Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “ALKALOSIS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 109 records · Page 6Linked to original sources
PubMed1990

Depressed distal tubule acidification corrects chloride-deplete alkalosis in rats.

We investigated the relative contributions made by the proximal and distal tubule to the correction of Cl-deplete metabolic alkalosis induced by systemic administration of NaCl. Free-flow micropuncture was used to examine net bicarbonate reabsorption in superficial proximal and distal tubules of anesthetized Munich-Wistar rats during maintenance and correction of chronic furosemide-induced Cl-deplete metabolic alkalosis. The distal tubule of animals with correcting vs. maintained alkalosis had a lower fractional reabsorption of bicarbonate (38 vs. 75%, P less than 0.001) and a lower slope of the linear regression comparing absorption to delivered load (0.48 vs. 0.99, P less than 0.02). By contrast, proximal tubule of animals with correcting vs. maintained alkalosis had fractional reabsorption (85 vs. 90%, P = 0.07) and slopes of the regression comparing reabsorption to filtered load (1.09 vs. 0.98, P = 0.48) that were not different. The data indicate that correction of Cl-deplete metabolic alkalosis induced by NaCl administration involves a qualitative decreased in bicarbonate reabsorption in distal tubule with maintenance of the same load-dependent relationship for bicarbonate reabsorption in proximal tubule.

Absorption↗
PubMed1985

Effect of respiratory alkalosis on skeletal muscle metabolism in the dog.

These experiments were conducted to determine whether changes in skeletal muscle metabolism contribute to the previously reported increase in whole-body O2 uptake (VO2) during respiratory alkalosis. The hind-limb and gastrocnemius-plantaris preparations in anesthetized and paralyzed dogs were used. VO2 of the hindlimb and gastrocnemius muscle was calculated from measurements of venous blood flow and arterial and venous O2 concentrations (Van Slyke analysis). Whole-body VO2 was measured by the open-circuit method. Minute ventilation (hence blood gases and pH) was controlled by a mechanical respirator. Whole-body, hind-limb, and gastrocnemius muscle VO2 increased 14, 19, and 20%, respectively, during alkalosis (P less than 0.05). In all experiments, arterial lactate concentration increased significantly (P less than 0.05) during alkalosis. A positive venoarterial lactate difference across muscle during alkalosis indicated that skeletal muscle is a source of the elevated blood lactate. We concluded that VO2 of resting skeletal muscle is increased during states of respiratory alkalosis and that this increase can account for much of the increase in whole-body VO2.

Alkalosis, Respiratory↗
PubMed1992

Brain glutamate metabolism during metabolic alkalosis and acidosis.

Glutamate modifies ventilation by altering neural excitability centrally. Metabolic acid-base perturbations may also alter cerebral glutamate metabolism locally and thus affect ventilation. Therefore, the effect of metabolic acid-base perturbations on central nervous system glutamate metabolism was studied in pentobarbital-anesthetized dogs under normal acid-base conditions and during isocapnic metabolic alkalosis and acidosis. Cerebrospinal fluid transfer rates of radiotracer [13N]ammonia and of [13N]glutamine synthesized de novo via the reaction glutamate+NH3-->glutamine in brain glia were measured during normal acid-base conditions and after 90 min of acute isocapnic metabolic alkalosis and acidosis. Cerebrospinal fluid [13N]ammonia and [13N]glutamine transfer rates decreased in metabolic acidosis. Maximal glial glutamine efflux rate jm equals 85.6 +/- 9.5 (SE) mumol.l-1 x min-1 in all animals. No difference in jm was observed in metabolic alkalosis or acidosis. Mean cerebral cortical glutamate concentration was significantly lower in acidosis [7.01 +/- 0.45 (SE) mumol/g brain tissue] and tended to be larger in alkalosis, compared with 7.97 +/- 0.89 mumol/g in normal acid-base conditions. There was a similar change in cerebral cortical gamma-aminobutyric acid concentration. Within the limits of the present method and measurements, the results suggest that acute metabolic acidosis but not alkalosis reduces glial glutamine efflux, corresponding to changes in cerebral cortical glutamate metabolism. These results suggest that glutamatergic mechanisms may contribute to central respiratory control in metabolic acidosis.

Acid-Base Equilibrium↗
PubMed1995

Chronic metabolic alkalosis: not uncommon in young children with severe cystic fibrosis.

The acid-base balance of 199 patients with cystic fibrosis, seen from 1987 through 1992 at the Bern Outpatient Clinic, were evaluated. Simple metabolic alkalosis was demonstrated in 16 and mixed metabolic alkalosis and respiratory acidosis in 9 patients. When compared with 10 patients with simple respiratory acidosis and 16 with normal hydrogen ion balance, those with simple metabolic alkalosis were significantly younger. The need for pancreatic enzymes was significantly higher and the relative underweight significantly more severe in patients with either simple or mixed metabolic alkalosis and respiratory acidosis. The results indicate the rather common occurrence of chronic metabolic alkalosis in cystic fibrosis. It is observed in young patients, in patients who need high doses of pancreatic enzymes and in the those with poor nutritional status.

Acidosis, Respiratory↗
PubMed1999

Blockade of ATP-sensitive potassium channels in cerebral arterioles inhibits vasoconstriction from hypocapnic alkalosis in cats.

BACKGROUND AND PURPOSE: Recent studies have shown that the cerebral arteriolar dilation from hypercapnic acidosis is blocked by agents which inhibit KATP channels. These findings suggested that this response is due to opening of KATP channels. Because the repose to CO2 is a continuum, with hypercapnic acidosis causing vasodilation and hypocapnic alkalosis causing vasoconstriction, it would be expected that the response to hypocapnic alkalosis would be due to closing of KATP channels. There are no studies of the effect of inhibition of KATP channels on the response to hypocapnic alkalosis. METHODS: We investigated the effect of 3 agents that in earlier studies were found to inhibit KATP channels--NG-nitro-L-arginine, hydroxylysine, and glyburide--on the cerebral arteriolar constriction caused by graded hypocapnia induced by hyperventilation in anesthetized cats equipped with cranial windows. RESULTS: Hypocapnic alkalosis caused dose-dependent vasoconstriction that was inhibited completely by each of the 3 inhibitors of KATP channels. The blockade induced by these agents was eliminated in the presence of topical L-lysine (5 micromol/L). CONCLUSIONS: The findings show that agents which inhibit ATP-sensitive potassium channels in cerebral arterioles inhibit the vasoconstriction from hypocapnic alkalosis. These and earlier results showing that inhibition of KATP channels inhibited dilation from hypercapnic acidosis demonstrate that the response to CO2 in cerebral arterioles is mediated by the opening and closing of KATP channels.

Adenosine Triphosphate↗
PubMed1967

Aldosterone in metabolic alkalosis.

Studies have been carried out in human volunteer subjects to evaluate the role of aldosterone in the development, maintenance, and correction of metabolic alkalosis induced by selective depletion of hydrochloric acid. During the first phase of our study the rate of aldosterone secretion was measured before the induction of alkalosis (while the subjects were on a low salt diet) and again after a steady state of metabolic alkalosis had been established. The data demonstrate a fall in aldosterone secretion from a value of approximately 500 mug/day to a value of approximately 200 mug/day. Thus, it appears that an increased rate of aldosterone secretion is not a prerequisite to the elevation of the renal bicarbonate threshold. During the second phase of our study, aldosterone was administered to the alkalotic subjects in doses of 1000 mug/day (or deoxycorticosterone acetate in doses of 40 mg/day) in order to determine the effects of a persistent steroid excess on the ability of sodium chloride to correct the acid-base disturbance. The data demonstrate that despite the administration of steroid, the ingestion of sodium chloride led to a reduction in plasma bicarbonate concentration from 39 to 29 mEq/liter, accompanied by a suppression of renal acid excretion. This reduction in plasma bicarbonate concentration occurred without a concomitant retention of potassium, a deficit of as much as 400-500 mEq of potassium persisting during repair of the acid-base disturbance. Our findings suggest that "saline-resistant" alkalosis, when it occurs in the absence of primary hyperadrenalism, cannot be attributed to aldosterone excess and/or potassium depletion of the magnitude seen in our study. We also suggest the need for a reappraisal of the way in which aldosterone excess contributes to the genesis and maintenance of alkalosis in primary aldosteronism.

Acid-Base Equilibrium↗
PubMed1983

Metabolic alkalosis in the rat. Evidence that reduced glomerular filtration rather than enhanced tubular bicarbonate reabsorption is responsible for maintaining the alkalotic state.

Maintenance of chronic metabolic alkalosis might occur by a reduction in glomerular filtration rate (GFR) without increased bicarbonate reabsorption or, alternatively, by augmentation of bicarbonate reabsorption with a normal GFR. To differentiate these possibilities, free-flow micropuncture was performed in alkalotic Munich-Wistar rats with a glomerular ultrafiltrate total CO2 concentration of 46.5 +/- 0.9 mM (vs. 27.7 +/- 0.9 mM in controls). Alkalotic animals had a markedly reduced single nephron GFR compared with controls (27.4 +/- 1.5 vs. 51.6 +/- 1.6 nl/min) and consequently unchanged filtered load of bicarbonate. Absolute proximal bicarbonate reabsorption in alkalotic animals was similar to controls (981 +/- 49 vs. 1,081 +/- 57 pmol/min), despite a higher luminal bicarbonate concentration, contracted extracellular volume, and potassium depletion. When single nephron GFR during alkalosis was increased toward normal by isohydric volume expansion or in another group by isotonic bicarbonate loading, absolute proximal bicarbonate reabsorption was not substantially augmented and bicarbonaturia developed. To confirm that a fall in GFR occurs during metabolic alkalosis, additional clearance studies were performed. Awake rats were studied before and after induction of metabolic alkalosis associated with varying amounts of potassium and chloride depletion. In all cases, the rise in blood bicarbonate concentration was inversely proportional to a reduction in GFR; filtered bicarbonate load remained normal. In conclusion, a reduction in GFR is proposed as being critical for maintaining chronic metabolic alkalosis in the rat. Constancy of the filtered bicarbonate load allows normal rates of renal bicarbonate reabsorption to maintain the alkalotic state.

Absorption↗
PubMed1993

Hyperoxia and alkalosis produce pulmonary vasodilation independent of endothelium-derived nitric oxide in newborn lambs.

Supplemental oxygen and alkalosis are the most effective treatments used to lower pulmonary arterial pressure in children with pulmonary hypertensive disorders. However, their mechanisms of action are unknown. Endothelium-derived nitric oxide (EDNO) is an important mediator of pulmonary vascular tone and produces potent pulmonary vasodilation during pulmonary hypertension. In vitro evidence suggests that EDNO may mediate the vasodilating effects of oxygen. To investigate whether EDNO synthesis mediates the pulmonary vasodilation produced by hyperoxia [normocarbic ventilation with 100% oxygen, arterial oxygen tension > 450 torr (60 kPa)] or alkalosis (hyperventilation with 21% oxygen, pH > 7.55) in vivo, eight intact newborn lambs were studied during similar degrees of pulmonary hypertension induced either by the infusion of U46619 (a thromboxane A2 mimic) or N omega-nitro-L-arginine (an inhibitor of EDNO synthesis). The lambs were sedated, paralyzed, and mechanically ventilated. Meclofenamic acid was infused to inhibit prostaglandin synthesis. During pulmonary hypertension induced by U46619, pulmonary arterial pressure and pulmonary vascular resistance were significantly decreased by acetylcholine (an EDNO-dependent vasodilator) (23.1 +/- 3.4% and 43.3 +/- 14.5%, respectively), hyperoxia (26.8 +/- 7.8% and 32.9 +/- 10.6%), and alkalosis (32.1 +/- 10.3% and 36.1 +/- 17.0%) (p < 0.05). During pulmonary hypertension induced by N omega-nitro-L-arginine, the decreases in pulmonary arterial pressure and pulmonary vascular resistance produced by acetylcholine (9.6 +/- 6.4% and 23.9 +/- 14.1%, respectively) were significantly attenuated (p < 0.05), but the decreases produced by hyperoxia or alkalosis were unchanged. Therefore, hyperoxia and alkalosis can produce pulmonary vasodilation independent of EDNO synthesis in the intact newborn lamb.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1997

Metabolic alkalosis.

In summary, the kidney possesses numerous mechanisms that help to prevent metabolic alkalosis. Maintenance of metabolic alkalosis for any length of time means that renal homeostatic mechanisms for HCO3- excretion have been disrupted. Understanding the mechanisms that may perturb the kidney's ability to correct alkalosis will lead to improved clinical approaches to differential diagnosis and treatment of the patient. Although metabolic alkalosis is frequently not dangerous, in certain settings metabolic alkalosis may contribute to mortality and should be treated aggressively.

Alkalosis↗
PubMed2002

[Hypertonic saline 7.5% in the treatment of severe hypochloremic metabolic alkalosis].

A 63 year-old man with a history of anal carcinoma treated by surgery, chemotherapy and radiotherapy was admitted to our hospital two years later with small bowel obstruction requiring emergency surgery. Fifteen days later, he had to be operated on once again. During the procedure, severe metabolic alkalosis developed: pH 7.58, CO3H- 47.7 mmol/L and a base excess of 24.3 mmol/L. The patient had the following preoperative risk factors for hypochloremic metabolic alkalosis: low levels of Cl and K, prolonged aspiration of gastric contents, low plasma volume and parenteral nutrition. Metabolic alkalosis was managed with 250 mL of 7.5% hypertonic saline, 40 mEq of KCl, readjustment of the ventilatory pattern, perfusion of lactated Ringer's solution instead of 0.9% saline and administration of omeprazole. Response to treatment was good as elevated values fell to acceptable levels within two hours. Metabolic alkalosis is a common acid-base balance disorder which arises for a variety of reasons and which has significant anesthetic implications. Hypertonic saline may be useful for treating severe, acute hypochloremic metabolic alkalosis.

Alkalosis↗
PubMed1991

[A case of the milk-alkali syndrome with a small amount of milk and magnesium oxide ingestion--the contribution of sustained metabolic alkalosis induced by hypertonic dehydration].

We described a patient with the milk-alkali syndrome induced by the ingestion of small amount of milk (200 ml/day) and ice cream (145 g/day) and the administration of small dose of absorbable alkali (magnesium oxide 2.0 g/day) for the treatment of chronic constipation. The present case shows not only triads, i.e., hypercalcemia (s-Ca 14.3 mg/dl), metabolic alkalosis (s-HCO3- 37.4 mEq/L), and renal insufficiency (s-Cre 2.3 mg/dl) but also hypernatremia (s-Na 161 mEq/L) and hypertonic dehydration after the frequent episodes of elevated body temperature. The milk-alkali syndrome has been defined as the hypercalcemia with a metabolic alkalosis from a high amount of calcium intake and long term administration of absorbable alkali in any form, usually as calcium carbonate for the treatment of peptic ulcer. As the present case could be distinguished from any other cases previously reported with regard to the amount of calcium (0.4 g/day) and alkali (36 mEq/day) intake and the clinical situations that induced the syndrome, we compared the present case with the previous reports, calculating the amount of calcium and alkali intake from milk and absorbable alkali. After the introduction of the H2 blockers for peptic ulceration, the most cases with milk-alkali syndrome had provoked by the smaller amount of calcium than previously reported, which were associated with the treatment of relatively large amount of alkali (50-150 mEq/day), suggesting the role of sustained metabolic alkalosis for the development. In the present case the metabolic alkalosis induced by hypertonic dehydration and enhanced by absorbable alkali intake also could cause an increase of renal tubular reabsorption of calcium and a decrease of ionized calcium which might produce increased secretion of parathyroid hormone followed by vitamin D3 activation and increased Ca absorption from the gut. The metabolic alkalosis might be essential to the development of the milk-alkali syndrome without a high calcium and absorbable alkali intake.

Aged↗
PubMed1994

Does saline "correct" the abnormal mass balance in metabolic alkalosis associated with chloride depletion in the rat?

An elevated plasma pH and bicarbonate are the clinical hallmarks of metabolic alkalosis. Nevertheless, to fully define its pathophysiology, one needs a quantitative interpretation of events in 3 areas - the ECF, ICF, and urine. Accordingly, our purpose was to study mass balance in Cl--depletion metabolic alkalosis with normal initial balance for Na+ and K+. In the 20 h following the "exchange" of Cl- (loss, 2455 mumol) and HCO(3-) (gain, 2455 mumol), only 334 mumol HCO(3-) remained in the ECF and 337 mumol were excreted. The remaining 1784 mumol disappeared primarily via titration because 3051 mueq of endogenous anions were produced and excreted largely with K+. Accordingly, metabolic alkalosis was associated with a deficit rather than a surplus of HCO(3-). To reflect the shift of H+ into cells driven by the exit of K+, the cumulative deficit of Cl- was replaced as KCl or NaCl. The fall in plasma [HCO(3-)] was larger in the KCl group (13.2 vs. 9.4 mmol/L); it was largely due to H+ exit from cells; in contrast, disappearance of HCO(3-) from the ECF was due to new endogenous acid production in the NaCl group. Thus, there was an overall deficit of HCO(3-) in metabolic alkalosis associated with KCl depletion (extracellular alkalosis and intracellular acidosis); processes in the ICF were not corrected by NaCl.

Alkalosis↗
PubMed1976

Importance of changes in plasma HCO-3 on regulation of CSF HCO-3 in respiratory alkalosis.

In respiratory alkalosis the fall in CSF bicarbonate is in part due to increased CSF lactate. The rest of CSF HCO3 fall may be actively regulated or as more recent evidence suggests is dependent on plasma HCO3 fall. Therefore, the relationship between plasma and CSF HCO3 changes was studied during 4 hours of respiratory alkalosis (PaCO2=20 mm Hg) in anesthetized dogs when plasma HCO3: (1) fell normally, (2) kept 'normal' by NaHCO3 infusion, (3) increased by infusing more NaHCO3, and (4) reduced by infusing HCl. In respiratory alkalosis plasma and CSF HCO3 fell 4.6 and 3.8 mEQ/L, respectively. In hypocapnia and 'normal' plasma HCO3 CSF HCO3 fell 2 mEq/L and lactate increased 1.33 mEq/L. In hypocapnia and metabolic alkalosis plasma HCO3 increased 6.5 mEq/L and CSF HCO3 remained unchanged and lactate increased 2.12 mEq/L. In combined hypocapnia and metabolic acidosis plasma HCO3 fall 10.5 mEq/L but CSF HCO3 fell 3.1 mEq/L and CSF pH returned to normal at 4 hours. Therefore CSF HCO3 fall in hypocapnia is primarily and critically dependent on the simultaneous fall in plasma HCO3 content, with a minimal contribution from CNS lactate increase. When CSF PH has returned to normal, however, CSF HCO3 fall is stopped despite further falls in plasma HCO3.

Acid-Base Equilibrium↗
PubMedDate not supplied

Red blood cell alkalosis and decreased oxyhemoglobin affinity.

The behavior of the oxyhemoglobin curve was studied in ten patients with respiratory alkalosis (arterial [H+] less than 37 nM, pCO2 less than 32 mmHg and HCO-3 less than 22.0 mEq/L) and ten patients with metabolic alkalosis ([H+] less than 34 nM, pCO2 greater than 37 mmHg and HCO-3 greater than 28.0 mEq/L) to determine whether different alkalotic states similarly affect the red blood cell [H+] and 2,3-diphosphoglycerate interaction and thus the oxygen affinity of hemoglobin. The findings were statistically indistinguishable in respiratory alkalosis and metabolic alkalosis: a) low plasma [H+], normal red blood cell [H+], and high transmembrane [H+] gradient; b) elevated red blood cell 2,3-diphosphoglycerate inversely proportional to low arterial plasma [H+]; c) decrease in oxygen affinity of hemoglobin when normalized for plasma [H+], but less decreased when normalized for red blood cell [H+]. Other factors capable of affecting the oxygen affinity of hemoglobin were: mean corpuscular hemoglobin concentration; red blood cell adenosine triphosphate; carboxyhemoglobin; and methemoglobin were not significantly different between groups. These results: 1) agree with data previously reported from this laboratory on patients with portal-systemic encephalopathy; 2) underscore the importance of RBC [H+] in defining the oxygen affinity of hemoglobin; 3) suggest the decrease in oxygen affinity of hemoglobin is mediated through the 2,3-diphosphoglycerate elevation; and 4) indicate the high transmembrane [H+] gradient is principally due to the cellular accumulation of [H+] (2,3-diphosphoglycerate ionization).

2,3-Diphosphoglycerate↗
PubMed1989

Aldosterone secretion during acute metabolic and respiratory alkalosis in the goat.

Metabolic and respiratory alkalosis were produced in goats with the primary aim of studying possible influence of a reduced blood hydrogen ion concentration on aldosterone secretion. Metabolic alkalosis was induced by 1 h i.v. infusion of hypertonic tris(hydroxy-methyl)aminomethane (THAM) solution. The infusion was associated with a significant reduction in plasma aldosterone concentration (PA). It occurred in the absence of a detectable fall in plasma K or obvious change in plasma renin activity, but simultaneously with a moderate increase in plasma cortisol concentration and a significant reduction of plasma Na concentration. It suggests that changes of the primary aldosterone regulators were not the cause of the fall in PA, but leaves open the possibility that either the decreased blood hydrogen ion concentration as such or THAM-induced blood hypertonicity reduced the aldosterone secretion. The respiratory alkalosis was due to heat polypnoea elicited by 2 h exposure of the goats to 45 degrees C. Here, no obvious change in PA was observed during the alkalotic period, which, however, was associated with a rise in plasma K. Increased K stimulation may therefore have masked a possible inhibitory influence of the alkalosis upon the aldosterone secretion.

Aldosterone↗
PubMed1979

Cimetidine in the management of metabolic alkalosis induced by nasogastric drainage.

Metabolic alkalosis resulting from nasogastric drainage is a well recognized and potentially serious clinical problem. In the postoperative patient with acute renal failure, the management of the metabolic alkalosis is particularly difficult, and established modalities of therapy are sometimes ineffective and can be hazardous to the patient. In this article, we report on the successful use of cimetidine (an H2-receptor antagonist) as an adjunct in the treatment of severe metabolic alkalosis in a postsurgical renal failure patient. To our knowledge, this is the first reported successful use of cimetidine in the treatment of metabolic alkalosis due to gastric acid loss.

Acute Kidney Injury↗
PubMed1993

The effects of acidosis and alkalosis on long bone vascular resistance.

This study used an ex vivo perfusion model to investigate the direct effects of acidosis and alkalosis on the vascular resistance of the canine tibia. Baseline vascular resistance (BVR) and the vascular smooth muscle response to bolus doses of norepinephrine (NE) (0.025-3.2 nmol) and periarterial sympathetic nerve stimulation (NS) (10-25 Hz: 9 V, 2 ms pulses, 10 s) were studied. In Group I, these parameters were measured at normal pH (duration 7.34-7.44) and then during acidosis (pH 7.2-7.33). In Group II, they were measured at normal pH and then during alkalosis (pH 7.47-7.58). In Group III (control), they were measured serially at a normal pH. Alkalosis increased BVR by 56% (p < 0.0001). Acidosis attenuated (18% reduction) and alkalosis enhanced (66% increase) the vasoconstrictor action of NE (p < 0.0001). Acidosis also attenuated (11% reduction) the effect of sympathetic NS (p = 0.012). It is concluded that perfusion pH influences the sensitivity of long bone resistance vessels to circulating NE and sympathetic NS. Thus, local concentration of hydrogen ions may provide bone with a mechanism to autoregulate blood flow.

Acidosis↗
PubMed1975

Lactic acid permeation rate in working gastrocnemii of dogs during metabolic alkalosis and acidosis.

In isolated, blood perfused, supramaximally stimulated, isotonically working gastrocnemii of dogs lactic acid (LA) output and O2-consumption (V O2) were measured according to the Fick principle. Simultaneously concentration of muscle tissue was determined at rest and at different times during exercise. In one series of experiments metabolic alkalosis was induced by infusions of THAM of Na bicarbonate. As a result arterial pH increased to about 7.5 and standard [HCO3-1] to 31-35 mmol per 1. In another group of experiments metabolic acidosis was induced by HCl infusions. In these experiments pH decreased to 7.0-7.1 and standard [HO301] to 8-11 mmol per 1. During the first 3-4 min after the onset of exercise LA concentration of muscle tissue rose to 18-19 mumol per g wet weight in both series of experiments. During acidosis the highest average values for LA release from the muscle were about 1.1 mumoles per g per minute. During alkalosis LA permeation rate was nearly three times as high. As a consequence of increased rate of permeation, LA concentration of muscle tissue decreased more rapidly in alkalosis than in acidosis. In both series of experiments work per time and VO2 were practically equal during the first 5-6 min of exercise. Thereafter work per time and VO2 decreased more rapidly in acidosis than in alkalosis, a result which probably is due to higher LA concentration in muscle at this time in acidosis. It is concluded that LA permeation rate across muscle cell membrane is increased by high extracellular HCO3- concentration in combination with low H+ activity and vice versa.

Acidosis↗