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PubMed1977

Relaxation of coronary artery strips by adenosine and acidosis.

Cumulative dose-response curves of Ca2+-induced tension increments were studied in K+-depolarized helical strips of dog coronary arteries. Adenosine 10(-4) M reduced the Ca2+ sensitivity of the strips without altering the maximal tension with full Ca2+ activation. In contrast, acidosis of pH 7.05 significantly diminished the maximal tension with full Ca2+ activation. The relaxing effect of acidosis was almost completely abolished by 10(-4) M adenosine. It is concluded that adenosine inhibits Ca2+ influx, whereas acidosis depresses the contractile process of vascular smooth muscle directly.

Acidosis↗
PubMed1990

Effects of hypoxia, acidosis, and simulated ischemia on repriming of caffeine contracture in rat myocardium.

This study was designed to examine the effects of hypoxia, acidosis, glucose-free medium and their combination on contraction and sarcoplasmic reticulum (SR) function in rat ventricular trabeculae. The isometric twitch tension was measured during superfusion with hypoxic (PO2 less than 30 mmHg), acidic (pH 6.80), glucose-free, or their combined ("ischemic") Tyrode's solution at 20 degrees C. The time needed to fully recover the contraction induced by 10 mM caffeine (repriming time) was measured to indirectly estimate the Ca2+ uptake of the SR. In "ischemia" and acidosis, the peak developed tension decreased progressively for the first 30 min (37.6 +/- 9.2% and 56.6 +/- 8.4% of control at 30 min, respectively), and then became steady. In hypoxic solution, the peak developed tension decreased moderately for the first 30 min (86.8 +/- 4.8% of control at 30 min), and thereafter remained steady. Developed tension did not change significantly during 60 min of superfusion with glucose-free solution. The repriming time of caffeine contraction was significantly delayed in both "ischemic" and hypoxic solutions, but was unchanged in acidic and glucose-free solutions. These results lead us to suggest that depressed SR function to accumulate Ca2+ may contribute to the decline in tension in ischemia and hypoxia, but that other mechanisms are important in the tension decline induced by acidosis.

Acidosis↗
PubMed1985

Effects of tissue acidosis on skeletal muscle microcirculatory responses to hemorrhagic shock in unanesthetized rats.

Arteriolar dilatation, loss of venous tone, and uptake of shed blood characterize decompensated hemorrhagic shock. The loss of compensatory constrictor responses to hemorrhage mainly occurs in the skeletal muscle microcirculation. Tissue acidosis may be an important mediator of this phenomenon. Using a decerebrate in vivo rat cremaster muscle preparation, we observed the microcirculatory responses to hemorrhagic hypotension with cremaster bath conditions of pH 7.4 and pH 7.0. Our data indicate that tissue acidosis attenuates constrictor responses of larger arterioles (100-170 micron) and venules to hemorrhagic hypotension but has no effect on the dilator responses of small arterioles (10-30 micron). We conclude that tissue acidosis contributes significantly to loss of arteriolar resistance and to decreased venous return in the decompensatory phase of hemorrhagic shock.

Acidosis↗
PubMed1982

Evaluation of sodium acetate as a source of alkali therapy in an experimental aerobic model of lactic acidosis due to decreased pyruvate oxidation.

An "in vitro" model of one type of lactic acidosis was produced in rat hemi-diaphragms with inhibitors of pyruvate oxidation. In order to obtain this inhibition in the absence of hypoxia, two actions were sought; inhibiting the mitochondrial pyruvate transporter and lowering the rate of pyruvate diffusion into these mitochondria. alpha-Cyano-3-hydroxy cinnamate (CNCM) was utilized because it is a specific inhibitor of the mitochondrial pyruvate transporter. Aminooxyacetate (AOA) was employed because it leads indirectly to inhibition of the entry of cytoplasmic reducing power into mitochondria. As a result of the addition of this latter compound, pyruvate levels fell and this should decrease the rate of pyruvate diffusion into the mitochondria. Glucose was the only substrate provided to this tissue and its entry into the cells was promoted by insulin. The oxidation of U-14C glucose to 14CO2 was significantly reduced in the presence of CNCM and AOA, presumably reflecting the inhibition of pyruvate oxidation. Under these conditions, lactate accumulated and pyruvate fell; however, there was a significant accumulation of lactate plus pyruvate during the incubation period. This "in vitro" lactic acidosis was markedly diminished when acetate was also present. These results are consistent with the hypothesis that provision of an alternate substrate to the TCA cycle for ATP synthesis could lead to a decreased rate of glycolysis and thereby to a decreased rate of lactic acid accumulation in this "in vitro" model of lactic acidosis.

Acetates↗
PubMed1984

Release of lactate by the liver in metabolic acidosis in vivo.

Chronic metabolic acidosis was induced in dogs by HCl. Pyruvate and lactate production and extractions were studied by arteriovenous sampling and electromagnetic flow probe measurements of gut and hepatic blood flows. The following results were obtained: (1) In control, overnight-fasted dogs, no net lactate or pyruvate was extracted by the liver. (2) In chronic acidosis, large amounts of lactate were produced. (3) Reduced tissue pyruvate levels and reduced activity of pyruvate dehydrogenase were found in the liver of these dogs compared with normal. These results demonstrate an unexpected effect of acidosis on hepatic lactate metabolism.

Acidosis↗
PubMed1987

Hypercalciuria and altered intestinal calcium absorption occurring independently of vitamin D in incomplete distal renal tubular acidosis.

Negative calcium balance and calcium nephrolithiasis are two sequelae of chronic metabolic acidosis. To establish the effects of acidosis on calcium and vitamin D metabolism, we have examined a group of nine patients with incomplete distal renal tubular acidosis. Patients were studied during a control phase and after eight months of potassium citrate treatment, 60 to 80 meq daily. Potassium citrate caused a significant decrease in urinary calcium. The fractional intestinal calcium absorption increased significantly, yet no change was observed in serum vitamin D levels. The estimated calcium balance increased significantly from -70.2 +/- 63.8 to +66.7 +/- 48.7 mg/d (P less than 0.01). Thus, potassium citrate treatment improved the estimated calcium balance by lowering urinary calcium while increasing the fractional intestinal calcium absorption. The original hypercalciuric state, its correction to normocalciuria, and the augmentation of intestinal calcium absorption seen in these patients are probably independent of vitamin D control since there was no change noted in serum 1,25-dihydroxyvitamin D levels.

Acidosis, Renal Tubular↗
PubMed1988

Role of glucocorticoids in regulating interorgan glutamine flow during chronic metabolic acidosis.

The role of glucocorticoids in external glutamine mobilization and renal utilization was evaluated in three groups of chronically acidotic rats: sham-treated controls, adrenalectomized, and adrenalectomized supplemented with triamcinolone. Chronic acidosis was induced by administering NH4Cl in their drinking solution over a three-day period. Adrenalectomized rats were supplemented by triamcinolone at a dose of 40 micrograms/100 g/d administered by pellet implantation. Interorgan glutamine flow was evaluated in the postabsorptive state by monitoring net balances across the hindquarters, gut, liver, and kidneys. In the adrenal-intact group, acidosis increased the flow of glutamine from the hindquarters to the kidneys; splanchnic bed uptake, the major glutamine sink in nonacidosis, was eliminated by virtue of hepatic reversal from net uptake to release. Adrenalectomy, in the absence of an exogenous acid load, reversed the flow of glutamine with the kidneys releasing and the hindquarters removing glutamine. Acid loading restored hindquarter glutamine release to levels seen in the intact chronically acidotic animals; however, renal extraction is much less than that exhibited by the intact animals. As a consequence, arterial glutamine concentration rose with the overflow removed by the splanchnic bed, the major glutamine sink in adrenalectomized acidotic rats. Supplementing adrenalectomized acidotic rats with triamcinolone restored glutamine extraction to values seen in intact acidotic rats. Despite the renal extraction, the large hindquarter glutamine release led to hepatic uptake and a high rate of ureagenesis. Glucocorticoids, the release of which is enhanced in metabolic acidosis, appear essential for renal glutamine extraction while playing a lesser role in modulating hindquarter glutamine release.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis↗
PubMed1994

Effects of EUK-8, a synthetic catalytic superoxide scavenger, on hypoxia- and acidosis-induced damage in hippocampal slices.

Anoxia produces deleterious effects on synaptic transmission in the hippocampal slice preparation. A proposed source of damage is the superoxide radical (.O2-) produced during the earlier period of reoxygenation. The present study tested the effects of a synthetic, catalytic superoxide radical scavenger (EUK-8) on CA1 pyramidal cell responses elicited by electrical stimulation of the Schaffer-commissural pathway after severe anoxic episodes. Following reoxygenation, slices incubated with EUK-8 (50 microM) exhibited significantly better recovery of excitatory postsynaptic potentials (EPSPs) than control slices. In addition, repeated episodes of anoxia produced irreversible loss of synaptic transmission in the majority of control slices (93 +/- 7%, n = 15), compared to a small fraction in EUK-8-incubated slices (27 +/- 12%, n = 15). A thiobarbituric acid (TBA) test was used to assess the effect of EUK-8 on lipid peroxidation elicited in hippocampal slices by acidosis and lactic acid (pH 5.0 and 30 mM lactic acid). Incubation in the presence of EUK-8 totally prevented the increase in lipid peroxidation produced by acidosis and lactic acid in both the incubation medium and the slice homogenates. These results indicate that a superoxide scavenger like EUK-8 prevents damage produced by acidosis and anoxia in hippocampal slices and suggest the possibility of using this type of molecule under various pathological conditions.

Acidosis↗
PubMed1976

Cardiac and skeletal muscle acid-base composition during metabolic acidosis in dogs.

Nephrectomized, open chested dogs were infused with 25-30 ml.kg(-1) body weight of 0.15 M NaCl (group I), 0.15 MHCl (Group II) or 0.3 M lactic acid (Group) III). Pulmonary ventilation was maintained constant in the three groups. Intracellular pH was calculated with the CO2 method. No significant intracellular or extracellular acid-base changes were produced in Group I. A similar degree of extracellular acidosis was achieved in Groups II and III. In spite of constant arterial PCO2, the PCO2 of mixed, coronary sinus and femoral vanous blood increased moderately after the infusion in Groups II and III. It was calculated that less than half of the HCl acid infused remained in the extracellular space. However, no significant changes were observed in the acid-base composition of skeletal muscle in either Group II or III. Comparison of the cardiac muscle cell acid-base composition of Group I with that of Groups II and III whows that metabolic acidosis of the degree and duration produced in these experiments does not produce appreciable myocardial acidosis.

Acid-Base Equilibrium↗
PubMed1991

Effects of anoxia and graded acidosis on the levels of circulating catecholamines in turtles.

We measured circulating levels of catecholamines in painted turtles subjected to anoxia with different degrees of concomitant acidosis at 20 degrees C and in turtles subjected to long-term submergence at 3 and 10 degrees C. Blood levels of both epinephrine (E) and norepinephrine (NE) increased during N2-breathing, N2/CO2 breathing and submergence, with NE generally being present in higher concentrations than E. During submergence at 20 degrees C, anoxic turtles experienced an extreme acidosis and NE levels exceeded 18,000 pg/ml. The greater the degree of acidosis in anoxic turtles the higher were the levels of plasma NE (log [NE; pg/ml] = 1.640 x pHa + 15.776, r = -0.826). Elevation of plasma E under anoxic conditions was more modest and the correlation between plasma E and pHa was less pronounced (log [E; pg/ml] = -0.329 x pHa + 6.069, r = -0.285). Submergence at lower temperatures also resulted in increases in plasma levels of NE, but while plasma E generally increased during anoxia, this elevation was less dramatic than that observed for NE. Exposure of turtles to either mild (6.5% CO2) or severe (14.5% CO2) normoxic hypercapnia resulted in no increase in E and only modest increases in NE. Upon resumption of air-breathing in all of the 20 degrees C protocols, turtles rapidly restored E and NE to control levels. The function of elevated plasma catecholamines during anoxia and acidemia in turtles is unknown but may be important in stimulating respiratory and cardiovascular recovery once air-breathing is resumed. Catecholamines may also play a role in mediating the rise in blood glucose we observed in this study, which may be an important factor in maintaining tissue viability during anoxic stress.

Acidosis↗
PubMed1995

Transient acidosis induces delayed neurotoxicity in cultured hippocampal slices.

It remains unknown if tissue acidosis contributes to neuronal loss during cerebral ischemia. We report that brief intracellular acidification (pH 6.62) results in delayed neuronal loss in cultured hippocampal slices. Cell loss was located primarily in stratum pyramidale and the hilus suggesting that neurons were preferentially damaged. Removal of molecular oxygen greatly attenuated cell loss suggesting that generation of reactive oxygen species may underlie acidosis-induced toxicity. These data suggest that acidosis and incomplete anoxia contributes to the delayed neuronal loss in the ischemic penumbra.

Acidosis↗
PubMed1984

The effects of chronic metabolic acidosis on patterns of protein synthesis in rat renal cortex.

In the rat chronic metabolic acidosis increases the net synthesis of 17 renal cortex proteins by amounts ranging from 1.5 to 4.5-fold. These proteins have molecular weights between 13,000 and 42,000 and isoelectric points between approximately 5.5 and 7.0. No new proteins not also present in normal animals are detected in renal cortex samples from acidotic animals. Three proteins undergo substantial reductions in their net synthetic rates in chronic metabolic acidosis. On the basis of their physical properties and similar alterations in net synthetic rate in acidosis some of these proteins appear to be closely related and may be coordinately expressed in the rat kidney.

Acidosis↗
PubMed1986

Effect of respiratory acidosis on glucose homeostasis in experimental intrauterine growth retardation in rats.

Hypoglycemia and asphyxia account for a significant proportion of morbidity in the infant with intrauterine growth retardation (IUGR). The purpose of this study was to evaluate changes in glucose homeostasis in IUGR rats during acute respiratory acidosis. IUGR was produced by bilateral uterine artery ligation at 17 days of gestation in 14 pregnant rats with 23 successfully delivered pups. The normal pups (n = 31) were those whose mothers were sham operated at the same gestational period. The IUGR and normal pups were studied at 2 days of age. One group of pups was studied under room air while another was subjected to 20 min of exposure to a gas mixture of 10% O2/15% CO2, balanced with N2. Gluconeogenesis in the liver and carcass, as well as plasma glucose and catecholamines were determined before and after the exposure to the gas mixture. The results showed that the 2-day-old IUGR rats have lower body weight (P less than 0.001), liver weight (P less than 0.001), plasma glucose (P less than 0.001), and rate of gluconeogenesis (P less than 0.01) when compared with the normally grown rats. During respiratory acidosis, the normally grown rats showed an increase in plasma epinephrine (P less than 0.005) without significant change in plasma glucose and rate of gluconeogenesis. The IUGR rats on the other hand, demonstrated a decrease in rate of gluconeogenesis (P less than 0.02), an increase in plasma glucose (P less than 0.001) while the plasma epinephrine level remained unchanged. We speculate that respiratory acidosis blunted cellular metabolism in the IUGR rat resulting in decreased peripheral glucose utilization.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis, Respiratory↗
PubMed1987

Convulsions as the etiology of lactic acidosis in acute diazinon toxicity in rats.

Diazinon, in acute doses (40 mg/kg, i.p.) in rats produced tremors and convulsions with lactic acidosis which was accompanied by depletion of glycogen and activation of glycogen phosphorylase activity in triceps and diaphragm muscles, 2 h after its administration. Prevention of convulsions with phenobarbitone administered immediately before diazinon, resulted in neither the development of lactic acidosis nor mobilization of muscle glycogen or activation of glycogen phosphorylase. Lactic acidosis was due to depletion of glycogen through enhanced activity of glycogen phosphorylase in muscles on account of tremors and convulsions induced by diazinon in rats.

Acidosis, Lactic↗
PubMed1985

Arterial pH in out-of-hospital cardiac arrest: response time as a determinant of acidosis.

It is unclear why some victims of out-of-hospital cardiac arrest are severely acidotic on arrival to the emergency department (ED), whereas others have a pH within normal limits. To explain the difference among patients, the authors collected data on 119 consecutive out-of-hospital adult nontraumatic cardiac arrest victims brought to the University of Nebraska Medical Center by paramedic rescue squad between December 1982 and January 1984. Patients who experienced restoration of spontaneous circulation (ROSC) in the field had a normal pH (7.40 +/- 0.13) as compared with the pH of patients still receiving cardiopulmonary resuscitation (CPR) on arrival at the ED (7.18 +/- 0.20). A rapid paramedic response time was the best determinant of ROSC and a normal pH on arrival at the ED. Bystander CPR neither significantly increased the number of patients with ROSC in the field nor protected against the development of acidosis, but did improve the neurological outcome of survivors. The presence of acidosis in patients still receiving CPR on arrival in the ED could not be predicted on the basis of paramedic response time, amount of sodium bicarbonate given in the field, whether or not the collapse was witnessed, or whether or not bystander CPR had been performed. Patients who were acidotic had a significantly higher (P less than 0.001) Paco2 (101 +/- 33 mm Hg) and a lower Pao2 (41 +/- 69 mm Hg) than patients with a normal pH (Paco2 37 +/- 10 mm Hg, Pao2 134 +/- 107 mm Hg). Adequacy of ventilation is the principal determinant of acidosis in patients who are still receiving CPR on arrival at the ED.

Acidosis↗
PubMed1988

Severe metabolic acidosis secondary to exertional hyperlactemia.

A case is presented of severe metabolic acidosis in a previously healthy man. The cause was attributed to lactic acidosis secondary to exertion. Although lactic acid is commonly produced with increased physical activity, it is usually cleared and buffered rapidly. The pathophysiology of lactic acidosis is discussed.

Acidosis, Lactic↗
PubMed1986

Acidosis-induced osteomalacia: metabolic studies and skeletal histomorphometry.

The pathogenesis of osteomalacia was investigated in three patients with chronic metabolic acidosis. Serum levels of parathyroid hormone and vitamin D metabolites were measured, and bone biopsy specimens were analyzed after double tetracycline labeling. Parathyroid hormone concentrations were normal in patients 1 and 3 and slightly elevated in patient 2. Vitamin D metabolism was undisturbed. Static indicators of bone remodeling substantiated the diagnosis of osteomalacia in each case. In patient 1 fluorescent microscopy revealed no evidence of tetracycline uptake. In patients 2 and 3 active mineralization was evident at all osteoid seams, but because double labels were rare, the mineral apposition rate appears to have been substantially reduced in most bone-forming units. Our results indicate that acidosis-induced osteomalacia, unlike that due to vitamin D deficiency, may be associated with mineral deposition at every possible site. Nevertheless, like other causes of osteomalacia, metabolic acidosis prevents mineral apposition at a normal rate even if mineral deposition is ubiquitous. We suggest that titration of newly deposited phosphate causes the observed impairment of mineral apposition and ultimately leads to osteomalacia.

Acidosis↗
PubMed2004

Are histopathologic chorioamnionitis and funisitis associated with metabolic acidosis in the preterm fetus?

OBJECTIVE: Perinatal infection increases the risk of neonatal neurologic injury. Our objective is to determine whether histologically confirmed chorioamnionitis and funisitis is associated with fetal metabolic acidosis. STUDY DESIGN: This is a retrospective cohort study of all infants 34 weeks or less born at a single tertiary hospital admitted to the neonatal intensive care unit (NICU) between April 1999 and September 2002. Maternal and neonatal records and placental pathology reports were reviewed. RESULTS: There were 392 infants at 23 to 34 weeks' gestational age admitted to the NICU during this period of whom 354 had placental pathology reported; 259 infants had umbilical cord gases available. These neonates were placed into 3 groups: group 1 (208 infants) had no signs of placental infection, group 2 (59 infants) had isolated chorioamnionitis, and group 3 (87 infants) had both chorioamnionitis and funisitis. The gestational age (30.2 +/- 2.8, 28.3 +/- 3.4, 27.8 +/- 2.8 weeks, P < .01) and birth weight (1358 +/- 520, 1242 +/- 547, 1103 +/- 381 g, P < .01) were significantly higher in group 1. There was an increase in neurologic morbidity in groups 2 and 3 (25.2%, 34.4%, 43.7%), which was not significant when corrected for gestational age. Groups 2 and 3 had a small but significant increase in umbilical arterial pH (7.25 +/- 0.10, 7.29 +/- 0.10, 7.30 +/- 0.08, P < .01) and base excess (-3.5 +/- 3.6, -2.2 +/- 3.6, -2.3 +/- 2.7 mmol/L, P = .02). When a single pathologist reviewed all placentas with any inflammation and staged them on the basis of the degree of the fetal inflammatory response, no relationship was found between the degree of fetal inflammation and umbilical arterial pH (stage 1, 7.27 +/- 0.09; stage 2, 7.30 +/- 0.09; stage 3, 7.30 +/- 0.08; P = .41) or base excess (stage 1, -2.82 +/- 3.47 mmol/L; stage 2, -1.95 +/- 3.17 mmol/L; stage 3, -2.23 +/- 3.07 mmol/L; P = .62). When stepwise multiple linear regression was performed, neither histologic chorioamnionitis nor histologic funisitis were associated with a change in umbilical cord pH or base excess. CONCLUSION: Intrauterine infection, as confirmed by histologic chorioamnionitis and funisitis, is not associated with fetal metabolic acidosis. Intrauterine infection may represent a nonhypoxic form of encephalopathy that produces neurologic morbidity by a mechanism independent of hypoxia-ischemia leading to metabolic acidosis.

Acidosis↗