Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

d-Tubocurarine (dTc) was infused intravenously into 35 cats anesthetized with chloralose and urethane at a constant continuous rate to produce and maintain 90 per cent depression of twitch height of the anterior tibial muscle following supramaximal stimulation of the peroneal nerve. The mean infusion rates that produced 90 per cent depression were not significantly altered by respiratory acid-base changes. Metabolic alkalosis decreased (32.5 per cent) and metabolic acidosis increased (27.7 per cent) the required infusion rate of dTc. When pH and Paco2 were maintained at 7.37 and 38 torr, respectively, the addition of a bolus of neostigmine, 10.5 mug/kg, intravenously, to the continuing infusion of dTc produced 50 per cent antagonism of the dTc-depressed twitch. Respiratory alkalosis and metabolic acidosis did not alter the dose of neostigmine needed to produce 50 per cent antagonism. However, during respiratory acidosis (pH 7.13, Paco2 66 torr) and metabolic alkalosis (pH 7.59, Paco2 36 torr) 20.0 and 18.0 mug/kg neostigmine, respectively, were needed to produce 50 per cent antagonism. Still larger doses of neostigmine (75 mug/kg) could not completely antagonize the block unless pH and Paco2 were returned to 7.30-7.50 and 35-45 torr, respectively. It is concluded that respiratory acidosis and metabolic alkalosis limit and oppose antagonism of dTc by neostigmine.
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PMID:The effect of acid-base balance on neostigmine antagonism of d-tubocurarine-induced neuromuscular blockade. 23 27

In 40 cases anesthetized with chloralose and urethane, pancuronium was infused i.v. at a constant rate to produce and maintain 90% depression twitch tension of the anterior tibialis muscle following supramaximal stimulation of the peroneal nerve. Neither respiratory alkalosis nor metabolic acidosis influenced the infusion rate required to produce 90% depression of twitch tension or antagonism of this depression yb neotigmine. Respiratory acidosis (pH 7.15; PaCO2 10 kPa) did not alter the required infusion rate but did prevent complete antagonism by neostigmine. Metabolic alkalosis (pH 7.65; PaCO2 4.8 kPa) reduced both the required infusion rate and prevented complete restoration of twitch tension by neostigmine. The duration of neostigmine antagonism was shortened by metabolic alkalosis. We conclude that respiratory acidosis and metabolic alkalosis prevent antagonism of pancuronium by neostigmine.
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PMID:Acid-base balance and neostigmine antagonism of pancuronium neuromuscular blockade. 65 47

Drug-induced acid-base disorders may be classified into four categories with respect to the mechanism. 1. Metabolic acidosis is induced by a large acid loads incurred from exogenous sources (e.g. NH4Cl, or toxin ingestion) or endogenous acid production (e.g. generation of ketoacids or lactic acids by alcohol or phenformin) or base loss (e.g. abuse of laxatives). 2. Metabolic alkalosis results from exogenous bicarbonate loads (e.g. milk-alkali syndrome) or effective extracellular fluid contraction, potassium depletion plus hyperaldosteronism (e.g. vomiting, diuretics, or licorice). 3. Renal tubular acidosis is induced by the drugs which mainly impair proximal and/or distal tubules (e.g. vitamin D, NSAID, acetazolamide or amphotericin B). 4. Respiratory acidosis or alkalosis results from drug-induced respiratory center depression or neuromuscular impairment (e.g. anesthetic, sedative overdosage or curare) or hyperventilation (salicylates, paraldehyde, epinephrine, or nicotine).
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PMID:[Drug-induced acid-base disorders]. 143 17

Two adult Hampshire rams, unrelated and from separate farms, were examined for the cause of intermittent bloat and, or anorexia which lasted for three to six weeks and caused depression and cachexia. The rumen of each ram was hypermotile and ballottement of the ventral abdomen of each animal revealed an enlarged doughy viscus. Mild prerenal azotaemia, hypokalaemia with metabolic alkalosis, and high rumen chloride concentrations were evident. One ram died during the induction of anaesthesia for an abomasotomy and the other was euthanased after unsuccessful medical therapy. The abomasum of each ram was four to six times larger than that of a normal adult ram and filled with coarse, semi-moist, impacted ingesta. This abnormality was clinically identical to the abomasal emptying syndrome which has been described only in the Suffolk breed.
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PMID:Abomasal dilatation and impaction in two Hampshire rams. 162 57

Ten male and 4 female dogs with chronic hypertrophic pyloric gastropathy were seen at the Sydney Veterinary Teaching Hospital in the period 1982-88. The most commonly affected breeds were the Shihtzu and Maltese. The mean age was 8.2 yr and the mean body weight 6.5 kg. The most common clinical signs were vomiting, weight loss, polydipsia and depression. Hypokalaemia was present in 11 of 12 dogs examined and hypochloraemia in 10 of 11 dogs examined. Five of the six dogs that had blood gases measured were found to have a metabolic alkalosis. Surgery was performed on 13 dogs; pyloromyotomy 7, pyloroplasty 4, gastroduodenostomy 2. There was a recurrence of symptoms in one pyloromyotomy dog, and fatal ulceration and perforation of the cardia occurred in one pyloroplasty case. The remaining 11 dogs had a mean known symptom-free survival time of 20 mo. This study confirms the preponderance of affected males, identifies electrolyte and blood gas disturbances as significant complication of chronic hypertrophic pyloric gastropathy, and suggests that relatively minor surgery (pyloromyotomy) may have a place in the treatment of a selected subgroup of cases.
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PMID:Chronic hypertrophic pyloric gastropathy in 14 dogs. 226 3

In vivo studies were performed in the dog to verify if sodium lactate had an important effect on the metabolism of glutamine by the kidney. The animals were infused with 0.6 M sodium lactate to induce acute metabolic alkalosis with plasma bicarbonate of 29.7 mM. During these experiments, it was demonstrated that the renal uptake of glutamine increased by 46%, while the renal production of ammonia was unchanged. The renal production of alanine rose from 6.0 to 16.8 mumol/min. Plasma concentration of lactate increased from 1.3 to 19.2 mM, while that of pyruvate increased from 0.075 to 0.454 mM. In the renal tissue, alpha-ketoglutarate, malate, oxaloacetate, lactate, pyruvate, citrate, and alanine increased significantly. Similar changes were found in the liver and skeletal muscle. The observed changes are best described by transamination of pyruvate and glutamate under the influence of alanine aminotransferase (GPT). It can be calculated that this reaction was responsible for 76% of the production of ammonia from glutamine, the latter being necessary to provide glutamate for the synthesis of alanine. Dogs infused with 0.3 M sodium bicarbonate instead of sodium lactate with the same degree of acute metabolic alkalosis, showed a depression of 40% in the renal uptake of glutamine with a 38% decrease in renal ammoniagenesis and a 20% fall in the production of alanine. The present studies demonstrate that the production of ammonia from glutamine is not necessarily related to changes in acid-base balance, but may be associated with biochemical alterations related to the synthesis of alanine by the kidney.
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PMID:The metabolic response of the kidney to acute sodium lactate alkalosis. 286 25

Although used as a condiment and essential supplement since pre-Biblical times, chlorine as a part of the molecule salt has received little research effort by large animal nutritionists. Its low cost and the continued popularity of salt as a condiment and sodium supplement has precluded the appearance of chloride deficiencies. There is great variation in the chloride and sodium content of feedstuffs fed to lactating cows so that some formulations require no supplemental chloride or sodium. Chloride is highly available from feedstuffs, and when dietary chloride is low, the cow can reduce sharply her losses of chloride in urine, feces, skin secretions, and to some degree in milk. Clinical symptoms of chloride deficiency in the lactating cow include pica, lethargy, anorexia, lowered milk yield, constipation, and cardiovascular depression. Metabolic changes are expressed as a severe primary hypochloremia, secondary hypokalemia, and metabolic alkalosis. Requirement for chloride by the lactating cow is about .20%; a working allowance of .25% seems reasonable for cows in positive energy balance. With gradual resolution of the requirements for chloride and more data on chloride in feedstuffs, use of supplemental salt for either sodium or chloride can be reduced greatly.
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PMID:Mineral utilization by the lactating cow--chlorine. 370 Jul 98

Forty-three patients with panic disorder or agoraphobia with panic attacks and 20 control subjects received 0.5 M racemic sodium lactate intravenous infusions, single-blind as to duration and sequence. During the procedure, pulse; blood pressure; blood L-lactate and pyruvate; plasma ionized calcium, phosphate, prolactin, epinephrine, norepinephrine, and cortisol levels; and venous PCO2, pH, and bicarbonate were measured in an attempt to clarify the mechanism of lactate-induced panic attacks. During the infusion, 72% of the patients but none of the control subjects had panic attacks. The laboratory findings suggest that peripheral catecholamine surge is not the mechanism by which lactate causes panic, although elevated epinephrine may be a predisposing factor. Heightened central noradrenergic activity was present in many but not all of the attacks. Contrary to previous hypotheses, neither depression of ionized calcium nor induction of metabolic alkalosis appears sufficient to cause panic during lactate infusion.
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PMID:Possible mechanisms for lactate's induction of panic. 395 91

Early-lactation Holstein cows fed a corn silage-based diet low in chloride and supplemented with sodium bicarbonate were observed for clinical, metabolic, and production alterations over the course of 8 to 11 weeks. In 3 of the more severely affected cows, metabolic derangements included a rapidly developing primary hypochloremic, secondary hypokalemic and hyponatremic metabolic alkalosis, and hemoconcentration. Clinical signs included severe hypophagia, weight loss, muscle weakness, hypogalactia, dehydration, constipation, cardiopulmonary depression, and a depraved appetite. It was concluded that the rapid progression of these derangements, apart from any anatomic abnormalities or infectious causes, emphasizes the need for rapid assessment and therapeutic intervention in primary imbalance associated with body chloride depletion and metabolic alkalosis.
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PMID:Effects of dietary chloride restriction in lactating dairy cows. 608 55

We investigated the relative contribution of peripheral and central chemosensory mechanisms to ventilatory responses to metabolic alkalosis in anesthetized cats by simultaneously measuring steady-state carotid body chemosensory activity and ventilation. The effects of graded steady-state levels of metabolic alkalosis at constant levels of arterial O2 and CO2 partial pressure (PaO2 and PaCO2, respectively) were studied first. Then the responses to isocapnic hypoxia and hyperoxic hypercapnia before and after the induction of a given level of metabolic alkalosis were studied. From the relationship between the carotid chemosensory activity and ventilation, the contribution of the two chemosensory mechanisms was estimated. The depression of ventilation that could not be accounted for by a decrease in the carotid chemosensory activity is attributed to the central effect. We found that metabolic alkalosis decreased both carotid chemosensory activity and ventilation at all levels of PaO2 or PaCO2. The ventilatory effect of alkalosis increased during hypoxia due to suppression of both peripheral chemosensory input and its interaction with the central CO2-H+ drive. During hyperoxia the central effect of alkalosis was predominant, although the peripheral effect increased with hypercapnia. We conclude that acute metabolic alkalosis suppresses both peripheral and central chemosensory drives, and its ventilatory effect grows larger with decreasing PaO2.
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PMID:Relative peripheral and central chemosensory responses to metabolic alkalosis. 631 76


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