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PubMed1975

[Study of fetal heart rate in deliveries complicated by fetal acidosis].

A study has been carried out on the parameters of the graph of the fetal heart rate (the basal rate and dips) in 44 cases of acute fetal distress with a pH lower than 7.2 in the blood and in 30 normal deliveries. The statistical analysis confirms that there is a significant rise in the number of heart rate abnormalities such as persistent bradycardia or persistent tachycardia and with dips during deliveries with fetal acidosis. The frequency of these abnormalities increases with the degree of acidosis. Sometimes the abnormalities in the fetal heart rate precede the appearance of the acidosis. All the same the discovery of these abnormalities does not by itself make a precise diagnosis of fetal distress because we do find these abnormalities in a certain number of cases even in normal deliveries. Only measuring fetal pH at a definite time can establish the diagnosis of fetal distress and the severity of the condition.

Acidosis↗
PubMed1983

Treatment of renal lithiasis associated with renal tubular acidosis.

In order to determine the incidence of renal lithiasis in patients with renal tubular acidosis and the effect of therapy on further stone formation, we reviewed the clinical and laboratory manifestations, X-ray findings, and treatment of 48 patients with renal tubular acidosis who were seen at the Mayo Clinic during the years 1970-1980. Thirty-four patients (70%) had radiological evidence of renal lithiasis which was the presenting symptom in 23 (48%) patients. In every instance the calculi were multiple and, with one exception, bilateral. While receiving therapy, 19 patients with renal lithiasis were followed for longer than one year with sequential uroradiographic studies. Fifteen of these patients were treated with oral base alone and thirteen had no evidence of new stone formation or continued growth of existing stones during therapy. The two patients with X-ray evidence of continued stone formation admitted to poor compliance. Four patients received initial treatment with an oral phosphorus supplement. Three of these four patients had radiographic evidence of continued renal stone formation during three, five and eight years of phosphate therapy. We conclude renal lithiasis is a frequent complication of renal tubular acidosis, and adequate base replacement is effective therapy to stop continued stone formation while oral phosphate therapy alone is often ineffective.

Acidosis, Renal Tubular↗
PubMed1984

Renal tubular acidosis following intestinal bypass: an etiological study.

Nine cases of the distal type of renal tubular acidosis (RTA) following intestinal bypass were found. Diagnosis was based on inability to acidify the urine to pH values below 5.40 despite systemic acidosis. Acidosis, if not present, was induced by giving ammonium chloride 0.1 g/kg body weight. Patients were examined for diseases known to cause RTA but no already known etiological factor was found. Hyperoxaluria was found in eight of the nine cases with RTA, while not present in patients without RTA or in obese control patients. A causal relationship between hyperoxaluria and RTA is suggested though not proved. Cases reported in the literature of renal damage following bypass are summarized and discussed in relation to presence of hyperoxaluria and RTA.

Acidosis, Renal Tubular↗
PubMed1984

Renal distal tubular acidosis in obstructive nephropathy.

The acidifying capacity of the kidney was studied in patients with obstructive nephropathy. After a loading test with ammonium chloride, incomplete renal tubular acidosis (RTA) could be observed in 22.5% and stone formation in 30% of the patients with renal tubular acidosis. Attention is called to the fact that, in addition to the known anatomical and physicochemical factors, the alkali fixed urine due to incomplete tubular acidosis due to urinary tract obstruction also predisposes to calculus formation.

Acidosis, Renal Tubular↗
PubMed1981

Congenital lactic acidosis associated with pyruvate carboxylase deficiency.

Two cases of congenital lactic acidosis associated with pyruvate carboxylase deficiency are described. One 2-mo-old infant had a fulminant clinical course with extremely severe intractable acidosis and died after 48 h in hospital. The second infant, aged 2 1/2 mo, had a milder clinical course, characterized by moderate acidosis and frequent convulsive episodes. He died at the age of 3 mo due to respiratory arrest following prolonged status epilepticus. Pyruvate carboxylase activity in liver biopsy specimens obtained from the two patients was 1 and 50% of normal, respectively. Both patients failed to respond to treatment, including massive doses of thiamine and high serum levels of lactate and pyruvate were found throughout their illnesses. Cerebral autopsy performed in both cases was unremarkable. Absence of neuropathological findings ruled out the possibility of Leigh's disease.

Acidosis↗
PubMed1983

Influence of phosphoenolpyruvate carboxykinase inhibition on the response of NH3 production to acute acidosis.

The role of PEPCK in the stimulation of NH3 production by acute acidosis was examined by perfusing isolated rat kidneys in the presence of the PEPCK inhibitor, MPA (0.15 mM). The response of kidneys perfused with physiologic quantities of glutamine to both acute respiratory (increase in pCO2) and metabolic acidosis (decrease in bicarbonate concentration) was assessed. Although MPA decreased renal NH3 production at pH 7.4, it had no effect on the stimulation of ammoniagenesis produced by either acute respiratory or acute metabolic acidosis. Thus the stimulation of NH3 production by an acute decline in pH must result from an effect on a metabolic step prior to the conversion of oxaloacetate to phosphoenolpyruvate.

Acidosis↗
PubMed1982

Depression of mechanical and electrical activity in muscle strips of opossum stomach and esophagus by acidosis.

We studied the effect of acidosis on nerve-muscle preparations from the opossum stomach and esophagus. All muscle strips were mounted in superfusion chambers and spontaneous contractile activity was recorded from longitudinal and transverse gastric muscle strips. Mechanical activity in esophageal and oblique gastric muscle strips was elicited by electrical stimulation of intrinsic nerves. The contractile activity of all types of strips changed when the pH of the superfusate was lowered for 30 min from 7.4 to 7.0. The baseline tension rose in strips from the lower esophageal sphincter and in oblique gastric muscle strips, and a baseline tension occurred de novo in longitudinal esophageal strips. Muscle relaxation was also impaired in these three types of strips. The amplitude of contractions declined in transverse strips from the esophageal body and in transverse and longitudinal strips from the stomach. The frequency of spontaneous contractions and of the pacesetter potential as recorded by extracellular electrodes was also reduced by acidosis in muscle strips from the stomach. Similar but less marked changes occurred when the pH was lowered from 7.4 to 7.2 for 30 min. Most changes related to a pH of 7.0 became irreversible after superfusion periods of more than 2 h. These findings indicate that acidosis alters a variety of neuromuscular functions and that its effects are determined by the electrical and contractile characteristics and the intrinsic innervation of individual segments and layers of the gut muscle coat.

Acidosis↗
PubMed1980

[Distal form of renal tubular acidosis and nephrolithiasis].

The distal form of the renal tubular acidosis is a causal factor of the formation of phosphate calculi which is not tao be neglected. Pathophysiology, diagnostics and therapy of the renal tubular acidosis are described under the point of view of the metaphylaxis of urinary calculi. The paraclinical findings of 7 patients with distal renal tubular acidosis and nephrolithiasis and nephrocalcinosis, respectively, are discussed.

Acidosis↗
PubMed1980

The effects of acidosis on canine hepatic and renal oxidative phosphorylation.

The intracellular effects of acidosis remain poorly defined. To examine the effects of acidosis on oxidative phosphorylation, liver biopsies and weight nephrectomies were performed on 10 adult German shepherd dogs. The mitochondria were isolated from each tissue and their respiratory activity was studied by the polarographic technique with the pH of the reaction media varied from 5.5 to 8.0. Glutamate and succinate substrates were employed. Results showed a dramatic reduction in the efficiency of oxygen utilization by mitochondria with glutamate as the reaction medium became more acidic. The efficiency of succinate oxidation was significantly (P less than 0.01) preserved. These findings were confirmed by both the respiratory control indices and by ADP:O ratios. Acidosis appears to result in severe inhibition of NAD-linked energy substrate oxidation.

Acidosis↗
PubMed1980

Lactic acidosis associated with metastatic breast carcinoma.

Occurrence of lactic acidosis with adequate tissue oxygenation (type B lactic acidosis) has been described in association with leukemia, lymphoma and a single case of Hodgkin's disease. No cases of this type have been reported in association with solid tumors. A case of type B lactic acidosis in a woman with rapidly progressing metastatic breast carcinoma is described.

Acidosis↗
PubMed1995

Induced acute ruminal acidosis in goats treated with yeast (Saccharomyces cerevisiae) and bicarbonate.

Ruminal acidosis was induced in twenty-one 10-month-old West African Dwarf Goats by feeding a suspension of 80 g wheat flour per kg bodyweight (day 0) through a stomach tube. Ruminal and systemic acidosis was diagnosed on day 1 in all goats. Clinical signs included loss of rumination and appetite, trembling, and watery diarrhoea. The detection of acidic faeces during the first 24h was considered of diagnostic importance. Subgroups were treated orally on days 1, 2, and 3 either with 1 g of sodium bicarbonate per kg bodyweight, with 1 g of baking yeast per kg, or with a combination of these treatments at 0.5 g of each per kg. A fourth group served as untreated controls. Peroral bicarbonate neutralization was highly effective in the treatment of rumen acidosis, whereas the use of yeast was found ineffective. The combined treatment had a moderate effect probably due to the bicarbonate. Three fatal cases (60%) occurred in the untreated group compared with none in the bicarbonate group, and 2 in each of the remaining groups. This corresponded to 33% of the yeast treated group and 40% of the combined treated group. Details were given on post mortem examinations performed on all survivors on day 11. Lesions included subacute rumenitis and abomasal ulcers. No lesions were found in 3 of the bicarbonate treated goats and in 2 of the animals receiving combined treatment.

Acidosis↗
PubMed1995

[Lactate acidosis: a rare or common disease?].

The authors present a survey of 50 documented cases of metabolic lactic acidosis (MLAC) recorded in the course of 5 years. To this study cases of severe hyperlactataemia (determined minimum lactate level of concentration 4 mmol/l) have been included. The sample consists of patients hospitalized at the Department of Internal Medicine Litomĕrice (hinterland of about 110,000 inhabitants). Liver involvement in 5 cases, cardiogenous shock in 6 cases, sepsis in 2 cases were the cause of lactic acidosis. The administration of biguanids (Adebit, Silubin R, Diformin) seems to be the probable cause in 21 cases, other cases were triggered by rarer causes. Dehydratation (16), vomiting (9), diarrhoea (11) dominate often in the clinical picture. The patients were admitted to the hospital often unconscious, with diagnose of vasculo-cerebral incidence, transitory ischaemic incidence... Quit rarely the typical Kussmaul's respiratory (only 9 cases) was recorded. Hyperlactatemia was usually associated with decrease of blood pH (theta = 7.12, pH less than 7.35 was recorded in 49 cases, pH less than 6.8 in 5 cases) and with decrease of BE value (= Ccoase, theta = -15.3 mmol/l). When the hypochloremia and/or hypocapnia was simultaneously more severe, only in these cases the value of pH was within physiological limits or even increased (10). The conclusions show that MLAC is not a rare disorder, however, its occurrence is depended rather on the clinician's capacity to diagnose this disorder and to indicate lactate examination. Usual signs of acidosis (Kussmaul's respiratory, decrease of pH, decrease of BE) can be missing in many cases.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis, Lactic↗
PubMed1994

Alterations in malondialdehyde concentration of jugular vein blood following transient brain ischemia. The effect of lactic acidosis.

Ischemia was induced for 10 min with a subsequent 60-min reperfusion and the changes of the malondialdehyde (MDA) concentration in the blood samples from the jugular vein were investigated in normo- and hyperglycemic dogs. Selective brain ischemia was evoked by the increase in cerebrospinal fluid (CSF) pressure. The experiments were carried out in 4 experimental groups. In sham operated animals (Group I) the blood MDA concentration did not change. The venous blood MDA content significantly elevated for 10 min after the start of reperfusion in normoglycemic animals (Group II). To study the effect of acidosis during ischemia and reperfusion on brain lipid peroxidation (LP) processes 1 and 2 g/kg glucose infusion was used in Groups III and IV. As an effect of ischemic lactic acidosis due to hyperglycemia the elevation of MDA concentration in the jugular vein blood was higher and it lasted longer than in the cases of normoglycemia. This finding supports the hypothesis that free radical reactions and LP processes play an important role in the enhanced brain damage caused by tissue acidosis.

Acidosis, Lactic↗
PubMed1994

[Metabolic acidosis in the 32nd week of pregnancy--uncontrolled diabetes in pregnancy, dehydration or sequela of tocolysis?].

We describe a case of keto- and lactic acidosis in a 22 year old, healthy woman hospitalized for preterm labor at week 32 of gestation. One former pregnancy was normal. Blood glucose level at admission was 115 mg/dl after 8 mg of betamethasone. Continuous salbutamol infusion was used for management of preterm labour. 18 hours later, the patient complained about nausea and dyspnoea followed by tachypnoea and hyperventilation. Blood gas analysis showed severe metabolic acidosis (ph 7.25, BE-17.5, pO2 114 mm Hg, pCO2 15.5 mm Hg). At this moment blood glucose level was 178 mg/dl. Ketone bodies in urine were positive, serum lactate level was also elevated at 8.6 mmol/l. Cesarean section was performed because of prolonged fetal bradycardia. 6 months post partum type-I-diabetes could be excluded. We conclude that this case of acidosis was due to both, beta-2-adrenergic treatment and beginning gestational diabetes.

Acidosis, Lactic↗
PubMed1994

Endotoxin and arachidonic acid metabolites in portal, hepatic and arterial blood of cattle with acute ruminal acidosis.

Ruminal acidosis was induced experimentally with 70 g barley/kg body weight in 2 rumen fistulated cows with chronic indwelling catheters in the portal vein, in a hepatic vein and the carotid artery. The cows were followed for 24 and 20h after the overfeeding and evaluated clinically and by clinical chemistry. The 2 cows exerted different responses to the treatment. Both cows showed signs of severe ruminal acidosis. Both cows had endotoxin in portal and hepatic vein blood, but only 1 of the cows convincingly developed a systemic endotoxaemia. A pre-hepatic release of the stable prostacyclin and thromboxane metabolites, 6-ketoprostaglandin F1 alpha and thromboxane B2 was demonstrated in this cow. The results of the present study show that endotoxin and arachidonic acid metabolites of pre-hepatic origin may be factors involved in the pathogenesis of ruminal acidosis, and that investigation of the factors affecting translocation of ruminal endotoxin and subsequent clearing in the liver, will be of importance.

6-Ketoprostaglandin F1 alpha↗
PubMed1995

Bicarbonate therapy in the treatment of lactic acidosis: medicine or toxin?

The metabolic acidosis resulting from poor tissue perfusion is considered to have several significant hemodynamic effects. Correction of the acidosis with sodium bicarbonate seems to be a rational approach to this problem. However, the current medical literature shows little clinical benefit to this tactic. In fact, indiscriminate bicarbonate administration may, itself, have deleterious effects. Concurring with the absence of a consistent therapeutic advantage to the use of sodium bicarbonate in the treatment of lactic acidosis due to inadequate tissue perfusion, the American Heart Association removed the routine use of sodium bicarbonate from the treatment of cardiac arrest in the algorithms of the Advanced Cardiac Life Support course. Although the debate continues, a detailed review of the medical literature does not support the use of sodium bicarbonate in this setting.

Acidosis, Lactic↗
PubMed1994

[The effect of chronic acidosis on the activity of renal glutamate decarboxylase and GABA-transaminase].

Chronic acidosis evoked by a 7-day application of ammonium chloride in concentration of 2% increased the activity of glutamate decarboxylase (GAD) in renal homogenates of rats to approximately 160%. The enzyme activators, chlorides and adenosine triphosphate influenced in varying measures the GAD activity in renal homogenates of both controlled and acidotic animals. Whilst ATP was gradually loosing the activating effect, chlorides preserved it. The renal GAD is firmly bound on insoluble structures. The increase in GAD activity due to acidosis was accompanied by increasing permanence of this bind. After the substitution of ammonium chloride by drinking water, the return of the increased GAD activity to previous normal values lasted 7 days, whilst apparent normalization of the weight of experimental animals reoccurred on the first day. Subfractionation of the crude renal mitochondrial fraction by use of enzyme markers localized GAD in mitochondria. In renal homogenates the activities of GABA-transaminases were assessed. GABA-alpha-ketoglutarate transaminase was 5x more active than GABA-pyruvate transaminase. Acidosis resulted in augmentation of both transaminases--the first to 130%, the second to 160%. (Tab. 5, Fig. 3, Ref. 25.)

4-Aminobutyrate Transaminase↗
PubMedDate not supplied

Bopindolol and its metabolite 18-502 attenuate regional myocardial acidosis during partial occlusion of the coronary artery in dogs.

The effects of bopindolol (a new, nonselective beta-adrenoceptor antagonist) and its active metabolite, 18-502, on the regional myocardial pH during coronary occlusion were studied. Mongrel dogs were anesthetized with pentobarbital and the thorax was opened to expose the heart. The left anterior descending coronary artery (LAD) was incompletely (or partially) occluded so that the LAD flow could be reduced to about one third of the original flow. Regional myocardial pH of the LAD area was continuously measured by a tissue pH monitor. Drugs were injected intravenously 30 minutes after LAD partial occlusion. The myocardial pH in the LAD area decreased in response to LAD partial occlusion (from 7.3-7.4 to 6.72-6.92), and the low pH value was sustained for 60 minutes after LAD occlusion. Atenolol (1 mg/kg) decreased heart rate markedly and attenuated the regional myocardial acidosis induced by LAD partial occlusion. Bopindolol (1 mg/kg) decreased heart rate and 18-502 (0.5 mg/kg) decreased heart rate and blood pressure. Both drugs attenuated to a similar degree the decrease of regional myocardial pH induced by LAD occlusion. In the dog whose heart rate was maintained constant, however, bopindolol (1 mg/kg) did not attenuate the decrease of regional myocardial pH induced by LAD occlusion. These results suggest that both bopindolol and 18-502 attenuate the ischemia-induced regional acidosis of the myocardium as does atenolol, and, hence, have an anti-ischemic action. The beneficial action of bopindolol on ischemia-induced myocardial acidosis is possibly due to a decrease of heart rate, which corresponds to a saving of energy in the myocardial cells.

Acidosis↗