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PubMed1989

Mechanisms of adaptation to chronic respiratory acidosis in the rabbit proximal tubule.

The hyperbicarbonatemia of chronic respiratory acidosis is maintained by enhanced bicarbonate reabsorption in the proximal tubule. To investigate the cellular mechanisms involved in this adaptation, cell and luminal pH were measured microfluorometrically using (2",7')-bis(carboxyethyl)-(5,6)-carboxyfluorescein in isolated, microperfused S2 proximal convoluted tubules from control and acidotic rabbits. Chronic respiratory acidosis was induced by exposure to 10% CO2 for 52-56 h. Tubules from acidotic rabbits had a significantly lower luminal pH after 1-mm perfused length (7.03 +/- 0.09 vs. 7.26 +/- 0.06 in controls, perfusion rate = 10 nl/min). Chronic respiratory acidosis increased the initial rate of cell acidification (dpHi/dt) in response to luminal sodium removal by 63% and in response to lowering luminal pH (7.4-6.8) by 69%. Chronic respiratory acidosis also increased dpHi/dt in response to peritubular sodium removal by 63% and in response to lowering peritubular pH by 73%. In conclusion, chronic respiratory acidosis induces a parallel increase in the rates of the luminal Na/H antiporter and the basolateral Na/(HCO3)3 cotransporter. Therefore, the enhanced proximal tubule reabsorption of bicarbonate in chronic respiratory acidosis may be, at least in part, mediated by a parallel adaptation of these transporters.

4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo↗
PubMedDate not supplied

Neonatal metabolic acidosis: effect of chloride from normal saline flushes.

Metabolic Acidosis is a reported complication of total parenteral nutrition (TPN). A large number of infants receiving TPN in an NICU were noted to have metabolic acidosis. We evaluated the effect of lowering the chloride intake on the incidence of metabolic acidosis in low birth weight (LBW) infants on TPN. Standard TPN solutions were adjusted to provide about 2-3 mEq/kg/day chloride instead of 5-7 mEq/kg/day provided previously. Most infants on TPN received approximately another 1-3 mEq/kg/day from intravenous and arterial line flushes with normal saline. Ten infants who had been on the original TPN solutions were compared to 10 infants who were on the revised TPN solutions. Serum pH, bicarbonate, and base deficit were used to measure acidosis. Medical records were reviewed for the number of days the infants had abnormal values. Serum chloride levels were also recorded. While similar in gestational age, birth weight, age during study period, days on TPN, and days on orally supplemented parenteral nutrition, the group with higher chloride intake had significantly more days of metabolic acidosis. They also had significantly higher serum chlorides. It is concluded that a total chloride load in excess of 6 mEq/kg/day in LBW infants receiving TPN is associated with more metabolic acidosis. Also, if saline is used for clearing of intravenous and arterial lines, standard TPN solutions should be formulated with consideration of the total chloride load.

Acidosis↗
PubMed1997

Metformin-associated nonketotic metabolic acidosis.

OBJECTIVE: To document a case of anion gap, nonketotic metabolic acidosis occurring in a patient with acute renal failure who was receiving metformin. CASE SUMMARY: A 67-year-old white man presented with a 9-day history of weakness, nausea, dizziness, and difficulty moving; he had also not eaten during the previous 2 days. The patient had numerous abnormalities on his serum chemistry panel and arterial blood gases, including a pH of 7.1 and an anion gap of 21 mEq/L No ketones were detected in the urine. The patient was treated with intravenous fluids, sodium bicarbonate, insulin, and hemodialysis. All medications were discontinued. The acidosis resolved shortly after hemodialysis. The hospital course was complicated by the onset of atrial fibrillation occurring on day 2 that did not respond to chemical cardioversion. On day 6 the patient was discharged home with resolving acute renal failure and normal serum pH. CONCLUSIONS: The mortality rate of biguanide-induced lactic acidosis is approximately 50%; thus, early recognition and treatment are essential. Suspicion of lactic acidosis should be high when diabetic patients who are taking a biguanide present with acidosis. The majority of cases of metformin-induced lactic acidosis have occurred in patients with contraindications to the drug (i.e., renal dysfunction). Thus, it is important to maintain strict adherence to these contraindications and monitor patients for deteriorating renal function.

Acidosis, Lactic↗
PubMed1980

The effects of acute total asphyxia and metabolic acidosis on cerebrospinal fluid bicarbonate regulation in newborn puppies.

We evaluated CSF [HCO3-] regulation in lightly anesthetized newborn puppies following: (1) acute total asphyxia; (2) metabolic acidosis; and (3) metabolic acidosis induced after acute asphyxia. Five and one-half min of total asphyxia resulted in a 4.4 mM/liter decrease in mean CSF [HCO3-]. During 65 min of recovery with mechanical ventilation mean CSF [HCO3-] increased 1.7 mM/liter. Mean plasma [HCO3-] decreased 7 mM/liter and recovered 4.5 mM/liter in the same period. We produced a stable metabolic acidosic for 4 hr using a peritoneal dialysis technique with PaCO2 maintained at the normal value. With acidosis in nonasphyxiated control puppies, CSF [HCO3-] decreased steadily. At 4 hr, the ratio, delta CSF [HCO3-]/delta plasma [HCO3-], was 0.43, a value close to that observed in adults of many species with metabolic acid-base disturbances, 0.41. With acidosis in asphyxiated puppies allowed 1 hr of recovery, the time course and mean values of plasma and CSF [HCO3-] were indistinguishable from those of the nonasphyxiated acidotic controls. Newborn puppies appear to regulate CSF [HCO3-] in response to acute asphyxia or metabolic acidosis, and acute asphyxia does not impair the puppy's ability to regulate CSF [HCO3-] in metabolic acidosis.

Acidosis↗
PubMed1986

Comparison of the effect of asphyxia, hypoxia, and acidosis on intestinal blood flow and O2 uptake in newborn piglets.

The aim of our study was to compare the effects of asphyxia and the two components of asphyxia, i.e. hypoxia and acidosis, on intestinal blood flow and oxygen consumption in anesthetized newborn piglets less than 3 days old. The first series of experiments, consisting of four groups of piglets, showed that blood flow to the proximal and distal small intestine and colon (as determined by the microsphere technique) significantly decreased after piglets were subjected to a sustained hypoxic hypoxemia (PaO2 50% of control) or asphyxia (acidosis plus hypoxia) for 90 min. A sustained acidosis (arterial pH = 7.0-7.15 for 90 min), however, decreased blood flow only to the proximal small intestine, and sham operation did not significantly alter any intestinal blood flow. All animals subjected to asphyxia and two of five of the animals subjected to hypoxia alone in this series, produced gross and microscopic intestinal lesions similar to those seen in human newborn with necrotizing enterocolitis. Acidosis alone, however, did not produce any pathologic lesions. The second series of experiments showed that the 90-min hypoxic hypoxemia decreased blood flow to both the mucosa and muscularis layers of the small intestine. The third series of experiments, consisting of four groups of piglets, determined the effects of 60-min acidosis, hypoxic hypoxemia, asphyxia, or sham operation on venous outflow and oxygen consumption of the isolated in situ terminal ileum. Acidosis or sham operation altered neither ileal blood flow nor oxygen consumption. Hypoxia or asphyxia, however, decreased ileal oxygen consumption without significantly decreasing blood flow.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis↗
PubMed1984

Rapid desensitization and uncoupling of human beta-adrenergic receptors in an in vitro model of lactic acidosis.

Adrenergic responsiveness in many tissues may be impaired in the presence of lactic acidosis. The purpose of this study was to examine how human neutrophil beta 2-adrenergic receptors may be altered in an in vitro model of lactic acidosis. Receptor coupling was assessed by constructing curves for the competition of isoproterenol with [125I]iodocyanopindolol for beta-adrenergic receptors. Receptors were exposed to control (2 mM lactate, pH 7.4), lactic acidosis (16 mM lactate, pH 7.1), lactate excess (16 mM lactate, pH 7.4), and low pH (2 mM lactate, pH 7.1) conditions. Prior exposure of beta-adrenergic receptors on whole cells to lactic acidosis resulted in a 61% reduction in isoproterenol-stimulated cAMP accumulation (P less than 0.005). This desensitization was not accompanied by down-regulation. After exposure to lactic acidosis, beta-adrenergic receptors were uncoupled sufficiently that a high affinity state could not be detected. Both lactate excess and low pH were necessary to fully express the desensitization and uncoupling defects. The uncoupling was rapid (40 min) and occurred in cell-free membrane preparations. Thus, in an in vitro model of lactic acidosis, rapid desensitization and uncoupling occur which do not appear to require protein synthesis.

Acidosis↗
PubMed1983

Cardiac performance in the in situ perfused fish heart during extracellular acidosis: interactive effects of adrenaline.

The physiological integrity of the in situ perfused heart of the ocean pout was established by its ability to maintain cardiac output (Q) over a range of work loads, and by the dependence of Q upon the filling pressure of the heart. Similar observations have been reported previously for the in situ perfused heart of the sea raven. Physiological levels of extracellular acidosis (pH 7.6/1% CO2 and pH 7.4/2% CO2) significantly depressed cardiac performance in sea raven and ocean pout hearts in situ. Negative chronotropic and inotropic responses were observed. Adrenaline (AD; 10(-7) M) under control conditions (pH 7.9/0.5% CO2) produced a sustained tachycardia. The tachycardia reduced filling time of the ventricle and stroke volume was compromised because of the constant preload to the heart. Consequently, AD produced only an initial, transient increase in stroke volume and Q. Thereafter, stroke volume was reduced in proportion with the increase in heart rate, and Q remained unchanged. The combined challenge of extracellular acidosis and AD demonstrated interactive effects between AD and acidosis in situ. Q and power output were maintained in both species at both levels of extracellular acidosis during the combined challenge. Thus AD alone can maintain (but not improve upon) basal Q during extracellular acidosis. The effects of extracellular acidosis, circulating catecholamines and venous return pressure to the heart are discussed in relation to the regulation of Q following exhaustive exercise.

Acidosis↗
PubMed2001

Acidosis inhibits gallbladder contraction mediated by protein kinase C activation.

The effects of extracellular acidosis on gallbladder contraction were investigated using gallbladder strips isolated from guinea pigs. In an acidic medium (pH 6.9), gallbladder contraction induced by histamine and prostaglandin E2 was significantly lower than that in a normal medium (pH 7.4). Acidosis affected neither gallbladder contraction induced by histamine in the absence of extracellular Ca2+ nor that induced by KCl. Acidosis significantly inhibited Ca2+-induced contraction in the presence of sodium fluoride and phorbol 12,13-dibutyrate but not that in the presence of KCl. Staurosporine (30 nM) significantly inhibited gallbladder contraction induced by histamine and prostaglandin E2, but not that by KCl. Histamine-induced contraction in the presence of staurosporine was not affected by acidosis. Acidosis significantly inhibited Ca2+-induced contraction in the presence of histamine but not that in the presence of both histamine and staurosporine. These results suggest that extracellular acidosis selectively inhibits gallbladder contraction mediated by protein kinase C activation.

Acidosis↗
PubMed1998

Trimethoprim/sulfamethoxazole and metabolic acidosis in HIV-infected patients.

OBJECTIVE: To describe a retrospective study of six HIV-positive individuals with compensated metabolic acidosis while receiving intravenous trimethoprim/sulfamethoxazole (TMP/SMX). CASE SUMMARY: Six HIV-infected patients were treated for Pneumocystis carinii pneumonia (PCP) with high-dose intravenous TMP/SMX. In spite of a favorable clinical and radiologic course, all six patients developed compensated metabolic acidosis 3-5 days after the start of treatment. This potential complication of TMP/SMX use was successfully managed with conservative treatment (cessation of therapy with or without additional administration of intravenous bicarbonate). DISCUSSION: TMP/SMX is first-line therapy for PCP in HIV-positive individuals, despite a high frequency of toxic effects in these patients. In addition to the cases reported here, only two other reports of metabolic acidosis secondary to TMP/SMX use in HIV-infected patients have been published in the literature. The precise mechanism of this untoward effect is not fully understood, although renal tubular acidosis induced by TMP/SMX could be implicated. CONCLUSIONS: TMP/SMX toxicity should be considered in the differential diagnosis of HIV-infected patients with acute metabolic acidosis. Metabolic acidosis can be expected to resolve shortly after discontinuation of the drug.

AIDS-Related Opportunistic Infections↗
PubMed2005

Propylene glycol-induced lactic acidosis in a patient with normal renal function: a proposed mechanism and monitoring recommendations.

OBJECTIVE: To report a case of severe propylene glycol-induced lactic acidosis not attributable to renal dysfunction that was secondary to administration of high-dose intravenous lorazepam. CASE SUMMARY: A 24-year-old female with community-acquired pneumonia presented with severe acute respiratory distress syndrome. To maintain adequate sedation and ventilation and reduce airway pressure, several relaxation strategies were used including high-dose intravenous lorazepam, fentanyl, and cisatracurium. After 18 days of high-dose continuous infusion of lorazepam (maximum dose 50 mg/h), the patient developed severe lactic acidosis secondary to propylene glycol toxicity, the main diluent of lorazepam. The acidosis temporarily resolved with bicarbonate administration and discontinuation of lorazepam. Her renal function remained stable for a time (serum creatinine 0.5 mg/dL, blood urea nitrogen 10 mg/dL, urine output 100-200 mL/h). However, after several more days, the patient's condition deteriorated, and she ultimately died. DISCUSSION: Previous cases of propylene glycol toxicity secondary to high-dose lorazepam infusion have occurred in patients with compromised renal function. Our patient's renal function remained stable throughout the hospital course, which caused us to look further for an explanation for the propylene glycol-induced lactic acidosis. Based on the Naranjo probability scale, propylene glycol was determined to be the probable cause of lactic acidosis. Since this case occurred, our intensive care unit has instituted recommendations for the prevention of lorazepam-associated propylene glycol toxicity. CONCLUSIONS: Our case highlights the development of propylene glycol-induced lactic acidosis secondary to high-dose lorazepam infusion not associated with renal dysfunction.

Acidosis, Lactic↗
PubMed2001

Lactic acidosis in status asthmaticus : three cases and review of the literature.

Lactic acidosis is a frequent laboratory finding in patients with severe exacerbations of asthma. The pathogenesis of lactic acidosis in asthma is not well understood, but it has been presumed, by some, to be generated by fatiguing respiratory muscles. We herein report the cases of three patients with status asthmaticus and lactic acidosis despite pharmacologic muscle relaxation. No common etiologies were found for lactic acidosis that abated after bronchospasm improved and the intensity of pharmacologic therapies was reduced. We review the literature describing lactic acidosis with asthma and discuss mechanisms by which lactic acidosis may occur in patients with status asthmaticus.

Acidosis, Lactic↗
PubMed2006

Hyperchloremic acidosis increases circulating inflammatory molecules in experimental sepsis.

RATIONALE: Hyperchloremic acidosis is common in the critically ill and is often iatrogenic. We have previously shown that hyperchloremic acidosis increases nuclear factor-kappaB DNA binding in lipopolysaccharide-stimulated RAW 264.7 cells. However, evidence that hyperchloremic acidosis leads to increased inflammation in vivo has been limited to nitric oxide. OBJECTIVES: To determine if acidosis, induced by dilute hydrochloric acid (HCl) infusion, will increase circulating inflammatory mediator levels in an experimental model of severe sepsis in rats. METHODS: Eighteen hours after inducing lethal sepsis by cecal ligation and puncture in 20 adult, male, Sprague-Dawley rats, we randomized animals into three groups. In groups 2 and 3, we began an IV infusion of 0.1 N HCl to reduce the standard base excess (SBE) by 5 to 10 mEq/L and 10 to 15 mEq/L, respectively. In group 1, we infused a similar volume of lactated Ringer solution. In all groups infusion continued 8 h or until the animal died. MEASUREMENTS AND MAIN RESULTS: We measured arterial blood gases, whole-blood lactate, and chloride, tumor necrosis factor (TNF), interleukin (IL)-6, and IL-10 levels at 0 h, 4 h, and 8 h. All measured cytokines increased over time. Compared to group 1, animals in groups 2 and 3 exhibited greater increase in all three cytokines, with the greatest increases seen with severe acidosis. CONCLUSION: Moderate (SBE, - 5 to - 10) and severe (SBE, - 10 to - 15) acidosis, induced by HCl infusion, increases circulating levels of IL-6, IL-10, and TNF in normotensive septic rats.

Acid-Base Equilibrium↗
PubMed2005

The syndrome of irreversible acidosis after prolonged propofol infusion.

INTRODUCTION: Propofol infusion syndrome is described in the pediatric literature as metabolic acidosis, rhabdomyolysis, and bradycardia that results in death. The pathogenesis of this syndrome is thought to be activation of the systemic inflammatory response, which culminates in acidosis and muscle necrosis. MATERIALS AND METHODS: Retrospective chart review of three patients in the Neurological Critical Care Units at Hahnemann and Massachusetts General Hospitals between October 2001 and September 2004. RESULTS: Patient 1: A 27-year-old woman had seizures secondary to hemorrhage from an arteriovenous malformation. Propofol coma was induced for sedation. After initiation of propofol, she developed a metabolic acidosis, hypotension, and bradycardia and expired. Patient 2: A 64-year-old man presented in status epilepticus. After prolonged propofol administration, he developed metabolic acidosis, hypotension, and rhabdomyolysis and expired. Patient 3: A 24-year-old woman presented in status epilepticus secondary to encephalitis. Propofol was added for seizure control. She developed hypotension, metabolic acidosis, and bradyarrhythmias. Despite transvenous pacing, she expired. CONCLUSION: These data show an association between extended propofol use and metabolic acidosis, rhabdomyolysis, and death in adults, as well as children. Risk factors for propofol infusion syndrome in adults include lean body mass index, high dose, and administration of more than 24-hour duration. Creatine phosphokinase, lactic acid levels, electrolytes, and arterial blood gases should be monitored frequently. Both bacterial and fungal cultures should be obtained. If this syndrome is suspected, hemodialysis should be considered. In fatal cases, autopsy should include electron microscopy of cardiac and skeletal muscle to look for mitochondrial dysfunction. Further study is warranted.

Acidosis↗
PubMed1975

Recognition and significance of maternogenic fetal acidosis during intensive monitoring of labor.

FHR monitoring and microanalysis of fetal blood are mutually complementary procedures, and optimal knowledge of the fetal state is achieved by making use of both, the former for the preliminary screening of all cases at risk and the latter for the purpose of deciding on obstetric management where pathological changes are evident in the FHR. The major difficulty in obtaining a precise value for the fetal acid-base balance lies in the occurence of "falsely abnormal" cases, i.e. cases in which the fetal pH falls during labor but the clinical condition at birth is good (APGAR greater than or equal to 7). In our own series the incidence of such cases among fetuses at risk was 11.2% (Tab. I). In the majority of these cases the fetal acidosis is thought to be a result of increased metabolic acidosis in the mother (maternogenic fetal metabolic acidosis). The importance of the maternogenic fetal acidosis during labor lies in the fact that unless it is recognised, rapid extraction of the fetus will appear necessary on clinical grounds, although it is in fact unnecessary, since this form of acidosis has no adverse effect on the fetus. Various parameters have been proposed for the differential diagnosis of the maternogenic fetal acidosis. These include the feto-maternal difference in base deficit (F/M deltaBD), the materno-fetal differences in pHqu 40 (M/F deltapHqu 40) the materno-fetal difference actual pH (M/F actual deltapH), and the materno-fetal difference in base deficit of the extra-cellular fluid (M/F deltaBDHb5). A critical analysis of these parameters has been carried out on the results of microtests performed during a 5 year period (1968-1972) at the First Clinic of Obstetrics and Gynecology of Milan University. The cases comprised 59 regarded as normal (normal course of pregnancy, spontaneous commencement of labor at term, clear amniotic fluid, regular FHR, spontaneous birth, APGAR at 90 sec between 8 and 10, weight at birth greater than 2500 g), and 335 considered to be at risk (maternal disease, presence of meconium stained amniotic fluid and/or abnormal changes in FHR). In all of these cases the FHR was recorded by cardiotokography, and the tracings were interpreted according to HON. Microsamples of blood were taken from both mother and fetus during labor and the following determinations were carried out: actual pH, pHqu 40, Hb concentration, hemoglobin oxygen saturation, base deficit Hb5 (BDHb5). The maternofetal differences were then calculated. The same determinations were carried out on samples of maternal blood and of arterial and venous cord blood taken immediately after delivery. The clinical condition of the infant was evaluated by the APGAR score at 90 seconds after birth.

Acid-Base Equilibrium↗
PubMed1991

Glue-sniffing and distal renal tubular acidosis: sticking to the facts.

An index case is presented to introduce the subject of the acid-base and electrolyte abnormalities resulting from toluene abuse. These include metabolic acidosis associated with a normal anion gap and excessive loss of sodium and potassium in the urine. The major question addressed is, what is the basis for the metabolic acidosis? Overproduction of hippuric acid resulting from the metabolism of toluene plays a more important role in the genesis of the metabolic acidosis than was previously believed. This conclusion is supported by the observation that the rate of excretion of ammonium was not low during metabolic acidosis in six of eight patients, suggesting that distal renal tubular acidosis was not an important acid-base abnormality in most cases where ammonium was measured. The excretion of hippurate in the urine unmatched by ammonium also mandates an enhanced rate of excretion of the cations, sodium and potassium. The loss of sodium causes extracellular fluid volume contraction and a fall in the glomerular filtration rate, which may transform the normal anion gap type of metabolic acidosis into one with a high anion gap (accumulation of hippurate and other anions). Continuing loss of potassium in the urine leads to hypokalemia. An understanding of the metabolism of toluene provides the basis for the unusual biochemical abnormalities seen with abuse of this solvent.

Acid-Base Equilibrium↗
PubMed1998

Tissue-specific responses of branched-chain alpha-ketoacid dehydrogenase activity in metabolic acidosis.

In adrenalectomized rats, acidosis does not increase whole-body leucine oxidation unless a physiologic amount of glucocorticoids (dexamethasone) is also provided; an equivalent dose of dexamethasone without acidosis does not change leucine catabolism. Because the influences of acidification and glucocorticoids on branched-chain amino acid metabolism in specific organs are unknown, the function of branched-chain alpha-ketoacid dehydrogenase (BCKAD), the rate-limiting enzyme in branched-chain amino acid catabolism, in adrenalectomized rat skeletal muscle and liver, the two major tissues that degrade branched-chain amino acid was measured. In muscle of acidotic adrenalectomized rats receiving dexamethasone, basal and total BCKAD activities were increased 2.6- (P < 0.05) and 2.8-fold (P < 0.05), respectively. Neither acidosis nor dexamethasone alone increased these activities. BCKAD E1alpha subunit mRNA in muscle of acidotic rats given dexamethasone was increased 1.89-fold (P < 0.05) in parallel with the change in BCKAD activity; BCKAD E2 subunit mRNA was increased by acidosis, dexamethasone, or a combination of both stimuli. In contrast, basal BCKAD activity in liver of rats with acidosis or dexamethasone was nearly threefold lower (P < 0.05) and changes in enzyme activity reflected reduced subunit mRNA. Thus, there are reciprocal, tissue-specific changes in BCKAD function in response to acidosis.

3-Methyl-2-Oxobutanoate Dehydrogenase (Lipoamide)↗
PubMed2002

Pathogenic mechanism, prophylaxis, and therapy of symptomatic acidosis induced by acetazolamide.

BACKGROUND: Acetazolamide, a noncompetitive carbonic anhydrase inhibitor, can produce symptomatic acidosis and bone marrow suppression by a mechanism that is still unknown. This presentation occurs in the elderly, patients with renal or liver failure, people with diabetes, and newborns. The objective of this study was to understand the pathogenic mechanism of these adverse effects and to propose a possible prophylaxis and therapy. METHODS: Four human clinical cases were studied, and one animal experiment was performed. Four preterm newborns with posthemorrhagic ventricular dilation developed severe metabolic acidosis after treatment with acetazolamide. The acidosis suddenly disappeared after a packed red blood cell transfusion. Metabolic studies were performed in one patient and in newborn guinea pigs treated with 200 mg/kg acetazolamide. RESULTS: Acetazolamide can produce severe lactic acidosis with an increased lactate-to-pyruvate ratio, ketosis with a low beta-hydroxybutyrate-to-acetoacetate ratio, and a urinary organic acid profile typical of pyruvate carboxylase deficiency. The acquired enzymatic injury resulting from the inhibition of mitochondrial carbonic anhydrase V that provides bicarbonate to pyruvate carboxylase can produce tricarboxylic acid cycle damage. We demonstrate that the dramatic disappearance of metabolic acidosis and normalizing metabolism after blood transfusion were due to the citrate contained in the packed red blood cell bag. This hypothesis was confirmed by animal experimentation. We argue that the metabolic disorder and bone marrow suppression may be related. CONCLUSION: We demonstrate how acetazolamide can lead to symptomatic metabolic acidosis and probably to bone marrow suppression. We suggest citrate as a possible prophylaxis and treatment for these adverse reactions.

Acetazolamide↗
PubMed1980

Control of wheat-induced lactic acidosis in sheep by thiopeptin and related antibiotics.

Thiopeptin, thiopeptin-like antibiotics and penicillin were shown previously to be highly active in vitro against Streptococcus bovis, the microorganism believed to be responsible for the initiation of ruminal lactic acidosis. The purpose of this work was to determine the efficacy of these antibiotics in preventing lactic acidosis in lambs challenged by intraruminal administration of ground wheat. Lambs, which were fasted and then given ground wheat at 40 g/kg body weight, showed dramatic increases in rumen and plasma lactate over the 30-hr experimental period. Rumen lactate increased from .2 to peak levels of approximately 150 mumoles/ml by 8 to 10 hr after wheat administration. Plasma lactate increased after rumen lactate was elevated and lambs succumbed when plasma levels exceeded 15 mumoles/ml. Ruminal volatile fatty acids were greatly reduced as rumen lactate increased. Over half of the lambs given ground wheat died within 30 hours. Thiopeptin given as a single dose completely prevented lactic acidosis by reducing rumen lactate 80 to 90%. In addition, thiopeptin permitted "normal" rumen fermentation to continue as indicated by a significant increase in volatile fatty acids. The minimum effective dose of thiopeptin to control acute lactic acidosis was .18 mg/kg body weight. Other members of the thiopeptin class, including sulfomycin, sporangiomycin, siomycin and taitomycin, prevented lactic acidosis in a manner similar to thiopeptin. Penicillin, however, inhibited ruminal volatile fatty acid production as well as lactate synthesis. In addition, the effective period for penicillin in the rumen was only 8 to 16 hr, after which lactate fermentation was reestablished. Thus, thiopeptin and thiopeptin-like antibiotics, but not penicillin, appear to provide prophylactic treatment against lactic acidosis in sheep.

Acidosis↗