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At least 865 records · Page 48Linked to original sources
PubMed1981

The prediction of intrapartum fetal metabolic acidosis by fetal heart rate monitoring.

Fetal heart rate characteristics during the 8 hours prior to delivery have been studied in 200 patients in whom the fetus had evidence of a metabolic acidosis at delivery, and compared to those in 200 patients in whom the fetus had a normal acid-base at delivery. Baseline fetal heart rate moderate bradycardia and tachycardia, decreased baseline variability, and decreased fetal heart rate accelerations are predictors of intrapartum fetal hypoxia with metabolic acidosis. Marked patterns of total decelerations and late decelerations are predictive of intrapartum fetal hypoxia with metabolic acidosis. The probability of fetal metabolic acidosis in the presence of a marked pattern of total decelerations is 25%, and with late decelerations it is 48%, in a population of high-risk pregnancies.

Acidosis↗
PubMed1995

Arterial oxygen saturation in relation to metabolic acidosis in fetal lambs.

OBJECTIVE: We studied the relationship between preductal arterial oxygen saturation and metabolic acidosis in 18 chronically instrumented fetal lambs (gestational age 119 to 133 days) in two experimental designs. In the first group the onset of metabolic acidosis was determined. In the second group the progression of metabolic acidosis was studied as was the cardiovascular and hormonal changes resulting from hypoxemia. STUDY DESIGN: In nine fetal lambs maternal fraction of inspired oxygen was lowered stepwise by increasing flows of nitrogen delivered into the trachea through a small indwelling catheter (group 1), and in nine fetal lambs maternal blood flow was reduced stepwise by means of a vascular occluder (group 2). RESULTS: Baseline arterial oxygen saturation values ranged from 26% to 67% with normal pH and extracellular fluid base excess values in both groups 1 and 2. In both groups pH and extracellular fluid base excess started to decrease below 30% arterial oxygen saturation, with a progressive decrease below 20% arterial oxygen saturation to an end value for pH of 7.14. In some fetal lambs pH and extracellular fluid base excess decreased initially at 20% to 30% arterial oxygen saturation and then stabilized at the lower level. Fetal heart rate in group 1 increased during hypoxemia from 155 to 179 beats/min. In group 2 baseline fetal heart rate was 153 beats/min and fell with every step change in arterial oxygen saturation but subsequently increased to 172 beats/min by the end of the period of hypoxemia. Baseline values for epinephrine, norepinephrine, dopamine, cortisol, and mean arterial pressure were not related to baseline arterial oxygen saturation levels, and each of these variables was increased at the end of hypoxemia in group 2. CONCLUSION: Preductal arterial oxygen saturation can reach values between 20% and 30% before anaerobic metabolism starts. During the progressive acidosis blood pressure was increased, which can be attributed to a strong rise in catecholamines.

Acidosis↗
PubMed1990

Acidosis reduces NMDA receptor activation, glutamate neurotoxicity, and oxygen-glucose deprivation neuronal injury in cortical cultures.

The acidosis which accompanies cerebral ischemia in vivo has been thought to contribute to subsequent neuronal injury. However, recent electrophysiological recordings from hippocampal neurons suggest that H+ can attenuate N-methyl-D-aspartate (NMDA) receptor-mediated cation influx, likely a key event in the pathogenesis of ischemic neuronal injury. Here we report that moderate extracellular acidosis (pH 6.5) markedly reduced the inward whole cell current induced by NMDA on cultured cortical neurons; at pH 6.1, kainate-induced current was additionally reduced. Furthermore, such acidosis reduced the cortical neuronal injury caused by toxic glutamate exposure, as well as the neuronal degeneration and accumulation of 45Ca2+ induced by combined oxygen and glucose deprivation. These findings raise the possibility that moderate acidosis may decrease cortical neuronal vulnerability to ischemic damage.

Acidosis↗
PubMed1985

Effect of different degrees of brain ischemia and tissue lactic acidosis on the short-term recovery of neurophysiologic and metabolic variables.

The recovery of the EEG and somatosensory evoked responses (SER) as compared with recovery of the cerebral energy state was studied in rats during recirculation following different degrees of brain ischemia with varying tissue lactic acidosis. Reversible complete and incomplete ischemia was induced either by increasing the intracranial pressure (compression ischemia) or by carotid artery clamping combined with arterial hypotension. In incomplete ischemia the degree of tissue lactic acidosis was varied by manipulations of blood and brain glucose levels. Animals with an increase in brain lactate to about 25 mumol X g-1 (whole brain wet weight) during ischemia showed persistent failure of both cerebral energy metabolism and neurophysiologic restitution during the recirculation phase; if less than 20 mumol X g-1 metabolic recovery was almost complete. Despite a similar restitution of tissue energy metabolism in these animals, neurophysiologic recovery was inversely proportional to brain lactate concentrations during ischemia. At similar levels of ischemic tissue lactic acidosis, and despite a similar recovery of cortical energy state, the neurophysiologic restitution was clearly inferior after complete ischemia to that following incomplete ischemia. Three conclusions were drawn: (i) neurophysiologic variables were more sensitive indicators of postischemic persistent cerebral dysfunction than the cerebral energy state; (ii) the degree to which lactate accumulated in the ischemic brain influenced neurophysiologic restitution even if concentrations critical for metabolic recovery were not attained; and (iii) incomplete ischemia was less harmful than complete ischemia provided that tissue lactic acidosis was not excessive.

Acidosis↗
PubMed1990

Lactic acidosis increases tumor necrosis factor secretion and transcription in vitro.

Lactic acid has been shown to affect numerous biologic processes. We investigated the role of lactic acidosis as a signal for the production of TNF by macrophages in vitro. Male F344 rats were administered thioglycolate media intraperitoneally. Macrophages were recovered 7 days later, cultured for 24 hr in complete media (CM), or CM with L-lactic acid (5, 10, or 15 mM), or with endotoxin (LPS) (10 micrograms/ml). TNF levels were measured in the supernatants. Female C57BL/6 mice were similarly treated, and macrophages were harvested and cultured in CM or CM containing lactic acid (15 mM), or LPS (10 micrograms/ml). RNA was extracted after 24 hr, separated by electrophoresis, and transferred to nitrocellulose. Human 32P-cDNA TNF and actin probes were used to determine relative TNF gene expression. Gel densitometry was used to calculate the TNF expression index (EI) in lactic acid and LPS treated cells as described. pH levels of the supernatant indicated that increasing concentrations of lactic acid caused increasing acidosis. Trypan blue exclusion demonstrated that lactic acidosis did not reduce cell viability. LPS significantly increased secretion of TNF relative to control (P less than 0.001). Each concentration of lactic acid significantly increased TNF secretion (P less than 0.05), but not in a dose-dependent manner. TNF gene transcription was elevated in macrophages cultured with lactic acid and LPS relative to control (EI = 1.13 and 1.18, respectively). This suggests that lactic acid concentration can regulate TNF secretion at the level of transcription, and is consistent with the hypothesis that local levels of lactic acid (lactic acidosis) may be a regulator of cytokine secretion.

Acidosis, Lactic↗
PubMed1976

Lactic acidosis: an experimental model.

A model of spontaneous lactic acidosis was developed in alloxan diabetic rabbits by infusing intravenously beta-hydroxybutyric acid followed by a continuous infusion of NaHCO3. In half of the animals, the arterial lactate/pyruvate ratio rose from 2.5 mM/0.19mM to 20.4 mM/0.28 mM, and arterial pH fell to 7.16. In animals with lactic acidosis, the calculated ratio in blood of NAD/NADH was 1437 +/- 230, versus a normal value of 6754 +/- 1250. Both arterial PO2 and blood pressure were normal. Continued infusion of NaHCO3 led to increased blood lactate levels, with cardiorespiratory arrest in 36% of animals. Lactic acidosis did not develop in normal rabbits who were similarly treated. It is concluded that spontaneous lactic acidosis can be produced in diabetic, but not in normal, rabbits by infusion of beta-hydroxybutric acid followed by infusion of NaHCO3.

Acidosis↗
PubMed1988

Effects of vasodilatation and acidosis on the blood-brain barrier.

Hypercapnia protects the blood-brain barrier against disruption during acute hypertension. Our goal was to determine whether protection of the blood-brain barrier by hypercapnia may be related to an affect of acidosis on the barrier, vasodilatation produced during hypercapnia, or attenuation of increases in cerebral venous pressure by hypercapnia. Pial vessels were examined in rats by means of fluorescent microscopy. We examined disruption of the blood-brain barrier in response to acute hypertension during hypercapnia (vasodilatation with acidosis), during topical adenosine (vasodilatation without acidosis), and during passive increases in cerebral venous pressure produced by venous occlusion during hypercapnia. Acute hypertension in normocapnic rats increased venular pressure and disrupted the blood-brain barrier and often produced bleeding from cerebral venules. Hypercapnia alone increased venular pressure, and acute hypertension produced only a modest further increase in venular pressure, with minimal disruption of the blood-brain barrier. Venous occlusion in hypercapnic rats increased venular pressure and disrupted the blood-brain barrier. We conclude that vasodilatation and acidosis produced by hypercapnia do not protect the blood-brain barrier from disruption during acute hypertension. Protection by hypercapnia during acute hypertension appears to be related to attenuation of increases in cerebral venous pressure.

Acidosis↗
PubMed1991

Fetal acidosis in labour: a prospective study on the effect of parity.

The effect of parity on intrapartum fetal scalp pH was investigated in 6466 patients in labour with a live fetus who were delivered in 1987. 350 (5.4%) required fetal scalp blood sampling for pH (FBS), 236 primigravidae (10.4%) and 114 multigravidae (2.7%) (P less than 0.001). Fetal acidosis (pH less than 7.20) was detected in 35 patients, 27 primigravidae (11.4%) and 8 multigravidae (7.0%) (P less than 0.001). The incidence of intrapartum acidosis in the 2275 primigravidae and the 4191 multigravidae was 1.2 and 0.2% respectively (P less than 0.001). The two deaths from birth asphyxia and three cases of neonatal seizures occurred in primigravidae. In primigravidae requiring FBS, fetal acidosis was not associated with the use of oxytocin or with increased duration of labour. Neonatal seizures were more common overall in primigravidae than in multigravidae and more common in patients requiring FBS than in those not requiring FBS (P less than 0.05). The higher incidence of FBS, fetal scalp acidosis and neonatal seizures in primigravidae has important implications for intrapartum fetal monitoring.

Acidosis↗
PubMed1979

Effect of hypocapnia on intracellular pH during metabolic acidosis.

Separate and combined effects of acute metabolic acidosis and hypocapnia were determined in skeletal and cardiac muscles of intact rats. Normocapnic metabolic acidosis, imposed by intraperitoneal injection of hydrochloric acid (6 mEq/kg), did not change skeletal muscle intracellular acid--base parameters. Hypocapnia, induced by mechanical hyperventilation, resulted in intracellular alkalosis within skeletal muscle during both respiratory alkalosis and compensated metabolic acidosis; changes of skeletal muscle intracellular bicarbonate concentration per unit change in carbon dioxide tension were identical during these two experimental procedures. These data suggest that processes other than physicochemical buffering neutralize protons taken into skeletal muscle cells during acute metabolic acidosis. The acid--base state of the heart was quite stable during these experimental manipulations; thus, it appears that cardiac muscle has an extraordinary buffering ability. Moreover, our data suggest that processes other than physicochemical buffering maintain cardiac intracellular pH normal during hypocapnia.

Acidosis↗
PubMed1989

Does acidosis contribute to stress-induced ulceration in rat stomachs?

The present study examines the involvement of acidosis in stress ulceration in rat stomachs. Cold restraint stress for 2 hr did not affect the blood lactate level; however, it produced respiratory acidosis, as reflected by the depressed respiratory rate which was associated with increased CO2 tension and a lowered blood pH. Severe hemorrhagic ulceration was found in the glandular mucosa. The effects of stress on blood pH and the stomach were reversed by IV infusion of NaHCO3. Infusion of HCl IV decreased the blood pH and HCO-3 level and produced gastric ulceration. It is concluded that respiratory acidosis could be involved in stress ulceration. The metabolic acidosis evoked by HCl also induced gastric damage, but the effect was much less.

Acidosis, Respiratory↗
PubMed1985

Clinical buffering of metabolic acidosis: problems and a solution.

Traditionally sodium bicarbonate has been the buffer of first choice in the treatment of metabolic acidosis. This treatment, however, involves risks of developing a hyperosmolar state, a high sodium concentration in the blood, increased arterial carbon dioxide tension and, as a result of the latter, intracellular and intracerebral acidosis and also cerebral oedema. The buffering effect occurs slowly and as a consequence of this, and of the titration curve of sodium bicarbonate, overcorrection of metabolic acidosis is often seen. Tris buffer was introduced as an alternative and has been claimed to solve most of these problems, but on the other hand it entails a very high risk of peripheral venous thrombosis and thrombophlebitic lesions owing to its local irritative effect. In order to overcome these disadvantages a new mixture of Tris, acetate, bicarbonate and phosphate has been designed. In the studies described it was shown to have an adequate buffering effect and to provide a solution to most of the problems connected with buffering of metabolic acidosis. The new Tris buffer mixture has a buffering effect in blood equivalent to 0.5 mol/l sodium bicarbonate, although its sodium content has been decreased to one-third of pure sodium bicarbonate. Its administration also results in predictable buffering in cerebrospinal fluid and skeletal muscle. In a clinical study it was demonstrated that the new Tris buffer mixture results in sufficient and adequate buffering without significant side-effects.

Acetates↗
PubMed1995

Effects of small-volume bolus treatment with intravenous normal saline and 7.5 per cent saline in combination with 6 per cent dextran-40 on metabolic acidosis and survival in burned mice.

Standard murine burn models include the administration of intraperitoneal (i.p.) saline solutions which are intended to resuscitate the animals during subsequent burn shock. Prehospital administration of small volumes of concentrated salt solutions has been recommended for the early treatment of haemorrhagic shock, and have also been utilized for burn shock. We studied the effects of bolus intravenous (i.v.) hypertonic saline (HS) or hypertonic saline/dextran-40 (HS + DEX) on animal survival and acid-base balance following 25 per cent total body surface area, full-thickness burn injury in mice. I.v. injections were administered via a tail vein immediately prior to burn injury. Some mice received 1 ml i.p. normal saline (NS) immediately after burn injury. Acid-base balance of vena caval blood was measured during the period of maximal metabolic acidosis following burn injury (12 h postburn). Preburn i.v. administration of 5 ml/kg of HS or HS+DEX, followed by 1 ml i.p. NS, only slightly decreased the degree of metabolic acidosis compared to animals receiving i.p. fluid alone, the standard resuscitation regimen for burned mice. Preburn i.v. administration of 0.2 ml volumes of HS or HS + DEX, without i.p. fluid administration, resulted in extremely high mortality. Immediate preburn i.v. administration of HS or HS + DEX did not eliminate metabolic acidosis in this murine burn model, and markedly increased the mortality when subsequent i.p. fluids were not administered. The degree of metabolic acidosis in the murine experimental burn model has not previously been clearly described. Furthermore, adequate fluid resuscitation of these animals may be difficult to achieve without indwelling vascular catheters which could deliver continuous i.v. fluids following burn injury.

Acid-Base Equilibrium↗
PubMed1989

Lactic acidosis in theophylline overdose.

An 18-year-old man with theophylline overdose developed an increased anion gap metabolic acidosis. Serum lactate levels were markedly elevated. A direct correlation was found between the increasing theophylline level, clinical hyperadrenergic state, and the worsening acidosis. Early hemoperfusion reversed the acidosis, the elevated serum theophylline level, and the hyperadrenergic state. This case substantiates the role of lactate accumulation in the metabolic acidosis associated with isolated theophylline toxicity.

Acidosis, Lactic↗
PubMed1994

Lactic acidosis and acute ethanol intoxication.

Ethanol intoxication has been widely reported as a cause of lactic acidosis. To determine the frequency and severity of ethanol-induced lactic acidosis, patients who presented to an emergency department with a clinical diagnosis of acute ethanol intoxication and a serum ethanol concentration of at least 100 mg/dL were studied. Arterial blood was sampled for lactate and blood gas determinations. A total of 60 patients (mean age, 41 years) were studied. Twenty-two patients sustained minor trauma. Ethanol concentrations ranged from 100 to 667 mg/dL (mean, 287 mg/dL). Lactate concentrations were abnormal (> 2.4 mmol/L) in seven patients (11.7%). In all cases, blood lactate was less than 5 mmol/L. Of the patients with elevated lactate, other potential causes for lactic acidosis, including hypoxia, seizures, and hypoperfusion, were also present. Only one case with elevated blood lactate concentration had associated acidemia. Significant elevations of blood lactate are uncommon in acute ethanol intoxication. In patients with ethanol intoxication who are found to have lactic acidosis, other etiologies for the elevated lactate level should be considered.

Acidosis, Lactic↗
PubMedDate not supplied

Lactic acidosis in childhood: Part I.

Lactic acidosis accompanies many acquired and inherited metabolic diseases. The role of lactic acid in anaerobic glycolysis, gluconeogenesis, and acid-base balance is key to the understanding of these disorders. Because lactic acid can be formed only from pyruvic acid, disorders which increase pyruvate production, inhibit its catabolism, or shift the equilibrium toward lactic acid formation cause lactic acidosis. Lactic acidosis results from systemic diseases and toxins which produce tissue hypoxia or mitochondrial injury. Abnormalities of other metabolites such as glucose, pyruvate, amino acids, and organic acids may provide clues to inborn metabolic errors. Treatment must first be directed toward removing precipitating causes of the acquired disorders and then toward correcting the acidosis and other metabolic complications such as hypoglycemia. Some of the inborn errors respond to specific therapies.

Acidosis, Lactic↗
PubMedDate not supplied

Lactic acidosis in childhood: Part II.

Lactic acidosis is associated with both inherited and acquired metabolic diseases. Lactic acid metabolism in the presence of altered gluconeogenesis, anaerobic glycolysis, and acid-base balance is a major factor in many disorders. Lactic acid can be formed only from pyruvic acid; therefore, disorders that increase pyruvate concentration, enhance lactic acid formation, or reduce lactic acid degradation cause lactic acidosis. Inborn metabolic errors that are accompanied by derangement of metabolic pathways of glucose, pyruvate, amino acids, and organic acids as well as toxic and systemic conditions that promote tissue hypoxia or mitochondrial injury result in lactic acidosis. In the presence of acquired disorders, treatment is directed initially toward modification or cure of the primary condition and then toward eliminating acidosis and other metabolic complications. Specific therapy is available for some inborn errors of metabolism.

Acidosis, Lactic↗
PubMed2006

[Metabolic acidosis after cardiac surgery with cardiopulmonary bypass revisited with the use of the Stewart acid-base approach].

INTRODUCTION: According to the Stewart approach of acid-base regulation, chloride from either volume replacement or cardiopulmonary bypass (CPB) priming solution may induce metabolic acidosis. The alternative hypothesis stands in volume dilution with solutions free of bicarbonate. OBJECTIVES: Evaluate the acid-base status of patients undergoing cardiac surgery with CPB priming containing chloride and bicarbonate. MATERIAL AND METHODS: Prospective study. METHODS: Twenty-eight patients were prospectively included. Priming of CPB contained 47.4 mmol/l of bicarbonate and 97.7 mmol/l of chloride. Arterial blood samples were taken at 3 timings: prior (T1) and after (T2) CPB, and on arrival in the ICU (T3). Following measurements were performed: Na(+), K(+), Cl(-), Mg(++), Ca(++), phosphates, albumin, lactate and arterial blood gases. RESULTS: After CPB respiratory acidosis was observed. There was a significant increase of chloride with a decrease in apparent strong ion difference (SIDa). At the same time bicarbonate and base excess (BE) remained constant. A significant but weak correlation between BE and SIDa existed (r(2) = 0.06, p=0.024). On the contrary, no correlation was found between variations of BE and SIDa. However, the correlation was stronger between values and variations of bicarbonate and BE (respectively r(2)=0.605, p<0.0001 and r(2)=0.495, p<0.0001). CONCLUSION: No metabolic acidosis occurred after cardiac surgery when CPB was primed with bicarbonate. Therefore, it appears that chloride administration is not the main mechanism being involved in the acid-base regulation. This reinforces the hypothesis that metabolic acidosis during CPB may mainly be due to dilution of bicarbonate.

Acid-Base Equilibrium↗
PubMed2005

Adverse 30-day outcomes after cardiac surgery: predictive role of intraoperative myocardial acidosis.

BACKGROUND: Regional myocardial acidosis in patients undergoing cardiac surgery has been shown to be reflective of regional myocardial ischemia. This study elucidates the relationship between intraoperative regional myocardial acidosis and 30-day postoperative outcomes after cardiac surgery. METHODS: Intramyocardial tissue pH in the anterior and posterior left ventricular walls was measured in 397 adult patients undergoing valve replacement or coronary revascularization surgery between 1987 and 2001. Dedicated nurses and research assistants prospectively collected preoperative, intraoperative, and outcomes data. Regional myocardial acidosis was defined in terms of pH thresholds identified by recursive partitioning. Adverse 30-day outcome, defined as death or any one of six complications, was the dependent variable in a multivariate logistic regression analysis. A morbidity score was developed on the basis of the sensitivity of each of the six complications in predicting death, and was the dependent variable in a multivariate linear regression analysis. RESULTS: During the period of aortic clamping, a mean intramyocardial tissue pH less than 6.85 was identified to be significant by recursive partitioning, and was encountered in either the anterior or posterior left ventricular wall in 85.4% of patients. After adjusting for preoperative and intraoperative variables, this pH threshold was found to be significantly associated with increased adverse outcomes within 30 days after surgery (p = 0.045). It was also significantly associated with increase in the morbidity score (p = 0.05). CONCLUSIONS: Regional myocardial acidosis of a magnitude frequently encountered during aortic clamping is an independent determinant of adverse 30-day outcomes after cardiac surgery. Its reversal by pH-guided myocardial management has the potential of improving postoperative patient outcomes.

Acidosis↗