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PubMed1996

High systemic HCO3(-) and topical 16,16-dimethyl-PGE2 protect gastric mucosa against luminal acid by enhancing its preepithelial buffer capacity.

Systemic metabolic alkalosis and topical prostaglandins protect the gastric mucosa against luminal acid. This study investigates whether this protection is mediated by increased epithelial HCO3(-) secretion with resultant alkalization of the pre-epithelial mucus-HCO3(-) buffer layer. surface pH of chambered ex vivo rat gastric epithelium was measured with liquid sensor pH microelectrodes during luminal perfusion of increasing acidities (0, 10, 30, 50, 100 mM HCL). The experimental groups were: (1) control, (2) topical 16,16-dimethyl-PGE2 treatment, (3) high-HCO3(-) metabolic alkalosis, and (4) low HCO3(-) respiratory alkalosis. The gastric mucosa of PGE2-treated and high-HCO3(-) alkalotic rats tolerated significantly better luminal acid than that of controls, but the tolerance of low-HCO3(-) alkalotic rats was significantly impaired. There was a significant correlation between arterial HCO3(-) concentration (but not arterial pH) and surface pH (r = 0.81, P < 0.01). This suggests that the gastric mucosa against luminal acid are, at least in part, mediated by enhanced buffer capacity of the pre-epithelial mucus-HCO3(-)layer.

16,16-Dimethylprostaglandin E2↗
PubMed1989

Simple acid-base disorders.

The body regulates pH closely to maintain homeostasis. The pH of blood can be represented by the Henderson-Hasselbalch equation: pH = pK + log [HCO3-]/PCO2 Thus, pH is a function of the ratio between bicarbonate ion concentration [HCO3-] and carbon dioxide tension (PCO2). There are four simple acid base disorders: (1) Metabolic acidosis, (2) respiratory acidosis, (3) metabolic alkalosis, and (4) respiratory alkalosis. Metabolic acidosis is the most common disorder encountered in clinical practice. The respiratory contribution to a change in pH can be determined by measuring PCO2 and the metabolic component by measuring the base excess. Unless it is desirable to know the oxygenation status of a patient, venous blood samples will usually be sufficient. Metabolic acidosis can result from an increase of acid in the body or by excess loss of bicarbonate. Measurement of the "anion-gap" [(Na+ + K+) - (Cl- + HCO3-)], may help to diagnose the cause of the metabolic acidosis. Treatment of all acid-base disorders must be aimed at diagnosis and correction of the underlying disease process. Specific treatment may be required when changes in pH are severe (pH less than 7.2 or pH greater than 7.6). Treatment of severe metabolic acidosis requires the use of sodium bicarbonate, but blood pH and gases should be monitored closely to avoid an "overshoot" alkalosis. Changes in pH may be accompanied by alterations in plasma potassium concentrations, and it is recommended that plasma potassium be monitored closely during treatment of acid-base disturbances.

Acid-Base Equilibrium↗
PubMed1980

Effects of changes in acid-base balance on neuromuscular blockade produced by ORG-NC 45.

The effects of acute acid-base changes on the neuromuscular blocking action of ORG NC 45 (a monoquaternary homologue of pancuronium) were measured in 10 cats, utilizing a constant infusion technique. Partial NC 45 blockade was antagonized slightly in the tibialis, soleus, and diaphragm during respiratory alkalosis (pH 7.53; PaCO2 1.9 kPa), whereas metabolic alkalosis (pH 7.64; Paco2 3.5 kPa) produced significant antagonism of NC 45 block in those muscles. Respiratory acidosis (pH 6.98; Paco2 10.3 kPa) and metabolic acidosis (p H 7.13; PaCO2 4.9 kPa) significantly potentiated partial NC 45 blocks in the tibialis, soleus, and diaphragm (except in the diaphragm during metabolic acidosis). Cumulative dose responses studied in six cats showed that the NC 45 dosage required to produce 85--95% tibialis block was slightly greater than controls during respiratory and metabolic alkalosis. Conversely, significantly less NC 45 was needed to produce the same degree of block during respiratory and metabolic acidosis. In vitro studies in rat hemidiaphragms likewise showed minimal NC 45 block antagonism when pH was raised to 7.68, and significant potentiation under acidotic conditions (pH 7.05). These actions are attributed in part to an increased rate of NC 45 metabolism by alkaline hydrolysis in alkalotic states and greater molecular stability during acidosis. Possible clinical implications are discussed.

Acidosis↗
PubMed1986

Increased arterial pH, not decreased PaCO2, attenuates hypoxia-induced pulmonary vasoconstriction in newborn lambs.

Mechanically induced hyperventilation is used in the treatment of newborn infants with persistent pulmonary hypertension syndrome to induce respiratory alkalosis, which may attenuate their pulmonary vasoconstriction. Whether this treatment is effective because of the increase in arterial pH or the decrease in Paco2 was investigated in nine sedated, mechanically ventilated newborn lambs with hypoxia-induced pulmonary vasoconstriction. We found that respiratory alkalosis and metabolic alkalosis were equally effective in attenuating hypoxia-induced pulmonary vasoconstriction, but that hypocapnia (low Paco2 with a normal arterial pH) was ineffective. These results indicate that increased arterial pH, not decreased Paco2, attenuates hypoxia-induced pulmonary vasoconstriction in newborn lambs and possibly the pulmonary vasoconstriction in newborn infants with persistent pulmonary hypertension syndrome.

Alkalosis↗
PubMed1990

Rational treatment of acid-base disorders.

Acid-base derangements are encountered frequently in clinical practice and many have life-threatening implications. Treatment is dependent on correctly identifying the acid-base disorder and, whenever possible, repairing the underlying causal process. Bicarbonate is the agent of choice for the treatment of acute metabolic acidosis. Controversy surrounds the use of alkali therapy in lactic acidosis and diabetic ketoacidosis, but bicarbonate should clearly be administered for severe acidosis. In most patients with mild to moderate chloride-responsive metabolic alkalosis, providing an adequate amount of a chloride salt will restore acid-base balance to normal over a matter of days. In contrast, therapy of the chloride-resistant metabolic alkalosis is best directed at the underlying disease. When alkalemia is severe, administering hydrochloric acid or a hydrochloric acid precursor may be necessary. Treatment of respiratory acidosis should be targeted at restoring ventilation; alkali should be administered only for superimposed metabolic acidosis. The therapy of respiratory alkalosis is centred on reversal of the root cause; short of this goal, there is no effective treatment of primary hypocapnia. The coexistence of more than one acid-base disorder (i.e. a mixed disorder) is not uncommon. When plasma bicarbonate concentration and arterial carbon dioxide tension (paCO2) are altered in opposite directions, extreme shifts in pH may occur. In such cases, it is imperative that the nature of the disturbance is identified early and therapy directed at both disorders.

Acid-Base Imbalance↗
PubMed1993

Effects of sodium bicarbonate and ammonium chloride on the incidence of furosemide-induced fetal skeletal anomaly, wavy rib, in rats.

Furosemide produces fetal wavy ribs when administered to pregnant rats during late gestation. The compound is also known to produce metabolic alkalosis in laboratory animals and man. In order to evaluate the effect of furosemide on maternal blood pH, Crj:CD(SD) female rats received an oral administration of 150 or 200 mg/kg of furosemide by gavage on day 16 of gestation and were bled at 4 hr post-dose. Compared to an average pH of 7.39 in control females, there was a significant elevation in blood pH in these furosemide-treated females (average pH of 7.44 to 7.48). When 2% sodium bicarbonate was provided in the drinking water for females treated with 150 mg/kg of furosemide, there was a further rise in maternal blood pH (7.52) compared to females treated with furosemide alone. Associated with this elevation in maternal blood pH was a marked increase in the incidence of fetal wavy ribs (87.6% compared to 27.6%). When females treated with 200 mg/kg of furosemide were provided with 0.5% ammonium chloride, furosemide-induced maternal alkalosis was corrected (pH decreased to 7.35) and there was a reduction in the incidence of fetal wavy ribs (7.0% compared to 37.2%). In addition, maternal blood pH among individual females was positively correlated with the incidence of fetal wavy ribs (r = 0.714). These results suggest that maternal metabolic alkalosis is involved in the pathogenesis of furosemide-induced wavy ribs.

Alkalosis↗
PubMed1995

Differential regulation of Na+/H+ exchange and H(+)-ATPase by pH and HCO3- in kidney proximal tubules.

This study examines the effects of acute in vitro acid-base disorders on Na+/H+ and H(+)-ATPase transporters in rabbit kidney proximal tubules (PT). PT suspensions were incubated in solutions with varying acid base conditions for 45 min and utilized for brush border membrane (BBM) vesicles preparation. BBM vesicles were studied for Na+/H+ exchange activity (assayed by 22Na+ influx) or abundance (using NHE-3 specific antibody) and H(+)-ATPase transporter abundance (using antibody against the 31 kDa subunit). The Na+/H+ exchanger activity increased by 55% in metabolic acidosis (pH 6.5, HCO3- 3 mM) and decreased by 41% in metabolic alkalosis (pH 8.0, HCO3- 90 mM). The abundance of NHE-3 remained constant in acidic, control, and alkalotic groups. H(+)-ATPase abundance, however, decreased in metabolic acidosis and increased in metabolic alkalosis by 57% and 42%, respectively. In PT suspensions incubated in isohydric conditions (pH 7.4), Na+/H+ exchanger activity increased by 29% in high HCO3- group (HCO3- 96 mM) and decreased by 16% in the low HCO3- groups (HCO3- 7 mM. The NHE-3 abundance remained constant in high, normal, and low [HCO3-] tubules. The abundance of H(+)-ATPase, however, increased by 82% in high [HCO3-] and decreased by 77% in the low [HCO3-] tubules. In PT suspensions incubated in varying pCO2 and constant [HCO3-], Na+/H+ exchanger activity increased by 35% in high pCO2 (20% pCO2, respiratory acidosis) and decreased by 32% in low pCO2 (1.5% pCO2, respiratory alkalosis) tubules. The NHE-3 abundance remained unchanged in high, normal, and low pCO2 tubules.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis↗
PubMedDate not supplied

Apparent normobasemia as a negative prognostic sign immediately after hepatectomy.

The acid-base balance from the postoperative day (POD) 1 to POD 3 after cirrhotic liver resection was investigated in relation to operative outcome by conducting a retrospective study on the changes in arterial ketone body ratio (AKBR), which reflects the hepatic mitochondrial redox state, and arterial blood gas analysis. Patients were grouped according to their outcome: hospital death (HD) and or good outcome, the latter group acting as controls (CTR). Metabolic alkalosis developed in a significant number of the CTR patients (p < 0.01), who had high AKBR values. By contrast, metabolic alkalosis did not develop in the HD group, with significantly lower AKBR (p < 0.001), and there was almost normobasemia. There were no significant differences in the need for mechanical respiratory assistance, the amounts of fresh frozen plasma administered, and renal function test results between the two groups on each of 3 postoperative days. These data indicated that the absence of metabolic alkalosis during the early postoperative days reflects disruption of energy metabolism in the remnant liver, and that the apparent normobasemia is a significant indicator of poor prognosis after cirrhotic liver resection.

Acid-Base Equilibrium↗
PubMed1993

Application of multivariate autoregressive modelling for analysing chloride/potassium/bicarbonate relationship in the body.

The authors repeatedly analysed course data of acid-base disturbances accompanying hypochloraemia and/or hypokalaemia by means of multivariate autoregressive modelling. It was found that the regulatory relationship between chloride and bicarbonate is inverse between the following two hypochloraemic hyperbicarbonataemic states: the one induced by chloride depletion and the other induced by CO2 retention. Also, the study revealed an independent role of potassium deficiency in the development of metabolic alkalosis, especially in cases with mineralocorticoid-induced alkalosis. The present approach enabled the authors to solve a long-standing problem, i.e. to differentiate between the roles of chloride and potassium in the development of metabolic alkalosis.

Alkalosis↗
PubMed2002

Effects of acid-base abnormalities on blood capacity of transporting CO(2): adverse effect of metabolic acidosis.

OBJECTIVE: To investigate the effects of some acid-base abnormalities on blood capacity of transporting CO(2). DESIGN: Prospective study. SETTING: General and Cardiosurgical ICUs of a University hospital. PATIENTS: Six groups of ten patients characterized by: metabolic alkalosis; respiratory alkalosis; absence of acid-base abnormalities; metabolic acidosis; uncompensated respiratory acidosis; and compensated respiratory acidosis. MEASUREMENTS AND RESULTS: The CO(2) dissociation curve, Haldane effect, and the ratio Ra-v between Ca-vCO(2) and Pa-vCO(2) were calculated from arterial and mixed-venous blood gas analyses. The CO(2) dissociation curve was shifted upwards by metabolic alkalosis and compensated respiratory acidosis and downwards by metabolic acidosis. The slope of the curve was unaffected, but CO(2) transport not due to Haldane effect was significantly lower in respiratory acidosis since the slope was less steep at higher PCO(2) values. In comparison with controls, patients affected by metabolic acidosis showed lower Haldane effect values (0.18+/-0.15 vs 0.59+/-0.26 ml of CO(2) per ml of arterial-mixed venous O(2) content difference; P <.05) and Ra-v values (0.43+/-0.10 vs 0.84+/-0.17 ml of CO(2) transported by 100 ml of blood per Torr of arterial-mixed venous PCO(2) gradient; P <.05). CONCLUSIONS: Our findings suggest that acid-base abnormalities, particularly metabolic acidosis, markedly affect blood capacity of transporting CO(2) and may worsen tissue hypercarbia associated with hypoperfusion. However, because of possible errors due to small measurements and the assumptions of the method, in the future definitive clarification will require the construction of original CO(2) dissociation curves for each acid-base abnormality.

Acidosis↗
PubMed1998

Concomitant occurrence of Gitelman and Bartter syndromes in the same family?

The molecular defects responsible for the two most-common forms of inherited normotensive hypokalemic metabolic alkalosis have recently been defined. Most patients with Bartter syndrome have defects in transporters in the thick ascending limb of the loop of Henle, such as the Na-K-2Cl cotransporter, NKCC2, or the ATP-sensitive potassium channel, ROMK. Patients with Gitelman syndrome usually have mutations in the thiazide-sensitive Na-Cl cotransporter in the distal convoluted tubule. The location of the affected transporters correlates well with the typical presentation of these syndromes. Patients with Bartter syndrome typically present with normal or increased calcium excretion. Hypomagnesemia is present in only one-third of affected individuals. In contrast, hypomagnesemia and hypocalciuria are considered hallmarks of Gitelman syndrome. This report describes siblings presenting as young adults with mild symptoms associated with normotensive hypokalemic metabolic alkalosis. One sibling has hypocalciuria and hypomagnesemia, consistent with Gitelman syndrome. Surprisingly, the other sibling has normal serum magnesium and urinary calcium excretion. These siblings demonstrate the biochemical heterogeneity that can exist in patients with normotensive hypokalemic metabolic alkalosis. This report indicates that hypocalciuria does not always distinguish Gitelman and Bartter syndromes.

Adolescent↗
PubMed1991

The time course in development of hypocalcemia and plasma lactate accumulation in mature and immature hyperthermic domestic fowl (Gallus domesticus).

1. During hyperthermia-induced thermal panting, there was a progressive development of alkalosis, hypocapnia, hypocalcemia and plasma lactate accumulation in both mature and immature domestic fowl. 2. The results of this study further demonstrate that hypocalcemia is a general consequence of respiratory alkalosis in animals. 3. The significant (P less than 0.05) regression analysis of plasma lactate vs arterial blood pH, suggest a relationship between these two variables. 4. Plasma lactate accumulation may therefore play an important role as an extrarenal buffering component in the normal defense against severe alkalosis.

Aging↗
PubMed1987

Interaction between calcium and hydrogen ions in canine coronary arteries.

In vitro experiments were carried out to study the effects of "respiratory" and "metabolic" acid-base alterations on canine coronary arteries precontracted by high potassium. Alkalosis (pH 7.70 +/- 0.02) increased the coronary tone by 33 +/- 3% (P less than 0.05) and acidosis (pH 7.10 +/- 0.01) decreased it by 30 +/- 3% (P less than 0.05). The tension stabilized in approximately 15 mins and its variation was of similar extent whether changes in extracellular pH were produced by changes in PCO2 or in bicarbonate concentration. The contractile changes were not abolished neither by alpha or beta adrenergic blockade nor by endothelium denudation. The effect of pH could not be offset by altering extracellular potassium or calcium when the plateau of the relationship between contractility of the smooth muscle and concentration of these ions was reached. When tonus developed by the strips and [Ca2+]0 were plotted reciprocally, DTmax significantly increased in alkalosis and decreased in acidosis. No significant changes in Ca50 ([Ca2+]0 necessary to obtain 50% of maximal force) were detected. pH changes did not modify Ca2+ influx but a relaxation of similar extent induced by nifedipine produced a detectable decrease in Ca2+ influx. Ca2+ efflux was augmented in acidosis and depressed in alkalosis. Our data do not support the hypothesis of hydrogen ion changes inducing calcium influx alterations in a competitive fashion as the mechanism involved to contract or relax conduit coronary arteries. On the contrary, they suggest that acid-base variations alter the contractile activity of vascular smooth muscle by modulating Ca2+ efflux.

Acid-Base Equilibrium↗
PubMed1981

The independent effects of hyperventilation, tolazoline, and dopamine on infants with persistent pulmonary hypertension.

We studied the separate and combined effects of hyperventilation and administration of dopamine and tolazoline in five infants with pulmonary hypertension managed with indwelling pulmonary artery catheters. In five infants the right-to-left shunt reversed during ventilator-induced respiratory alkalosis (pH greater than 7.6). Response to drugs was variable and unpredictable. One infant could be oxygenated at normal pH during combined dopamine and tolazoline infusion. Other infants showed no response to drugs, or became worse during infusion. The ratio of pulmonary artery to systemic artery pressure averaged 1.14 with standard therapy, but decreased to 0.98 following respiratory alkalosis alone, to 0.87 following drug infusions, and to 0.70 following the combination of alkalosis and drug infusion. These changes were significant by analysis of variance at P less than 0.02, P less 0.001, and P less than 0.001, respectively. Systemic oxygenation was satisfactory in all cases when the pulmonary to systemic pressure ratio was less than 1.0.

Alkalosis, Respiratory↗
PubMed1985

Furosemide decreases ventilation in young rabbits.

To test the hypothesis that furosemide would cause metabolic alkalosis and thus alveolar hypoventilation, normal rabbit pups were given either furosemide (4 mg/kg/day) or saline solution for the first 8 to 10 days of life. Pups given furosemide developed primary metabolic alkalosis and reduced ventilation, which resulted in secondary respiratory acidosis. Lung compliance was improved by furosemide, and the ventilatory response to CO2 was unaffected. KCl injection in alkalotic pups increased ventilation and decreased pH. The data show that conventional doses of furosemide can (1) cause metabolic alkalosis and reduce ventilation; (2) increase the PaCO2, which reflects changes in acid-base status and not changes in lung function; and (3) increase lung compliance, perhaps by decreasing lung water. When these effects occur in infants with chronic lung disease, the beneficial effect of furosemide may be obscured.

Acidosis, Respiratory↗
PubMed2001

Effect of acute metabolic acid/base shifts on the human airway calibre.

Acute metabolic alkalosis (NaHCO(3)), acidosis (NH(4)Cl), and placebo (NaCl) were induced in 15 healthy volunteers (12 females, median age 34 (range 24-56) years) in a double blind, placebo controlled study to evaluate the presence of the effects on airway calibre. Acid-base shifts were determined by capillary blood gas sampling. Measurements were performed at the maximal acid-base shift, 90 min after intervention. Airway resistance (R(aw)) and specific airway conductance (sG(aw)), were evaluated, as primary variables, pre and post intervention. Secondary variables, including bronchial responsiveness to histamine, maximal respiratory mouth pressures and grip strength, were evaluated post intervention. In alkalosis, base excess (BE) increased from -0.3 (-3.0-1.9) to 3.0 (1.0-4.8) mmol/l and pH increased from 7.41 (7.37-7.43) to 7.44 (7.39-7.47) (both P<0.01), accompanied by an increase in Pa(CO(2)): 4.7 (4.0-5.7) to 5.0 (4.7-6.1) kPa (P<0.05). R(aw) increased from 0.156 (0.134-0.263) to 0.169 (0.132-0.271) kPa s/L (P<0.05), sG(aw) decreased, but this was not statistically significantly. In acidosis, BE decreased from -0.2 (-2.0-2.2) to -3.5 (-6.3-1.1) mmol/l and pH decreased from 7.41 (7.39-7.45) to 7.36 (7.31-7.40) (both P<0.01), accompanied by a non-significant decrease in Pa(CO(2)). Changes in R(aw) and sG(aw) were contrary to those in alkalosis, but did not reach statistical significance. Acute metabolic acid-base shifts mildly influence the airway calibre in healthy human subjects.

Acidosis↗
PubMed1997

Possible role of sweating in the pathophysiology of panic attacks.

In recent years the role of hyperventilation in the generation of panic attacks has attracted a considerable amount of interest. According to these studies hyperventilation can elicit the somatic symptoms of panic due to systemic alkalosis. We suggest that since in the case of panic, sweating might cause alkalosis, it could also contribute to the generation of panic attacks. In light of this hypothesis we made a statistical analysis of the panic symptoms of 111 panic patients diagnosed according to DSM-III criteria. The analysis revealed that: (1) there was a well identified group of panic patients who had minor breathing difficulties with heavy sweating; and (2) that all the patients sampled had either severe breathing, or sweating symptoms, or both. We conclude that in the absence of the intensive physical activity of the 'flight or fight' reaction, sweating as well as hyperventilation can cause alkalosis, which in turn might generate panic attacks.

Alkalosis, Respiratory↗
PubMed1981

The effect of chronic acid/base disturbances on renal amino acid clearances in the rat.

Since the few data available concerning the effect of acid/base disturbances on renal amino acid reabsorption were conflicting, and there were sound theoretical reasons for an effect, we have studied the clearance of endogenous amino acids in the rat in vivo under control conditions and after induction of either metabolic acidosis or alkalosis by administration of NH4Cl or NaHCO3, respectively. The effectiveness of treatment was assessed by examination of plasma and urinary levels of HCO3, Cl, Na and K. It was found that the renal clearance of amino acids, measured during acidosis or alkalosis, did not differ from those found under control conditions, the majority of values being less than 1% of the glomerular filtration rate. Thus, the amino acid reabsorptive mechanism appears unaffected by changes in the pH of the glomerular filtrate and/or by changes in tubular hydrogen ion secretion which would accompany such disturbances. These data are thus in agreement with findings during acidosis in man and in both acidosis and alkalosis in the dog. The findings are contrary to earlier reports from in vitro studies in the rat, and suggest the presence of severe functional impairment in the isolated perfused kidneys used in these earlier studies where very large changes in amino acid clearance were obtained.

Acid-Base Imbalance↗