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PubMed1987

Effect of lidocaine on the myocardial acidosis induced by coronary artery occlusion in dogs.

The effect of lidocaine on ischemic myocardial acidosis was investigated in the dog heart, in which the left anterior descending coronary artery was occluded to reduce to about one-third (partial occlusion). Myocardial pH (MpH) was measured by means of a micro glass pH electrode. MpH before partial occlusion was 7.52 to 7.66. Partial occlusion decreased the left anterior descending coronary artery flow by 49 to 68%, MpH by 0.58 to 0.76 and myocardial contractile force by 26 to 43%, and increased ST segment (surface electrocardiogram) by 3.2 to 11.7 mV. Lidocaine (injected i.v. 30 min after partial occlusion) decreased heart rate, blood pressure and myocardial contractile force, and attenuated the decrease in MpH during ischemia. Lidocaine in doses of 2, 5 and 10 mg/kg restored the myocardial [H+], that had been increased by partial occlusion, by 23, 38 and 50%, respectively. Even in the paced heart, lidocaine (10 mg/kg) attenuated the myocardial acidosis, although the degree of attenuation was smaller (36%). Partial occlusion elevated the ST segment even in the presence of 5 or 10 mg/kg of lidocaine. In the nonischemic heart, however, lidocaine (2, 5 or 10 mg/kg) did not change in MpH. It is concluded that lidocaine attenuates the myocardial acidosis during ischemia, and the primarily important mechanism of pH attenuation is not a decrease in heart rate.

Acidosis↗
PubMed1986

Comparison of lidocaine and bupivacaine depression of sinoatrial nodal activity during hypoxia and acidosis in adult and neonatal guinea pigs.

High blood concentrations of local anesthetics are cardiotoxic. The aim of this study was to compare the effects of lidocaine and bupivacaine on the intrinsic pacemaker activity of in vitro sinoatrial nodal cells of the adult and neonatal guinea pig in the presence and absence of hypoxia and acidosis. Fifteen pairs of adult (greater than 80 days old) and neonatal (0-3 days old) hearts were isolated. Nodal tissues were suffused with Krebs-Ringer solution at 37 degrees C and exposed to increasing concentrations of either lidocaine (0.05-0.8 mM) or bupivacaine (0.01-0.4 mM). The suffusate was equilibrated either with 5% CO2, 95% O2 (pH 7.40, PO2 482 torr) or with 12% CO2, 88% N2 (pH 7.01, PO2 58 torr). Transmembrane action potentials were recorded from sinoatrial nodal cells and impulse intervals were converted to rates. We found that hypoxia and acidosis alone reduced rates in both adults and neonates, and that the reduction was additive to the effects of local anesthetics. Bupivacaine was 4-5 times more potent in decreasing rates than was lidocaine in both age groups. Lidocaine was about twice as effective in depressing neonatal rates as adult rates, and bupivacaine caused cessation of pacemaker activity in a greater percentage of nodes than did lidocaine. Our results demonstrate, in vitro, that the neonatal sinoatrial node is more sensitive to lidocaine and bupivacaine than is the adult node, that bupivacaine is more potent in depressing and stopping nodal activity, and that hypoxia and acidosis enhance pacemaker depression caused by these agents.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis↗
PubMed1986

Metabolic acidosis enhances 1,25(OH)2D3-induced intestinal absorption of calcium and phosphorus in rats.

The effect of metabolic acidosis on the intestinal absorption of calcium (Ca) and phosphorus (P), plasma vitamin D metabolites and urinary excretion of Ca in adult rats treated with a small dose of 1,25(OH)2D3 were investigated. The rats in the experimental group received 1.8% ammonium chloride (NH4Cl) and a commercial chow, and their pair-fed controls received 0.45% NaCl. Both groups were given subcutaneously 1,25(OH)2D3. Intestinal absorption of Ca and P was measured by gut sac uptake of 45Ca and 32P. In the acidotic rats, duodenal, jejunal and ileal 45Ca uptake as well as jejunal and ileal 32P uptake were significantly increased. Plasma 1,25(OH)2D, 25(OH)D and 24,25(OH)2D were similar in both groups. 1,25(OH)2D3 treatment induced a greater calciuria in acidotic rats and increased their fractional excretion (FE) of Ca. An additional experiment showed increased 45Ca uptake by duodenum at a pH of 7.0 compared to pH 7.4. The present study suggests that NH4Cl-induced metabolic acidosis may enhance the effect of 1,25(OH)2D3 on intestinal absorption of Ca and P in the rat. However, the data from the study cannot exclude the possibility that acidosis may have a direct, vitamin D-independent effect on the intestine.

Acidosis↗
PubMedDate not supplied

[Effect of infusion acidosis on the condition of the fetus--animal experiment studies].

In order to assess the effect of acid infusion on fetal cardiovascular functions, oxygenation, glucose and electrolyte concentrations, 8 experiments were performed on chronically instrumented ewes. A severe metabolic acidosis (pH less than 7.10, BDECF = 13.5 mmol/l) was induced by intravenous infusion of L(+) lactate into the fetus. There was no significant alteration of baseline fetal heart rate and oscillation amplitude. The blood pressure exhibited a slight increase, probably due to the administration of volume (87-204 ml in 90-210 min). PO2 remained constant while SO2 showed a decrease in the order of 10%, due to the change in oxygen affinity of the fetal blood produced by the Bohr effect. Levels of glucose increased significantly, whereas electrolyte concentrations remained unchanged. After the end of infusion, pH-values returned to the normal range within 110 min. Lactate and BDECF decreased with a half life time of 95 and 48 min, respectively (mean SO2 = 28%). We conclude that a severe metabolic acidosis in the extracellular space does not affect the normal fetal heart rate pattern (baseline, oscillation amplitude) and has no acute deleterious effects on the fetus. Hence, when the actual fetal pH during labor is found to be low, a maternogenic infusion acidosis should be excluded by a simultaneous feto-maternal blood gas analysis.

Acidosis↗
PubMed1985

[Type IV renal tubular acidosis: pathogenetic role of aldosterone deficiency and hyperkalemia].

Type IV renal tubular acidosis (RTA) is a syndrome of tubular dysfunction manifested clinically by persisting hyperkalemia and metabolic acidosis that occurs usually in patients with mild to moderate chronic glomerular insufficiency. The pathophysiologic characteristics include: reduced renal clearance of potassium; a reduced rate of renal bicarbonate reabsorption at normal plasma bicarbonate concentrations (the magnitude of which is insufficiently great to implicate the proximal tubule); an unimpaired ability to maintain a steep hydrogen ion concentration gradient between blood and urine during acidosis; and a reduced rate of renal net acid excretion despite highly acidic urine, due in part to reduced urinary excretion of ammonium, which in turn appears to be due in part to suppression of renal ammoniagenesis by hyperkalemia. Many patients with type IV RTA, but not all, have hyporeninemic hypoaldosteronism. The roles of mineralocorticoid deficiency and hyperkalemia in the pathogenesis of type IV RTA will be considered and the ameliorative effects of treatment with fludrocortisone, furosemide, and dietary potassium restriction reviewed.

Acidosis, Renal Tubular↗
PubMed1985

Actions of parathyroid hormone are not impaired during chronic metabolic acidosis.

The effect of parathyroid hormone (PTH) on renal excretion of calcium, phosphate, and bicarbonate was studied in acutely thyroparathyroidectomized dogs with metabolic acidosis. Ammonium chloride 10 gm/day for 3 days was given to 15 dogs to induce chronic metabolic acidosis. Clearance results obtained from these experiments showed that infusion of Beckman 1-34 PTH into normal and acidotic dogs resulted in a marked increase in phosphate and bicarbonate excretion, accompanied by a small reduction in calcium excretion and a slight but significant increase in plasma ultrafilterable calcium. Complementing our clearance data, micropuncture results obtained from the proximal and distal tubules of these animals indicated an enhancement of calcium reabsorption in the distal tubule after administration of PTH. Phosphate reabsorption by the proximal and distal tubules was reduced after infusion of PTH in both normal and acidotic dogs. The fraction of bicarbonate reabsorbed in the proximal tubule was reduced after PTH infusion, but the fraction of bicarbonate reabsorbed in the distal tubule remained unchanged. These data suggest that the phosphaturic, the hypocalciuric, and the bicarbonaturic effects of PTH were not impaired during chronic metabolic acidosis.

Acidosis↗
PubMedDate not supplied

Thalassemia B with distal renal tubular acidosis: a previously undescribed association.

An infant with beta thalassemia major and distal renal tubular acidosis is described. Screening of forty patients with beta thalassemia major revealed no evidence of renal tubular acidosis. Although the possibility of coincidence cannot be completely excluded, we suggest that beta thalassemia major should be added to the list of conditions associated with distal renal tubular acidosis.

Acidosis, Renal Tubular↗
PubMed1985

Electrophysiologic effects of enflurane and halothane on isolated rabbit hearts in the presence and absence of metabolic acidosis.

Electrophysiologic effects of halothane and enflurane in the presence of a normal pH and during metabolic acidosis were examined in isolated rabbit hearts perfused at a constant rate. During exposure to a normal pH, both halothane and enflurane produced concentration-dependent suppression of sinus node automaticity and atrioventricular conduction. Intraatrial and intraventricular conduction times during constant pacing were slightly but significantly prolonged by these anesthetics at 2 MAC. The magnitudes of these electrophysiologic changes were similar with halothane and enflurane when compared at the same MAC. These electrophysiologic effects became more marked during metabolic acidosis (pH 6.9). These results suggest that enflurane and halothane have direct depressant actions on the cardiac conduction system and that these electrophysiologic effects may be augmented by metabolic acidosis.

Acidosis↗
PubMed1985

[Type II pseudohypoaldosteronism: proximal tubular acidosis and distal tubular hyperkalemia corrected by DDAVP].

The mechanisms of metabolic acidosis and hyperkalemia were investigated in a patient with chronic mineralocorticoid-resistant renal hyperkalemia (5.3 to 6.8 mM), metabolic acidosis (arterial blood pH 7.27, total CO2 17 mM), arterial hypertension, undetectable plasma renin activity (less than 0.10 ng/ml/hr), high plasma aldosterone (32 to 100 ng/dl), normal GFR (131 +/- 2.5 ml/min/1.73 m2). During hyperkalemic period, urine was highly acidic (pH 4.6 to 5.0), urinary NH4 excretion (13 mumoles/min) and urinary net acid excretion (24 mumoles/min) were not supernormal as expected from a chronic acid load. During NaHCO3 infusion, maximal tubular HCO3 reabsorption (Tm HCO3) was markedly diminished (19 mmoles/liter GF), fractional excretion of HCO3 (FE HCO3) when plasma HCO3 was normalized, was 20%. Urine-minus-blood PCO2 increased normally (31 mmHg) during NaHCO3 infusion, and urinary pH remained maximally low (less than 5.3) when buffer urinary excretion sharply increased after NH4Cl load. When serum K was returned toward normal limits, metabolic acidosis disappeared, urinary NH4 excretion rose normally after short NH4Cl loading while urinary pH remained maximally low (4.9 to 5.2), Tm HCO3 returned to normal value (24.8 mmoles/liter GF), and FE HCO3 became nil. The renal handling of K was improved with acute NaHCO3 loading and normalized after DDAVP nasal insufflation.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis, Renal Tubular↗
PubMed1985

Effect of ionophore antibiotics on experimentally induced lactic acidosis in cattle.

Salinomycin, a new ionophore antibiotic, was tested and compared with lasalocid and monensin for preventing experimentally induced lactic acidosis. Five rumen-fistulated adult cattle were used in a 5 X 5 Latin square design, and the treatments were as follows: no treatment (control), 0.11 mg of salinomycin/kg of body weight (S1), 0.22 mg of salinomycin/kg (S2), 0.66 of lasalocid/kg, and 0.66 mg of monensin/kg. Acidosis was induced by intraruminal administration of a ground corn-corn starch mixture (50:50, 12.5 g/kg) once a day for up to 4 days. Antibiotics were administered along with grain-starch mixture. Rumen and blood samples were obtained before and at 6, 12, and 24 hours after each carbohydrate-antibiotic dosing to monitor acid-base status. Control and S1-treated cattle became ruminally acidotic within 54 hours, whereas cattle treated with S2, lasalocid, and monensin resisted acidosis for up to 78 hours after dosing. Cattle treated with S2, lasalocid, or monensin had higher rumen pH and lower L(+)- and D(-)-lactate concentrations than did control or S1-treated cattle. Rumen pH decrease to below 5.0 in S2-, lasalocid-, and monensin-treated cattle was not due to lactic acid, but to increased production of volatile fatty acids. Rumen propionate proportion increased initially in antibiotic-treated cattle, but after 48 hours, butyrate proportion increased significantly. Despite low rumen pH and high lactate concentration, lacticacidemia was not evident, and the systemic acid-base disturbance was mild in control cattle.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis↗
PubMed1975

[Blood sugar and hypoxic dynamics in metabolic acidosis and alkalosis (experimental data)].

The dynamics of the glucose concentration and arterovenous glucose gradient was examined during different metabolic deviations in the acid-base balance. The metabolitic acidosis increased the level of sugar in the blood. A definite influence on the latter had the gravity of the acidosis and to a certain degree its pathogenetic form. The arterio-venous glucose difference changed from negative to positive with the increase of proton activity. The type of the peripheral hypoxic structure, formed during the state of acidosis influenced both the glucose gradient and its quantitative relations to the acid-base and oxygen indices. The sugar content in the blood during metabolitic alcalosis was not changed significantly. There was an increase in the arterio-venous gradient and inverse correlation between the glucose level and the arterio-venous oxygen difference with the increase of the bicarbonate concentration.

Acid-Base Equilibrium↗
PubMed1979

Effects of acute lactic acidosis on some hemodynamic and hematologic values in three cows.

Some hemodynamic and hematologic effects of acute experimental lactic acidemia in 3 healthy cows are presented. Lactic acidemia was induced by intravenous infusion of a 10% solution of racemic lactic acid. The prominent features of the acidification of the blood were increases in carotid artery blood pressure and responses to intravenously injected norepinephrine, slight bradycardia and slight hyperventilation. Intravascular hemolysis with hemoglobinuria was a constant finding. Otherwise, no adverse effects of the acidemia were noted. These changes were paralleled by a progressive fall in arterial blood pH, base excess and PCO2 and increasing venous blood L (+)-lactate concentrations A reasonable explanation for the hemodynamic effects of the acidemia is peripheral vasoconstriction elicited by either stimulation of the sympathetic nervous system or increased sensitivity of vasoconstrictive receptors. The results are discussed with special reference to primary lactic acidosis encountered in grain engorgement in ruminants and to the secondary lactic acidosis of shock. These conditions are characterized by hemoconcentration and hypovolemia. Therefore, the results of this study of healthy normovolemic cows may not be valid in the severely dehydrated, hemoconcentrated and acidemic cow as hypotension is reported in the literature in connection with ruminal acidosis in sheep.

Acidosis↗
PubMed1979

Treament of biguanide-induced lactic acidosis with dichloroacetate. 3 case histories.

The administration of dichloroacetate (DCA) in cases of biguanide-induced lactic acidosis (LA) improves pyruvate oxidation and therefore increases energy production from glucose. Preliminary results of treatment of LA in humans are reported. A continuous fall in pyruvate was observed in all 3 cases after administration of at least 20 g of DCA (4 g i.v. bolus, then continuously 12 g/h). In Case 1, in which no supplementary measures for controlling the acidosis were applied, the acidosis did not improve and the patient died. In Case 2, despite administration of tris-buffer and dialysis, pH-values could not be raised sufficiently. The production of hydrogen ions persisted and lactate continued to rise. This patient also died. Case 3 was admitted in the beginning stages of a phenformin-induced LA, and in this case therapy was successful. The decline in pyruvate was accompanied by a slow fall in lactate, and a further fall in pH was averted. The clinical condition of the patient improved markedly after i.v. administration of a total of 34 g of DCA.

Acetates↗
PubMed1977

[Renal tubular acidosis during a course of liver cirrhosis].

In a group of 23 patients suffering from liver cirrhosis, metabolic acidosis was always observed, in most cases corrected by respiratory alkalosis. In 8,6% of cases a tubular renal acidosis (type I), in 8,6% (type II) and 8,6% a loss of urinary bicarbonate without acidosis were observed.

Acidosis, Renal Tubular↗
PubMed1984

Differential effects of acetazolamide, benzolamide and systemic acidosis on hydrogen and bicarbonate gradients across the apical and basolateral membranes of the choroid plexus.

The effect after 1 hr of sulfonamide agents and systemic acidosis on pH (dimethyloxazolidinedione method) and [HCO3-] (calculated from pH and estimated cell pCO2) of choroid plexus epithelium was analyzed in adult Sprague-Dawley rats anesthetized with ether. Acetazolamide (20 mg/kg i.p.) caused a striking increase in choroid cell pH (7.0-7.45) and a substantial elevation in [HCO3-]i, and an alkalinization of cerebrospinal fluid (CSF); effects of benzolamide (3 mg/kg i.v.) were less marked. Acetazolamide-induced augmentation of steady-state pH was found in choroid plexus (0.45 pH unit) but not in submaxillary salivary gland, skeletal muscle, erythrocytes and cerebral cortex. Respiratory acidosis (blood pH 6.94) caused choroid cell pH to decrease less extensively than in the other tissues analyzed; metabolic acidosis (blood pH 7.23) did not significantly alter choroid plexus pH. Both sulfonamide agents and systemic acidoses significantly decreased the pH gradient between arterial blood and cisternal CSF. The sulfonamide-induced increase in choroid cell pH is attributed to suppression of buffering of OH- by CO2, leading to elevated [OH]i; and to a build-up in [HCO3-]i. Acetazolamide caused a reversal of the H+ and HCO3- gradients across the basolateral (plasma-facing) membrane of the choroid plexus. It is postulated that carbonic anhydrase inhibitors decrease CSF formation primarily by reducing Na+-H+ exchange at the basolateral membrane of the choroidal epithelium, and secondarily by slowing down HCO3- and Cl- exit across the CSF-facing membrane.

Acetazolamide↗
PubMedDate not supplied

A comparative study of the renal glutaminase response to acidosis.

The rates of ammonia excretion and the activities of renal glutaminase were measured in the rat, dog, guinea pig and chicken. The rate of ammonia excretion and the activity of renal glutaminase were less in guinea pig than in the other species. Renal glutaminase from all four species was activated by phosphate, but the degree of activation varied between species. Many organic acids activated renal glutaminase in the rat, dog and chicken, but these compounds were without affect or decreased glutaminase activity in the guinea pig. The optimal pH for renal glutaminase was 7.4, 8.0 and 8.8 for the guinea pig, rat and dog respectively, while in the chicken a plateau was reached between pH 7.5 and 9.5. The activation of renal glutaminase by phosphate in the chicken was greater at sub-optimal pH values than in the plateau region. In the absence of an activator acidosis did not affect glutaminase activity in any species. When phosphate was present in the incubation medium acidosis increased glutaminase activity in the rat and chicken, but did not alter enzyme activity in the guinea pig or dog. Acidosis did not affect the optimal pH or the shape of the activity versus pH curve in any of the species.

Acidosis, Renal Tubular↗
PubMed1983

[The effect of zeolite on experimentally induced acidosis in sheep].

The effect of zeolite (clinoptilolite) on experimentally induced metabolic acidosis was studied in sheep under experimental conditions. Sucrose was administered at the doses of 10 and 15 g per kg l. w. either alone or, in other groups, together with 0.45 g zeolite per kg l. w. The content of volatile fatty acids in rumen contents and the indices of acid-base homeostasis of blood were monitored in the subsequent 24 and/or 48 hours. The examinations showed that simultaneous administration of zeolite with sucrose failed to prevent the rise of metabolic acidosis but the drop in the indices of acid-base homeostasis was less severe, or was delayed by three to six hours. The dose of 0.45 g zeolite per kg l. w. was found to be insufficient for the prevention of a medium-severe or severe course of metabolic acidosis.

Acidosis↗
PubMed1984

Response of intercalated cells of rat outer medullary collecting duct to chronic metabolic acidosis.

The outer medullary collecting duct which is composed of both principal and intercalated cells is involved in hydrogen ion secretion. In the turtle urinary bladder stimulation of hydrogen ion secretion is associated with ultrastructural changes in the mitochondria-rich cells, suggesting that membrane and possibly a proton pump are being transferred from apical tubulovesicular structures and inserted into the apical plasma membrane. Since the intercalated cells resemble the mitochondria-rich cells, this study was initiated to determine whether or not similar changes occur in the outer medullary collecting duct during chronic metabolic acidosis. Rats received ammonium chloride in their drinking water for 15 days and as a daily gavage for 3 days before sacrifice. Control rats received regular tap water. After collection of physiologic data the kidneys were fixed by in vivo perfusion with glutaraldehyde and processed for electron microscopy. No changes were observed in the principal cells. Morphometric analyses of the intercalated cells in both the outer and inner stripe revealed a significant increase in the surface density of the apical plasma membrane concomitant with a striking depletion of the tubulovesicular structures in the apical plasma region of the cell with chronic metabolic acidosis. These findings suggest that in response to chronic metabolic acidosis membrane, possibly containing a proton pump, is transported from the tubulovesicular membrane compartment to the apical plasma membrane of the intercalated cell.

Acidosis↗