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PubMed1994

[Changes in cerebral extracellular pH, cerebral blood flow and intracranial pressure induced by hypercarbic ventilation--assessment as a potential in vivo model of cerebral acidosis].

The effects of acidosis on ischemic brain damage are unclear and probably diverse. To establish an in vivo model of acidosis, the authors assess changes in extracellular brain pH (pHe), CBF and ICP induced by hypercarbic ventilation, and discuss the reliability and short comings of this experimental model. Acidosis was induced by increasing the inspired CO2 concentration in mechanically ventilated rats. pHe was measured with a pH-sensitive electrode implanted into the cortical mantle. The rats were divided into five groups according to the CO2 concentrations inspired: G-1, 0% control; G-2, -5-% CO2; G-3, -10-% CO2; G-4, -20-% CO2; G-5, -25-% CO2. Cortical blood flow was measured using a laser Doppler flowmeter, and ICP was also determined in each of the experimental groups. pHe decreased rapidly after the CO2 supply was turned on and remained almost constant at fixed concentrations of inspired CO2. pHe values diminished as the concentration of inspired CO2 decreased, as follows: G-2, -0.10 +/- 0.03; G-3, -0.31 +/- 0.08; G-4, -0.49 +/- 0.09; G-5, -0.64 +/- 0.10. The changes in pHe almost perfectly paralleled the changes in blood pH. The percentage increase in CBF was more than 200% in the G-2 groups and minimal increases in CBF, probably due to changes in blood pressure, were observed in from G-2 to G-5. Changes in CBF paralleled changes in systemic blood pressure, especially after the CO2 supply was turned off. ICP also rose after increasing the CO2 supply, and the pattern of changes was similar to that of CBF.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis, Respiratory↗
PubMed1994

Renal tubular acidosis in Kelantan, Malaysia--a case review.

Renal tubular acidosis (RTA) is a defect in urinary acidification in the absence of renal failure. All records of patients admitted to adult medical wards at the University Hospital USM (HUSM), Kelantan between 1986 to 1990 with the diagnosis of renal tubular acidosis were reviewed. Sixteen (16) patients were identified and fulfilled the diagnostic criteria. Their mean age at presentation was 28.9 +/- 0.74 years. The triad of muscle weakness, hypokalaemia and systemic metabolic acidosis were the characteristic features at presentation. Normal serum alkaline phosphatase and skeletal X-rays were noted. Their prognosis were generally good. Their mean serum bicarbonate and potassium on follow up were 17.84 +/- 0.35 and 3.82 +/- 0.05 mmol/L respectively. The importance of regular follow-up and long-term management is emphasised.

Acid-Base Equilibrium↗
PubMed1994

Mild acidosis delays hypoxic spreading depression and improves neuronal recovery in hippocampal slices.

Severe tissue acidosis has been viewed traditionally as a damaging component of cerebral hypoxia. However, a neuroprotective action of low pH during hypoxia has been described in primary neuronal cultures. To identify and characterize this effect in mature brain tissue, adult rat hippocampal slices were made hypoxic after adjusting pHo with HCl or NaOH. Ion-selective microelectrodes were positioned in CA1 to record evoked field potentials, extracellular DC voltage (Vo), pHo, and [Ca2+]o. Orthodromic population spike amplitude was used as a measure of slice recovery 2 hr after reoxygenation. All slices became markedly acidotic during hypoxia (delta pHo approximately 0.4 pH unit). Following restoration of O2 and bath pH to 7.4, slice pHo returned to its pretreatment level regardless of experimental treatment, hypoxic duration, or the degree of electrophysiological recovery. When either the period of hypoxia or the duration of HSD was held constant, acid-treated slices exhibited a significant improvement in recovery. However, in neither paradigm did the recovery of alkaline-treated slices differ from controls. Mild acidosis (bath pH = 6.9-7.3) caused a reversible depression of the orthodromic population spike, an increase in the latency of hypoxic spreading depression-like depolarization (HSD), and a decrease in the magnitude of the associated negative Vo shift. For each of these parameters, mild alkalinity (bath pH = 7.7) had the opposite effect. Acid treatment did not affect the decrease in [Ca2+]o during HSD but accelerated its recovery after reoxygenation. These results suggest that mild acidosis may limit hypoxic neuronal injury in vitro by delaying HSD onset and by additional mechanisms unrelated to the degree of calcium influx during neuronal depolarization.

Acidosis↗
PubMed1994

Stromal acidosis modulates corneal swelling.

PURPOSE: Studies have shown that stromal acidosis reduces the rate of corneal thickness recovery after induced edema, providing the first human in vivo evidence that corneal pH can influence corneal hydration control. This finding raises the question of the possible effect that pH may have on induced corneal swelling. To explore this question, the corneal swelling response to hypoxia was measured while stromal pH was controlled. METHODS: Corneal edema and stromal acidosis was induced in ten subjects by passing a mixture of nitrogen and carbon dioxide gas across the eyes through tight-fitting goggles. One eye of each subject received 100% N2, whereas the contralateral eye received a mixture of 95% N2 and 5% CO2. Exposures of 95% N2 + 5% CO2 lower pH on average to 7.16 versus 7.34 for 100% N2 alone. Before and after 2.5 hours of gas exposure, central corneal thickness (CCT) was measured. RESULTS: Eyes exposed to the lower pH environment (eg, N2 + CO2) developed less change in CCT compared to the eyes receiving N2 alone. Overall increase in CCT was 29.9 +/- 5.3 microns for eyes exposed to the 95% N2 + 5% CO2 gas mixture, versus 37.1 +/- 4.8 microns for 100% N2 eyes (P < 0.0001). CONCLUSIONS: The corneal swelling response to hypoxia can be reduced by lowering stromal pH. Because changes in corneal pH alone have not been found to alter steady-state CCT, it is proposed that pH exerts its effect only under non-steady-state conditions (ie, corneal swelling and deswelling). This suggests that acidosis may produce changes in the rate of lactate metabolism or alter endothelial hydraulic conductivity.

Acidosis↗
PubMed1994

[Effects of NaHCO3 on cardiac function and metabolism during hypoxic metabolic acidosis--1: Slow infusion of NaHCO3].

Effects of NaHCO3 on metabolic acidosis during hypoxia and after reoxygenation were studied in 18 anesthetized dogs. Metabolic acidosis was produced by inhalation of low fraction of oxygen (9%) for 2 hours. NaHCO3 1M was infused intravenously during hypoxia (n = 12) and 30 minutes after reoxygenation (n = 6) at the rate of 100 ml.min-1 (total 0.2 x body weight x base excess mEq). After reoxygenation, NaHCO3 significantly increased blood and intramyocardial pH and decreased blood lactate (LA) level. Maximal rate of rise of left ventricular pressure (LV dP/dt max) and cardiac index (CI) increased significantly, and left ventricular end-diastolic pressure (LVEDP) and LVEDP/left ventricular pressure (LVP) were unchanged. During hypoxia, NaHCO3 also significantly increased blood and intramyocardial pH but those changes were less than the values after reoxygenation, while blood LA level increased significantly. LVP and LV dP/dt max tended to decrease, while LVEDP and LVEDP/LVP increased significantly. In 8 of 12 dogs, myocardial glucose uptake increased but was not correlated with myocardial LA uptake and LV dP/dt max. Blood LA level correlated significantly with LV dP/dt max (r = 0.534, P < 0.01). It appears that during hypoxia, differing from reoxygenation, NaHCO3 may depress cardiac function due to intramyocardial acidosis.

Acidosis, Respiratory↗
PubMedDate not supplied

[Risk of neonatal acidosis and maternal respiration during labor].

BACKGROUND: The reported incidence of neonatal acidosis varies++ significantly in different obstetrical departments. We wanted to investigate to which extend neonatal acidosis is depended on maternal respiration patterns during the third stage of labor. METHODS: Maternal arterial blood gas analysis was performed in 101 term pregnancies. Fetal acid-base parameters from arterial and venous umbilical blood were assessed simultaneously. SPEARMAN rank correlation (rs) was used to investigate the statistical relationship of maternal and fetal blood gas parameters and pH-values. Moreover a computer model was developed to describe the influence of maternal respiration on neonatal acidotic risk figures. RESULTS: A highly significant correlation was established between corresponding variables in maternal arterial blood and in venous umbilical blood (rs > or = 0.500, 2P < 0.001). These correlations were not as striking when comparing maternal parameters with corresponding variables in arterial umbilical blood. The partial oxygen pressure in arterial and venous umbilical blood did not show any correlation with the variables of the maternal acid-base status. In the computerized simulation model mild maternal hyperventilation during the third stage of labor decreased the risk of neonatal acidosis (pH, UA < 7.100%) by approximately 25% without evidence of lack of fetal oxygen supply. CONCLUSIONS: A mild maternal hyperventilation synchronized with uterine contractions during the third stage of labor in combination with rapid breathing when delivering the fetal head has a favourable influence on the neonatal acid-base balance. In this study there is no indication that such an obstetrical management results merely in a laboratory artifact, because according to our data there was indeed no indication of compromised fetal oxygen supply. Routine fetal blood sampling also from venous umbilical blood appears to be useful in differentiating between combined feto-maternal and isolated fetal variations in actual pH-values.

Acid-Base Equilibrium↗
PubMed1993

Brain acidosis induced by hypercarbic ventilation attenuates focal ischemic injury.

Intracellular calcium toxicity appears to play a major role in cell death during cerebral ischemia. Such calcium enters the cell mainly through the N-methyl-D-aspartate subclass of the postsynaptic glutamate receptor. Increased extracellular hydrogen ion concentration has been shown recently to reduce N-methyl-D-aspartate-activated divalent cation currents. Therefore, we studied the effect of induced brain acidosis, via hypercarbic ventilation, as a potential therapeutic modality in focal cerebral ischemia. Brain acidosis reduced infarct volume in a biphasic manner, with maximal protection at approximately brain pH 6.8. The effect was lost at pH 6.5, presumably due to the effect of acidosis on glial glutamate uptake.

Acidosis, Respiratory↗
PubMed1993

Hyperplasia of pulmonary arterial media in infantile familial pulmonary hypertension associated with severe metabolic acidosis.

Two female siblings, offspring of consanguinous parents, died at 10 and 12 wk of age following short illnesses characterized clinically by hypoxia and severe metabolic acidosis. Cardiac catheterization confirmed severe pulmonary hypertension in the second infant, who survived 6 wk after onset of symptoms and 4 wk after admission to hospital; extensive investigations failed to identify any inborn metabolic error. At autopsy, small pulmonary arteries/arterioles in both cases showed marked medial thickening due to smooth muscle hyperplasia; concentric intimal fibrosis was present focally in the older infant. Compared morphometrically with small pulmonary arteries in 20 infantile controls who died of Reye's syndrome (n = 8), a Reye's-like illness (n = 5) or an identified metabolic error associated with metabolic acidosis (n = 7), intraacinar pulmonary arteries in both cases, were significantly more numerous and had a significantly greater relative medial thickness. We suggest that an autosomal recessive gene caused or potentiated the pulmonary medial hyperplasia. The latter finding, compared with medial hypertrophy, is rarely described as the morphologic basis of pulmonary hypertension, and its occurrence may be restricted to early infancy. In this family, the relationship between hypertensive pulmonary arteriopathy and severe metabolic acidosis remains speculative.

Acidosis↗
PubMed1993

Lactic acidosis.

Lactic acidosis is the most common metabolic acidosis. At clinical presentation, several causes usually can be identified. The liver is a major site of removal of lactate and hydrogen ions, and abnormalities in the aerobic metabolism of lactate by mitochondria in hepatocytes and other cells may contribute to many clinical conditions in which overproduction and underuse of lactate occur. To date, no therapy specifically designed to lower arterial blood lactate levels has reduced mortality significantly. Prompt recognition and treatment of the underlying causes of lactic acidosis remain the cornerstone of treatment.

Acidosis, Lactic↗
PubMed1977

Effect of amphotercin B on urine acidification in rats: implications for the pathogenesis of distal renal tubular acidosis.

It has been proposed that distal renal tubular acidosis is a gradient-limited disorder an that the low urine Pco2 observed in this condition is caused by back diffusion of carbonic acid. This study was designed to examine this hypothesis using the amphotericin B model of gradient-limited distal renal tubular acidosis in rats. After induction of acute metabolic acidosis the minimum urine pH in 12 of 24 amphotericin B-treated rats exceeded 5.63 (mean 5.76 +/- 0.04), whereas it was 5.41 +/-0.04 in control rats. These animals with impaired urine acidification were presumed to have a gradient lesion and were studied in bicarbonate-loading experiments. The urine minus blood Pco2 gradient in these rats was 24.9 +/- 1.5 mm. Hg, a value similar to that of the control rats (26.7 +/- 2.1 mm. Hg). The presence of a normal urine minus blood Pco2 value in this experimentally induced gradient-limited type of acidification lesion indicates that a permeability defect for hydrogen ions was not associated with a similar defect for carbonic acid and that the urine minus blood Pco2 gradient is a valid index of distal nephron hydrogen ion secretion in amphotericin B-like gradient-type lesions.

Acidosis, Renal Tubular↗
PubMed1993

[Growth and protein metabolism in chronic metabolic acidosis from experimental renal insufficiency].

Two studies of uremia-induced chronic metabolic acidosis (CMA) were carried out to determine: 1) the level of acidosis beyond which growth failure occurs; 2) the protein metabolism anomalies which are associated with growth failure. Rats rendered uremic by subtotal nephrectomy were fed a diet containing sufficient protein amounts (30% casein) to induce CMA. CMA was left uncorrected in half the rats (group A) and was corrected by administration of bicarbonate in the other half (group B). 1) Fifty-two group A rats were compared with 52 group B rats matched for renal function. Results showed that a) CMA failed to reduce food intake; b) weight gain decreased only when CMA was profound (pH < 7.20) whereas reductions in length gain occurred at less severe levels of acidosis (pH < 7.25) suggesting that bone may be more susceptible to CMA than muscle mass. 2) Protein fractional synthesis rate was evaluated in skeletal muscle after a flooding dose of 3H-phenylalanine in group A rats (pH 7.22 +/- 0.01, HCO3-: 15.2 +/- 0.8 mmol/l) and group B rats matched for renal function. Values were identical in both groups (10.4 +/- 0.5 vs 10.8 +/- 0.5%/day). However, fractional muscle protein accretion rate was decreased in group A rats. These data demonstrate that CMA-associated growth failure in uremia is due to increased breakdown of protein with no change in protein production.

Acidosis, Lactic↗
PubMed1993

[Infusion therapy in newborn calves with diarrhea from the area of Ankara with special reference to acidosis (part 1)].

Characteristic changes (hyperkalemia, metabolic acidosis and azotemia) occurred in the blood of 54 calves 1 to 15 days old with diarrhoea. Clinical signs of dehydration were observed. Average values were: Potassium 6.37 mmol/l, pH 7.17, bicarbonate 18.76 mmol/l, base excess (BE)-10.01 mmol/l, urea % 78.2 mg. The amount of 1.3% sodium bicarbonate solution to be given to calves with patent metabolic acidosis was determined according to the following formula: HCO3- (mmol/l = body weight (kg) x 0.5 x BE. In most of the cases with severe metabolic acidosis (pH < 7.0), a good compensating effect was obtained. Infusion treatment brought blood pH and base excess values near to normal, and bicarbonate concentration to within the physiological range. Balanced solutions were used in the regulation of electrolyte-fluid balance. Hematocrit, potassium and urea values, which had been pathologically high, returned to normal following infusion treatment. Apart from this, patients were given symptomatic treatment according to the important clinical findings. Forty-two animals recovered completely after intravenous infusion of buffer and electrolyte solutions. Twelve out the total of 54 animals died within 1-5 days despite infusion treatment.

Acidosis↗
PubMed1977

[Lactic acidosis after administration of guanidine derivatives (buformine, phenformine) (author's transl)].

Three patients are reported on, who at the time of admittance showed a decompensated metabolic acidosis, elevated concentrations of serum lactate and a reduced kidney funktion. All the patients had taken guanidine derivates (phenformine, buformine) because of diabetes mellitus. The serum biguanid concentrations, however, were elevated in only two cases. Therapy of the lactic acidosis has to be directed at the underlying disease. In biguanid incluced acidosis, haemodialysis with simultaneous administration of sodium bicarbonate is indicated.

Acidosis↗
PubMed1995

Metabolic acidosis and osteodystrophic bone disease in predialysis chronic renal failure: effect of calcitriol treatment.

The role of metabolic acidosis on osteodystrophic bone lesions of chronic renal failure has been studied retrospectively in 24 patients, divided into two equal groups of 12, one with normal acid-base equilibrium (group A) and one with metabolic acidosis (group B). The two groups were found to differ significantly in serum levels of BGP (23.7 +/- 18 vs. 42.3 +/- 24 ng/ml, p < 0.02) and in several bone histomorphometric parameters such as osteoid volume (4.5 +/- 3.4 vs. 10.2 +/- 6.6%, p < 0.01), osteoid surface (27.7 +/- 18 vs. 48.4 +/- 19%, p < 0.01), single-labelled surface (7.94 +/- 2.9 vs. 15.8 +/- 9.9%, p < 0.02), mineralizing surface (60.69 +/- 26 vs. 30.89 +/- 15.8%, p < 0.003) and mineralization lag time (56.5 +/- 54 vs. 170.5 +/- 189 days, p < 0.05), with the acidotic group showing excess osteoid and a defect in mineralization. Osteomalacia was found only in the acidotic group, while the only 2 cases of adynamic bone disease (ABD) were in the nonacidotic group. Calcitriol administration, 0.25 micrograms daily for a period of 1 year, in 5 cases in group A and 6 cases in group B induced significant improvement of bone lesions mainly in group A. Two of these patients following treatment acquired the characteristics of ABD. In group B, the response to treatment was very limited, with 5 patients still showing persistence of the histological mixed type of bone disease. In conclusion, metabolic acidosis is accompanied by osteomalacia, pure or mixed variety, and shows a relative resistance to calcitriol administration. Normal acid-base equilibrium is more frequently associated with mild hyperparathyroidism and ABD, spontaneously or as a consequence of calcitriol administration.

Acid-Base Equilibrium↗
PubMed1995

Induction of lactic acidosis in cattle with sucrose: relationship between dose, rumen fluid pH and animal size.

To determine an efficient way to induce rumen lactic acidosis (rumen fluid pH 4.2 to 3.9 at 20 h after dosing), different dosages of sucrose on a basis of body weight (BW; 12 g/kg BW), metabolic weight (MW; 60 g/kg BW0.75 and corrected metabolic weight (CMW; y = 1057 + 43.1 BW0.75) were used in cattle of different size. In all cases rumen lactic acidosis occurred, although yearling steers given sucrose on a basis of BW had higher rumen fluid pH than yearlings given sucrose on a basis of MW and CMW. The heavier the yearlings given sucrose were (on a basis of BW and MW), the lower the rumen fluid pH. Bullocks given sucrose on a basis of BW and MW presented lower rumen fluid pH than those given sucrose on a basis of CMW. The heavier the bullocks given sucrose on a basis of BW and MW, the lower the rumen fluid pH. Only cattle given sucrose on a basis of CMW had a predictable rumen fluid pH within the desired range in both animal sizes. Larger cattle were more vulnerable to rumen lactic acidosis than smaller ones.

Acidosis, Lactic↗
PubMed1996

Forestomach acidosis in six New World camelids.

Forestomach acidosis was diagnosed in 2 llamas and 4 alpacas. All were young, group-housed, sexually intact males. Clinical signs included forestomach atony, lethargy, ataxia, diarrhea, and tachycardia. Forestomach distention was observed in only 1 llama. Clinicopathologic abnormalities included low forestomach fluid pH, hyperchloremia, hypokalemia, and metabolic acidosis. Although camelids differ from domestic ruminants in typical management practices and behavioral, anatomic, and physiologic characteristics, they are, nonetheless, susceptible to forestomach acidosis. Gastric fluid analysis was essential for an accurate diagnosis. Four of 6 camelids recovered after PO and IV treatment with alkalinizing agents and fluids, antibiotics, and thiamine.

Acid-Base Equilibrium↗
PubMed1996

Muscle protein turnover in chronic renal failure patients with metabolic acidosis or normal acid-base balance.

It is currently unknown if metabolic acidosis has any effect on muscle protein metabolism in patients with chronic renal failure (CRF). To address this question, muscle protein turnover was studied in patients with CRF and controls in the postabsorptive state by using the forearm perfusion method together with the 3H-phenylalanine kinetics. Nine patients were acidotic ([HCO-3]a = 20 +/- 0.5 mEq/l) whereas 4 patients had a normal acid-base balance ([HCO-3]a = 25 +/- 0.3 mEq/l). In patients with metabolic acidosis the rates of phenylalanine appearance and disposal from the forearm were increased as compared to controls. Phenylalanine net balance, i.e. net proteolysis, was only slightly higher than in controls. In patients under a normal acid-base balance both rates of appearance and disposal of phenylalanine as well as phenylalanine net balance were similar to controls. These preliminary data suggest that metabolic acidosis can enhance the rate of muscle protein degradation in patients with CRF.

Acidosis↗
PubMed1996

Acidosis and glucocorticoids induce branched-chain amino acid catabolism.

Chronic renal failure (CRF) is frequently complicated by malnutrition and wasting. The loss of lean body mass in CRF is the result of accelerated protein and amino acid degradation. Both appear to occur via acidosis-induced, glucocorticoid-dependent processes. In skeletal muscle, acidosis stimulates the activity of the rate-limiting enzyme in branched-chain amino acid metabolism, branched-brain ketoacid dehydrogenase (BCKAD). The activation of BCKAD in acidosis is likely to be glucocorticoid-dependent.

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