidine-treated dogs, intravenous administration resulted in more rapid sedation and the effects of the higher dose were deeper and longer lasting. The small dogs receiving 40 micrograms/kg may have been underdosed. The initial analgesic effects in response to a pin prick to the body surface were sufficient and similar for both drugs, except for the intramuscular dose of 40 micrograms/kg medetomidine. Analgesia for the clinical procedures was less reliable with medetomidine and was not always adequate even at the high dose, but xylazine plus l-methadone assured analgesia in almost every case. Medetomidine resulted in marked bradycardia, lasting as long as the sedation and the ECG revealed a sinus arrhythmia with sinoatrial and atrioventricular blocks grade I and II as a sign of interference with transduction. The bradycardia with xylazine plus l-methadone was less pronounced. A decrease in respiratory rate accompanying sedation had no influence on blood gases and blood acidity in the dogs treated with medetomidine but caused a respiratory acidosis with xylazine plus l-methadone. Body temperature decreased with all treatments for the duration of the period of sedation. Blood glucose concentration increased to a similar extent in all treatment groups, but all other haematological and clinicochemical variables remained unchanged. Treatment with the specific alpha 2 antagonist, atipamezole, reversed the sedation and cardiovascular and pulmonary effects due to medetomidine within minutes.

Analgesics↗
PubMed1999

Comparison of two combinations of sedatives before anaesthetising pigs with halothane and nitrous oxide.

Two groups of 21 three-month-old Landrace x Large White pigs were sedated with either azaperone (2 mg/kg), butorphanol (0.2 mg/kg) and ketamine (5 mg/kg) (group A), or detomidine (100 microg/kg), butorphanol (0.2 mg/kg) and ketamine (5 mg/kg) (group D) administered intramuscularly, before being anaesthetised with halothane, oxygen and nitrous oxide for a bilateral stifle arthrotomy. The pigs' heart rate, respiratory rate, mean arterial blood pressure, electrocardiogram, arterial oxygen saturation, arterial blood gases, and oesophageal and rectal temperature were measured while they were anaesthetised and five minutes after they were disconnected, and their recovery times and any complications were recorded. Both groups were well sedated. Their heart rate was unchanged during the period of anaesthesia but increased when they recovered. The respiratory rate, mean arterial blood pressure and rectal temperature were lower in group A than in group D (P<0.05). Mild respiratory acidosis developed during anaesthesia in both groups. Both groups recovered equally rapidly and complications were generally minor, though two pigs in group D appeared to develop malignant hyperthermia.

Anesthesia, Inhalation↗
PubMed1999

Effects of glucose infusion on the endocrine, metabolic and cardiorespiratory responses to halothane anaesthesia of ponies.

Glucose was infused intravenously into six ponies during halothane anaesthesia, to evaluate its effect on their endocrine response to anaesthesia. The ponies were premedicated with acepromazine, and anaesthesia was induced with thiopentone and maintained with halothane in oxygen for two hours. Glucose was infused to maintain the plasma glucose concentration above 20 mmol/litre. Anaesthesia was associated with hypothermia, a decrease in haematocrit, hypotension, hyperoxaemia, respiratory acidosis and an increase in the plasma concentrations of lactate and arginine vasopressin. The concentration of beta-endorphin in plasma increased transiently after 20 minutes but there were no changes in concentrations of adrenocorticotrophic hormone, dynorphin, cortisol or catecholamines. These data suggest that the glucose infusion attenuated the normal adrenal response of ponies to halothane anaesthesia.

Adrenal Glands↗
PubMed2003

The essential role of carotid body chemoreceptors in sleep apnea.

Sleep apnea is attributable, in part, to an unstable ventilatory control system and specifically to a narrowed "CO2 reserve" (i.e., the difference in P(a)CO2 between eupnea and the apneic threshold). Findings from sleeping animal preparations with denervated carotid chemoreceptors or vascularly isolated, perfused carotid chemoreceptors demonstrate the critical importance of peripheral chemoreceptors to the ventilatory responses to dynamic changes in P(a)CO2. Specifically, (i) carotid body denervation prevented the apnea and periodic breathing that normally follow transient ventilatory overshoots; (ii) the CO2 reserve for peripheral chemoreceptors was about one half that for brain chemoreceptors; and (iii) hypocapnia isolated to the carotid chemoreceptors caused hypoventilation that persisted over time despite a concomitant, progressive brain respiratory acidosis. Observations in both humans and animals are cited to demonstrate the marked plasticity of the CO2 reserve and, therefore, the propensity for apneas and periodic breathing, in response to changing background ventilatory stimuli.

Animals↗
PubMed2004

Entristar skin-level gastrostomy tube: primary placement with radiologic guidance in patients with amyotrophic lateral sclerosis.

PURPOSE: To retrospectively review the authors' experience with a radiologic method of primary insertion of a skin-level gastrostomy tube (Entristar; Tyco Healthcare, Mansfield, Mass) in patients with amyotrophic lateral sclerosis (ALS). MATERIALS AND METHODS: Over a 12-month period (September 2002 through September 2003), 25 patients with ALS (mean age, 62.4 years; age range, 41-83 years; 15 men, 10 women) who had bulbar impairment and a body mass index of less than 20 kg/m(2) or weight loss of greater than 10% were selected for placement of an enteral feeding tube. Patients with overnight oxygen desaturation or respiratory acidosis were referred for placement of the Entristar tube with radiologic guidance. This procedure was performed with local anesthesia and without sedation by using a modified percutaneous lateral fluoroscopic technique that aided tube insertion in patients with elevation of the hemidiaphragm and a "high" stomach position. Technical success and immediate and delayed procedure complications were recorded. RESULTS: The Entristar tube was successfully inserted in all 25 patients. Pneumoperitoneum as an early complication was documented in one patient, and one patient developed a pelvic abscess that required drainage. Follow-up for a median of 112 days (range, 14-343 days) revealed superficial wound infections in four patients and weight gain in two patients; weight gain necessitated tube replacement in one patient. There were no procedure-related deaths. CONCLUSION: Radiologically guided insertion of the Entristar skin-level gastrostomy tube is a safe procedure in patients with ALS that allows the creation of a permanent feeding gastrostomy without the need for sedation or endoscopy.

Adult↗
PubMed1980

Effect of NH4Cl on phosphaturic response to PTH in the hamster: dissociation from acidemia.

Previous studies indicate that the hamster fasted for 16 h fails to demonstrate a significant phosphaturic response to parathyroid hormone (PTH). However, when hamsters were infused with ammonium chloride, a phosphaturic response to PTH was observed. The present studies evaluate the respective roles of acidemia and the ammonium ion in this response. As in previous studies, fasted thyroparathyroidectomized (TPTX) hamsters infused with PTH showed no significant increase in the fractional excretion of phosphate (FE rho), from 19 +/- 2 to 22 +/- 1%. Neither respiratory acidosis (hypercapnia) nor metabolic acidosis (HCl infusion) enhanced the phosphaturic effect of PTH, FE rho 21 +/- 4 to 20 +/- 6 and 15 +/- 2 to 16 +/- 3%, respectively. Both ammonium chloride and ammonium bicarbonate infusions enhanced the phosphaturic response; FE rho increased from 15 +/- 5 to 27 +/- 5% (P < 0.02) and 17 +/- 3 to 25 +/- 3% (P < 0.05), respectively. We conclude that the enhancement of the phosphaturic effect of PTH in the fasted hamster by ammonium chloride infusions can be dissociated from acidemia.

Acidosis↗
PubMed1985

Effect of systemic acid-base disorders on colonic intracellular pH and ion transport.

We have previously reported that changes in colonic net Na and Cl absorption correlate with arterial CO2 partial pressure (PCO2) and that changes in colonic net Cl absorption and HCO3 secretion correlate with the plasma HCO3 concentration during the systemic acid-base disorders. To determine whether changes in intracellular pH (pHi) and HCO3 concentration [( HCO3]i) mediate these effects, we measured pHi and calculated [HCO3] in the distal colonic mucosa of anesthetized, mechanically ventilated Sprague-Dawley rats using 5,5-[14C]dimethyloxazolidine-2,4-dione and [3H]inulin. Rats were studied during normocapnia, acute respiratory acidosis and alkalosis, and uncompensated and pH-compensated acute metabolic acidosis and alkalosis. When animals in all groups were considered, there were strong correlations between mucosal pHi and both arterial PCO2 (r = -0.76) and pH (r = 0.82) and between mucosal [HCO3]i and both arterial PCO2 (r = 0.98) and HCO3 concentration (r = 0.77). When we considered the rates of colonic electrolyte transport that characterized these acid-base disorders [A. N. Charney and L. P. Haskell. Am. J. Physiol. 246 (Gastrointest. Liver Physiol. 9): G159-G165, 1984], we found strong correlations between mucosal pHi and net Na absorption (r = -0.86) and between mucosal [HCO3]i and both net Cl absorption (r = 0.98) and net HCO3 secretion (r = 0.83). These findings suggest that the systemic acid-base disorders cause changes in colonic mucosal pHi and [HCO3]i as a consequence of altered arterial PCO2 and HCO3 concentration. In addition, the effects of these disorders on colonic electrolyte transport may be mediated by changes in mucosal pHi and [HCO3]i.

Acid-Base Imbalance↗
PubMed1986

Effect of systemic acid-base disorders on ileal intracellular pH and ion transport.

We previously reported that changes in ileal net Na absorption correlated with arterial pH, changes in net HCO3 secretion correlated with the plasma HCO3 concentration, and changes in net Cl absorption correlated with arterial CO2 partial pressure (PCO2) during the systemic acid-base disorders. To determine whether changes in intracellular pH (pHi) and HCO3 concentration [( HCO3]i) mediated these effects, we measured pHi and calculated [HCO3]i in the distal ileal mucosa of anesthetized, mechanically ventilated Sprague-Dawley rats using 5,5-[14C]dimethyloxazolidine-2,4,-dione and [3H]inulin. Rats were studied during normocapnia, acute respiratory acidosis, and alkalosis, and uncompensated and pH-compensated acute metabolic acidosis and alkalosis. When animals in all groups were considered, mucosal pHi was not altered, but there were strong correlations between mucosal [HCO3]i and both arterial PCO2 (r = 0.97) and [HCO3] (r = 0.61). When we considered the rates of ileal electrolyte transport that characterized these acid-base disorders [A. N. Charney and L.P. Haskell, Am. J. Physiol. 245 (Gastrointest. Liver Physiol. 8): G230-G235, 1983], we found strong correlations between mucosal [HCO3]i and both net Cl absorption (r = 0.88) and net HCO3 secretion (r = 0.82). These findings suggest that the systemic acid-base disorders do not affect ileal mucosal pHi but do alter mucosal [HCO3]i as a consequence of altered arterial PCO2 and [HCO3]. The effects of these disorders on ileal net Cl absorption and HCO3 secretion may be mediated by changes in [HCO3]i. Arterial pH does not appear to alter ileal Na absorption through changes in the mucosal acid-base milieu.

Acid-Base Imbalance↗
PubMed1976

Importance of pulmonary ventilation in respiratory control in the bullfrog.

Pulmonary and cutaneous O2 consumption (Vo2) and CO2 production (Vco2) were measured simultaneously in bullfrogs Rana catesbeiana at 20 degrees C. The lungs were responsible for 77.3-91.0% of the total Vo2 and 28.5-74.9% of the total VCO2. The distribution of the total exchange between the lungs and skin depended on metabolic rate; frogs with higher rates relied more heavily on the pulmonary mode for both Vo2 and Vco2. When prevented from ventilating their lungs in an O2-rich environment, bullfrogs developed severe respiratory acidosis, demonstrating the importance of lung exchange in normal acid-base balance. When frogs were totally submerged in an O2-saturated medium, skin Vco2 increased linearly to a steady-state value which approximated the preapneic total Vco2. In these same animals, arterial Pco2 increased proportionately to the increase in skin Vco2, indicating that skin diffusion capacity for CO2 was unaffected. We conclude that the control of breathing in the bullfrog in response to changes in metabolic rate relies predominantly on changes in lung ventilation while the skin plays a more passive role.

Animals↗
PubMed1977

Acid-base balance and plasma composition in the aestivating lungfish (Protopterus).

Upon entering into aestivation, Protopterus aethiopicus develops a respiratory acidosis. A slow compensatory increase in plasma bicarbonate suffices only to partially restore arterial pH toward normal. The cessation of water intake from the start of aestivation results in hemoconcentration and marked oliguria. The concentrations of most plasma constituents continue to increase progressively, and the electrolyte ratios change. The increase in urea concentration is disproportionately high for the degree of dehydration and constitutes an increasing fraction of total plasma osmolality. Acid-base and electrolyte balance do not reach a new equilibrium within 1 yr in the cocoon.

Acclimatization↗
PubMed1987

Membrane-associated carbonic anhydrase in gills of the blue crab, Callinectes sapidus.

The presence of the enzyme carbonic anhydrase (CA) on the basal membrane of the branchial endothelial cells in the blue crab and its physiological significance were studied in vivo using a membrane-impermeant CA inhibitor, quaternary ammonium sulfanilamide (QAS). Injection of QAS into the hemolymph of Callinectes sapidus resulted in the rapid development of a respiratory acidosis; PCO2 rose almost 2 Torr, pH was lowered by approximately 0.25 units, and total CO2 rose by 2 mM. These results support the hypothesis that membrane-associated CA exposed to hemolymph is present in the crustacean gill and that it is physiologically significant in mobilizing hemolymph HCO-3 to CO2 to facilitate CO2 excretion across the gill. The recovery from this acidosis coincides with the clearance of the inhibitor from the hemolymph. Hemolymph osmotic and ionic parameters were unaffected by QAS, reconfirming the role of branchial cytoplasmic CA in ion regulation and also providing a convenient bioassay for determining CA inhibitor permeability in the intact organism.

Acid-Base Equilibrium↗
PubMed2001

Developmental changes in intracellular pH regulation in medullary neurons of the rat.

We examined intracellular pH (pH(i)) regulation in the retrotrapezoid nucleus (RTN), a CO(2)-sensitive site, and the hypoglossal nucleus, a nonchemosensitive site, during development (postnatal days 2-18) in rats. Respiratory acidosis [10% CO(2), extracellular pH (pH(o)) 7.18] caused acidification without pH(i) recovery in the RTN at all ages. In the hypoglossal nucleus, pH(i) recovered in young animals, but as animal age increased, the slope of pH(i) recovery diminished. In animals older than postnatal day 11, the pH(i) responses to hypercapnia were identical in the hypoglossal nucleus and the RTN, but hypoglossal nucleus and RTN neurons could regulate pH(i) during intracellular acidification at constant pH(o) at all ages. Recovery of pH(i) from acidification in the RTN depended on extracellular Na+ and was inhibited by amiloride but was unaffected by DIDS, suggesting a role for Na+/H+ exchange. Hence, pH(i) regulation during acidosis is more effective in the hypoglossal nucleus in younger animals, possibly as a requirement of development, but in older juvenile animals (older than postnatal day 11), pH(i) regulation is relatively poor in chemosensitive (RTN) and nonchemosensitive nuclei (hypoglossal nucleus).

Acidosis↗
PubMed2006

Roles of cytosolic and membrane-bound carbonic anhydrase in renal control of acid-base balance in rainbow trout, Oncorhynchus mykiss.

We tested the hypothesis that cytosolic and membrane-associated carbonic anhydrase (CA IV) are involved in renal urinary acidification and bicarbonate reabsorption in rainbow trout. With the use of homological cloning techniques, a 1,137-bp cDNA was assembled that included an open reading frame encoding for a deduced protein of 297 amino acids. Phylogenetic analysis revealed that this protein was likely a CA IV isoform. With the use of this sequence and a previously described trout cytosolic isoform [tCAc (13)], tools were developed to quantify and localize mRNA and protein for the two CA isoforms. Unlike tCAc, which displayed a broad tissue distribution, trout CA IV mRNA (and to a lesser extent protein) was highly and preferentially expressed in the posterior kidney. The results of in situ hybridization, immunocytochemistry, and standard histological procedures demonstrated that CA IV was likely confined to epithelial cells of the proximal tubule with the protein being expressed on both apical and basolateral membranes. The CA IV-containing tubule cells were enriched with Na(+)-K(+)-ATPase. Similar results were obtained for tCAc except that it appeared to be present in both proximal and distal tubules. The levels of mRNA and protein for tCAc increased significantly during respiratory acidosis (hypercapnia). Although tCA IV mRNA was elevated after 24 h of hypercapnia, tCA IV protein levels were unaltered. By using F3500, a membrane-impermeant (yet filtered) inhibitor of CA, in concert with blood and urine analyses, we demonstrated that CA IV (and possibly other membrane-associated CA isoforms) plays a role in urinary acidification and renal bicarbonate reabsorption.

Absorption↗
PubMed1981

Determination of disequilibrium pH in the rat kidney in vivo: evidence of hydrogen secretion.

The recent demonstration of elevated PCO2 in structures of the rat renal cortex indicated that previous determinations of disequilibrium pH (pHDq), and thus the differentiation of H+ secretion from bicarbonate reabsorption per se, required further evaluation. A new aspiration pH electrode was developed to allow tubule fluid to achieve chemical equilibrium at the PCO2 prevailing in vivo. In control and bicarbonate-loaded rats a pHDq was not observed in either proximal or distal tubules. After intravenous benzolamide a significant acid pHDq was observed in the proximal (but not the distal) nephron, and increased further during metabolic alkalosis. During combined metabolic alkalosis and respiratory acidosis a significant pHDq was present in the distal but not in the proximal tubule. Aldosterone administration to bicarbonate-loaded, hypercapnic rats did not alter the distal pHDq further. When present, the pHDq in the distal tubule was obliterated by carbonic anhydrase infusion. We conclude that proximal but not distal tubule fluid is in functional contact with carbonic anhydrase; the enzyme is in excess in the proximal lumen and H2CO3 did not accumulate even during conditions associated with increased H+ secretion; the basal rate of H+ secretion in the distal nephron accessible to cortical micropuncture is less than previously assumed. The data support the view that H+ secretion is the major mechanism of renal bicarbonate reabsorption.

Acid-Base Equilibrium↗
PubMed1986

ATP turnover and renal response of dog tubules to pH changes in vitro.

In vivo the dog kidney responds to metabolic or respiratory acidosis by a marked increment of its ammonia production (expressed per 100 milliliters glomerular filtration rate). This phenomenon is related to a switch from metabolic utilization of nonammoniagenic (lactate) to ammoniagenic (glutamine) substrates to support ATP turnover in the proximal tubules. We have proposed that in vivo the maximum activity of the ammoniagenic process is fixed by the ATP turnover in this segment of the nephron. The maximal glutamine metabolism is reached when 100% of this turnover is supported by glutamine metabolism. We have studied how these concepts apply to the adaptation of glutamine metabolism and ammonia production to a low pH in vitro using proximal tubules of dogs incubated when one (lactate or glutamine) or several (glutamine plus lactate or plus palmitate) substrates are provided. At pH 7.4 glutamine alone supports already 71-76% of the tissue ATP turnover (minimal and maximal values). With acidification this fraction rises to nearly 87-94%, but this increases only modestly the ammonia production. Reducing the ATP turnover with ouabain at pH 7.4 decreases the absolute glutamine utilization, which now supports only 45-50% of the ATP turnover. Again acidification increases this fraction to 90-99%. Addition of lactate with glutamine displaces part of the glutamine metabolized, but greatly stimulates the synthesis of alanine. Fatty acids depress ammonia production and blunt the tissue response to acidification. Gluconeogenesis from lactate is minimally influenced by incubation pH. It is concluded that the ATP turnover limits the metabolism of glutamine by proximal tubules in vitro as in vivo in the dog, and that the response to acidification is small in vitro because of the absence of alternative substrates.

Adenosine Triphosphate↗
PubMed1990

PCO2 in renal cortex.

In a number of recent investigations a renal cortical PCO2 higher than that of systemic blood was reported. We have studied this problem with the use of micro-Severinghaus electrodes based on antimony, H+ liquid ion exchange, and glass pH electrodes with an inner buffer solution containing 0.5 mg/ml carbonic anhydrase (CA). Measurements in renal cortical structures (renal tubules, star vessels, capillaries, and glomeruli in Munich-Wistar rats) were compared with determinations in renal vein or artery performed with the same electrode in sequence. No significant differences in PCO2 were found between cortical structures and renal vein in control rats, in metabolic alkalosis, respiratory acidosis and alkalosis, and after CA inhibition. Nevertheless, absolute PCO2 levels, which followed the PCO2 of systemic blood, were markedly different in these groups. Measurements of pH and PCO2 at the same tubule site were compatible with HCO3- determinations in tubule fluid in vitro (made with use of the Henderson-Hasselbalch equation) in control rats. When proximal tubules were pump-perfused in vivo with a solution containing 30 mM NaHCO3, measured PCO2 approached that of the perfusing solution at high pump rates, and approached the free-flow value as rates were reduced to zero, indicating that the CO2 generated in the lumen equilibrated rapidly across the epithelium. Reducing renal blood flow by aortic clamping reduced renal cortical PCO2. In conclusion, in a large number of experimental conditions renal cortical PCO2 was never higher than that measured in systemic blood.

Animals↗
PubMed1975

Effect of chronic hypercapnia on body temperature regulation.

Guinea pigs and rats exposed to 15% CO2 for 7 days showed a parallel time course of changes in pH, body temperature (TB), and oxygen consumption (VO2). Between 1 and 6 h of exposure the maximal drop in actual pH occurred in guinea pigs simultaneously with the maximal fall in TB and VO2. During the subsequent period pH TB, VO2 rose again. Skin blood content (heat loss) also exhibited a biphasic pH-dependent time course. Animals showing no partial compensation of respiratory acidosis during 3 days exposure also failed in raising their TB back to normal in this time. The behavior of TB was found to be a good indicator of the acid-base status and adaptive potential of the animals to hypercapnia. Similar results were obtained in rats. Thermo-regulatory processes in the hypothalamus were affected during exposure to 15% CO2. Both guinea pigs and rats showed a decrease in norepinephrine content of the hypothalamus during the first part of exposure reaching a maximal fall at the end of 24 h. The serotonin content increased slightly during this period. During prolonged exposure to 3% CO2 for 7 days, TB showed a transient rise, and VO2 was slightly elevated.

Adaptation, Physiological↗