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PubMed1976

Acid-base status in liver cirrhosis. Disturbances in stable, terminal and portal-caval shunted patients.

Acid-base status was determined in 86 patients with cirrhosis of the liver. Group I comprised 55 patients living more than 3 months after examination (stable). Another 18 stable patients with a surgical porta-caval shunt (p.c.a.) formed group II. Group III consisted of 12 terminal patients without p.c.a. examined within the last week of life. With respect to liver function group II was intermediate between I and III. The most common acid-base disturbance in group I was compensated respiratory alkalosis (20%) followed by compensated metabolic alkalosis (15%). 50% of group II presented compensated respiratory alkalosis. 85% of group III showed metabolic acidosis, which was compensated in only half of the patients. Respiratory alkalosis seemed more related to impairment of liver function than to portasystemic shunting. The genesis of the terminal metabolic acidosis was complex. Renal function was reduced in 92% of group III, and lactic acidosis was found in 36%. In this group hepatic function was most severely impaired, and 60% were hypotensive. These disturbances were not related to aetiology or treatment of the liver disease.

Acid-Base Equilibrium↗
PubMed1975

The physiological assessment of acid-base balance.

Acid-base terminology including the sue of SI units is reviewed. The historical reasons why nomograms have been particularly used in acid-base work are discussed. The theoretical basis of the Henderson-Hasselbalch equation is considered. It is emphasized that the solubility of CO2 in plasma and the apparent first dissociation constant of carbonic acid are not chemical constants when applied to media of uncertain and varying composition such as blood plasma. The use of the Henderson-Hasselbalch equation in making hypothermia corrections for PCO2 is discussed. The Astrup system for the in vitro determination of blood gases and derived parameters is described and the theoretical weakness of the base excess concept stressed. A more clinically-oriented approach to the assessment of acid-base problems is presented. Measurement of blood [H+] and PCO2 are considered to be primary data which should be recorded on a chart with in vivo CO2-titration lines (see below). Clinical information and results of other laboratory investigations such as plasma bicarbonate, PO2,P50 are then to be considered together with the primary data. In order to interpret this combined information it is essential to take into account the known ventilatory response to metabolic acidosis and alkalosis, and the renal response to respiratory acidosis and alkalosis. The use is recommended of a chart showing the whole-body CO2-titration points obtained when patients with different initial levels of non-respiratory [H+] are ventilated. A number of examples are given of the use of this [H+] and PCO2 in vivo chart in the interpretation of acid-base data. The aetiology, prognosis and treatment of metabolic alkalosis is briefly reviewed. Treatment with intravenous acid is recommended for established cases. Attention is drawn to the possibility of iatrogenic production of metabolic alkalosis. Caution is expressed over the use of intravenous alkali in all but the severest cases of metabolic acidosis. The role of 2,3-diphosphoglycerate on tissue oxygenation is stressed and use of intravenous sodium phosphate as an alternative to intravenous bicarbonate is mentioned.

Acid-Base Equilibrium↗
PubMed1979

Effect of pH on the calcium metabolism of isolated rat kidney cells.

The effects of metabolic and respiratory acidosis and alkalosis on cellular calcium metabolism were studied in rat kidney cells dispersed with collagenase. In both types of acidosis, the intracellular pH, total cell calcium, and the cell relative radioactivity after 60 min of labeling are significantly depressed. Kinetic analysis of 45-ca desaturation curves shows that acidosis decreases all three cellular calcium pools and depresses calcium fluxes between the superficial and cytosolic pools and between the cytosolic and mitochondrial pools. In alkalosis the intracellular pH, the total cell calcium, and the cell relative radioactivity are significantly increased. Kinetic studies show that in alkalosis, only the mitochondrial pool is consistently increased. Calcium exchange between the mitochondrial and cytosolic pool is increased in metabolic alkalosis only. These results suggest that hydrogen ion is an important modulator of calcium metabolism, and that the intracellular pH rather than extracellular pH is the critical factor in determining the calcium status of cells during altered acid-base conditions.

Acidosis↗
PubMed2005

Na(+)/H(+) exchanger isoforms are differentially regulated in rat submandibular gland during acid/base disturbances in vivo.

Acute metabolic acidosis and alkalosis cause a series of homeostatic adaptive responses in the kidney and other epithelia. We hypothesized that acid/base disturbances might affect the expression of Na(+)/H(+) exchanger (NHE) isoforms in salivary glands and determined the expression and cellular distribution of NHE3 and NHE4 in rat submandibular glands of controls and after imposed acute or chronic metabolic acidosis or alkalosis in vivo. Reverse transcription/polymerase chain reaction, in situ hybridization, and immunohistochemistry were applied by using specific primers, antisense probes, and antibodies, respectively. The results showed NHE3 and NHE4 transcript expression and protein abundance in rat submandibular gland. NHE3 was apically localized in duct cells, whereas NHE4 was found basolaterally distributed in acinar and duct cells. Acute acidosis and alkalosis and chronic acidosis had no effect on NHE3 and NHE4 expression and localization. In contrast, chronic metabolic alkalosis significantly decreased the number of apically stained NHE3 duct cells but had no effect on NHE3 mRNA expression. The results demonstrate, for the first time, the presence of NHE4 protein in salivary glands. The data also indicate the distinct regulation and adaptive changes of different isoforms of the same transporter in rat submandibular gland as a response to acid/base disturbances.

Acid-Base Equilibrium↗
PubMed1983

Effects of acute metabolic acid-base changes and furosemide on magnesium excretion in rats.

The effect of acute metabolic acid-base changes on renal magnesium transport is not well defined. We have examined renal magnesium handling in three groups of ten acutely thyroparathyroidectomized rats infused with isotonic NaCl (controls), NH4Cl (acidosis), and NaHCO3 (alkalosis). To define the interactions of furosemide with acid-base changes and in an attempt to localize the site of action of acidosis and alkalosis on tubular magnesium transport, the rats were studied in a second phase after administration of a maximal dose of furosemide. Before furosemide, the blood pH was 7.40 in the controls, 7.27 (P less than 0.001) in the acidotic rats, and 7.56 (P less than 0.001) in the alkalotic rats. The filtered magnesium load was not significantly different in the three groups, but fractional excretion of magnesium (FEMg) was 33.7%, 37.4%, and 13.3% in the controls, the acidosis group, and the alkalosis group, respectively. Following furosemide, the blood pH was unchanged in each group, but FEMg increased significantly to 55.4%, 71.1% (P less than 0.01 compared with controls), and 41.4% (P less than 0.01 compared with controls) in the controls, the acidotic rats, and the alkalotic rats, respectively. These data indicate that metabolic alkalosis per se enhances renal magnesium transport, and this effect is also evident after blockade of loop magnesium reabsorption by a maximal dose of furosemide. Acidosis per se does not significantly alter magnesium transport, but an inhibitory effect of acidosis on magnesium reabsorption becomes evident when distal magnesium delivery is greatly increased by furosemide. These interactions suggest that metabolic acid-base changes and furosemide may influence magnesium reabsorption at different tubule sites.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Imbalance↗
PubMed1984

The effects of hypocapnia on intracellular pH and bicarbonate.

The intracellular pH (pHi) and bicarbonate concentration ([HCO3-]icw) of cardiac and skeletal muscles were monitored during respiratory alkalosis in order to further elucidate the homeostatic processes which operate in these tissues to ameliorate deviations from normal acid-base status. Rats were mechanically hyperventilated to induce hypocapnia, pHi was determined by the DMO method, and [HCO-3]icw was calculated from the Henderson-Hasselbalch equation using pHi and the partial pressure of carbon dioxide of vena caval blood. A significant intracellular alkalosis occurred in both cardiac and skeletal muscles during hypocapnia, but the changes in pHi were less in the heart than in skeletal muscle. The decreases in cardiac [HCO-3]icw were greater than those attributable to the physicochemical buffering of the heart. These data are consistent with an intramyocardial source of protons other than physicochemical buffering during respiratory alkalosis. The decreases in skeletal muscle [HCO-3]icw were less than those due to physicochemical buffering. These data are consistent with a net extrusion from skeletal muscles cells of the protons derived from physicochemical buffering during respiratory alkalosis.

Acid-Base Equilibrium↗
PubMed2004

Central neurogenic hyperventilation in a conscious child associated with glioblastoma multiforme.

Central neurogenic hyperventilation refers to progressive tachypnea leading to hypocarbia and respiratory alkalosis caused by cortical disorders, initially reported in comatose patients with mainly pontine infarction. Central neurogenic hyperventilation in conscious patients is even rarer, numbering around 30 reported cases including seven children, mainly associated with infiltrative gliomas and lymphomas of the brainstem and pons. We report the evolution of central neurogenic hyperventilation in a conscious child associated with an infiltrative glioblastoma multiforme diagnosed 1 year before admission. He presented with progressive tachypnea and dyspnea of 1 week duration. On examination he was fully alert and aware of his respiratory disorder. Respiratory rate was 56 breaths per minute using accessory respiratory muscles. Hyperventilation was unchanged during sleep. Arterial blood gases disclosed marked hypocarbia: Pco(2) of 8 mm Hg resulting in severe respiratory alkalosis at pH of 7.8. Central neurogenic hyperventilation was therefore suggested after exclusion of other respiratory or cardiac disorders. The exaggerated tachypnea persisted along with respiratory alkalosis. Over a period of 2 months his overall state markedly deteriorated; he lapsed into coma, and finally succumbed after involvement of medullary cardiovascular centers. Although extremely rare in the pediatric age group, central neurogenic hyperventilation should be suspected in any alert child presenting with unexplained increasing tachypnea and hypocarbia leading to respiratory alkalosis. The evolution of such a disorder may be an alarming sign of ensuing deterioration in patients with tumors of the brainstem and medulla before cardiovascular derangement.

Alkalosis, Respiratory↗
PubMed1999

Ammonium prepulse: effects on intracellular pH and bioelectric activity of CA3-neurones in guinea pig hippocampal slices.

The ammonium prepulse technique was used to study influences of intracellular pH (pH(i)) on bioelectric activity of CA3-neurones in hippocampal slices. 60, 180 or 600 s lasting NH(4)Cl (10 mM) pulses led to a transient intracellular alkalosis (DeltapH(i): up to 0.2 pH-units) in about one-half of the neurones loaded with 2', 7-bis(2-carboxyethyl)-5(6)-carboxyfluorescein-acetoxymethylester (BCECF-AM). No alkalosis was seen in the remainder cells. The amount of alkalosis depended on the actual pH(i) of each neurone and increased when the pH(i) decreased. Washout of NH(4)Cl induced a fall in pH(i) (DeltapH(i): 0.12-0.54 pH-units) which recovered within <20 min. Frequency of spontaneous action potentials remained unchanged during washin of ammonium (60 or 180 s). However, pre-treatment with low concentrations of bicuculline-methiodide (0. 01 microM) or caffeine (0.1 mM), both of which did not change bioelectric activity per se, permitted a burst-activity to occur during ammonium-washin in about one-half of the neurones. In all neurones, washout of ammonium inhibited spontaneous and epileptiform activity (elicited by 1 mM caffeine, 20-50 microM bicuculline-methiodide, or 50-75 microM 4-aminopyridine) for </=20 min. This inhibition was accompanied by an increased membrane conductance (up to 20%) and a hyperpolarisation of up to 10 mV. We conclude that intracellular alkalosis augments, whereas intracellular acidosis depresses bioelectric activity of CA3-neurones.

Alkalosis↗
PubMed1988

Effect of pH and PCO2 on pulmonary and systemic hemodynamics after surgery in children with congenital heart disease and pulmonary hypertension.

Fourteen children with congenital heart disease and associated pulmonary hypertension (preoperative mean pulmonary artery pressure (MPAP) 48 mm Hg +/- 1 SEM were examined to determine the effect of arterial carbon dioxide tension (PaCO2) and pH on pulmonary and systemic hemodynamics after surgical repair. Baseline measurements were obtained with hyperventilation to PaCO2 20 to 30 mm Hg (pH 7.56 +/- 0.01 mm Hg). The addition of carbon dioxide to inspired gas to achieve a PaCO2 40 to 45 mm Hg (pH 7.35 +/- 0.01) resulted in a significant increase in MPAP, from 32 +/- 5 mm Hg to 47 +/- 8 mm Hg (p less than 0.05). An increase in mean cardiac index (CI) from 2.7 +/- 0.3 L/min/m2 to 3.3 +/- 0.3 L/min/m2 (p less than 0.05) explained in part the associated increase in MPAP. For a subgroup of eight patients with postoperative MPAP greater than 30 mm Hg (at pH 7.35 to 7.40), pulmonary vascular resistance index (PVRI) also significantly increased (p less than 0.05) as PaCO2 was increased, implying a direct pulmonary vasodilating effect of alkalosis. Removal of carbon dioxide from inspired gas returned hemodynamic values to baseline. The higher the MPAP at physiologic pH the greater the absolute amount of MPAP reduction and PVRI reduction (p less than 0.05) with alkalosis. No complications from alkalosis were seen. We suggest that a trial of hypocarbic alkalosis in the child with severe residual pulmonary hypertension after surgical repair of congenital heart disease is warranted to reduce right ventricular afterload.

Adolescent↗
PubMed1994

[Acid-base equilibrium and the brain].

In physiological conditions, the regulation of acid-base balance in brain maintains a noteworthy stability of cerebral pH. During systemic metabolic acid-base imbalances cerebral pH is well controlled as the blood/brain barrier is slowly and poorly permeable to electrolytes (HCO3- and H+). Cerebral pH is regulated by a modulation of the respiratory drive, triggered by the early alterations of interstitial fluid pH, close to medullary chemoreceptors. As blood/brain barrier is highly permeable to Co2, CSF pH is corrected in a few hours, even in case of severe metabolic acidosis and alkalosis. Conversely, during ventilatory acidosis and alkalosis the cerebral pH varies in the same direction and in the same range than blood pH. Therefore, the brain is better protected against metabolic than ventilatory acid-base imbalances. Ventilatory acidosis and alkalosis are able to impair cerebral blood flow and brain activity through interstitial pH alterations. During respiratory acidosis, [HCO3-] increases in extracellular fluids to control cerebral pH by two main ways: a carbonic anhydrase activation at the blood/brain and blood/CSF barriers level and an increase in chloride shift in glial cells (HCO3- exchanged for Cl-). During respiratory alkalosis, [HCO3-] decreases in extracellular fluids by the opposite changes in HCO3- transport and by an increase in lactic acid synthesis by cerebral cells. The treatment of metabolic acidosis with bicarbonates may induce a cerebral acidosis and worsen a cerebral oedema during ketoacidosis. Moderate hypocapnia carried out to treat intracranial hypertension is mainly effective when cerebral blood flow is high and vascular CO2 reactivity maintained. Hypocapnia may restore an altered cerebral blood flow autoregulation. Instrumental hypocapnia requires a control of cerebral perfusion pressure and cerebral arteriovenous difference for oxygen, to select patients for whom this kind of treatment may be of benefit, to choose the optimal level of hypocapnia and to avoid any deleterious effect. If hypocapnia is maintained over several days, an adaptation of CSF pH may limit the therapeutic effect on the cerebral blood flow and the intracranial pressure.

Acid-Base Equilibrium↗
PubMed1999

Segmental pulmonary vascular responses to changes in pH in rat lungs: role of nitric oxide.

BACKGROUND: Respiratory or renal failure is associated with changes in blood pH. Changes in pH may have profound effects on vascular tone and reactivity. Site of action of acidosis in the pulmonary vasculature and the role of nitric oxide production remain unclear. METHODS: We utilized isolated rat lung preparation perfused with autologous blood (Hct = 20%, flow rate = 33 ml/min), and investigated the effect of acidosis and alkalosis (induced by ventilation with high and low inspired CO2) on vascular resistance and the role of nitric oxide during resting and elevated tone conditions. Changes in resistance were described in terms of small and large arteries and veins, using the vascular occlusion technique. RESULTS: Acidosis (Pco2 = 66.7 +/- 0.7 mmHg, pH = 7.17 +/- 0.01, Po2 = 255 +/- 3 mmHg) caused vasoconstriction under resting and increased vascular tone conditions (U46619-induced). The changes in resistance occurred primarily in the small arteries. In contrast, alkalosis (Pco2 = 20.1 +/- 0.3 mmHg, pH = 7.61 +/- 0.01, Po2 = 244 +/- 3 mmHg) caused vasodilation only at elevated tone conditions. Nitro-L-arginine (LNA), an inhibitor of nitric oxide synthase, increased vascular resistance slightly but did not modulate the responses to pH, suggesting that such responses are not nitric oxide dependent. During KCl-induced contraction, the effects of pH were abolished. CONCLUSIONS: We conclude that in rat lung, acidosis causes an increase in pulmonary vascular resistance at normal and elevated tone conditions. Furthermore, the response is limited primarily to the small arteries, and is not mediated by nitric oxide. Alkalosis tends to cause the opposite effects. The effects of acidosis and alkalosis were abolished when vascular tone was elevated with a low dose of KCl, suggesting that vascular response to pH may involve changes in membrane potential.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1984

Halothane diminishes changes in cardiac fiber action potential duration induced by hypocarbia and hypercarbia.

Both halothane (HAL) and acid-base changes produce cardiac arrhythmias in humans. The authors' aim was to determine if HAL alters the effects of hypercapnic acidosis and hypocapnic alkalosis on action potential (AP) properties of ventricular muscle fibers. They superfused the paced right ventricle of 15 guinea pig hearts with non-HCO3- buffered salt solution and recorded transmembrane APs with 3 M KCl microelectrodes in 35 subendocardial cells. Random changes in the fractions of HAL were made during low (12% CO2 in O2), normal (5% CO2 in O2), and high (0% CO2 in O2) pH. Compared with controls at pH 7.44, AP duration (APD) and effective refractory period (ERP) significantly decreased by 7 and 4% at pH 8.08 and increased by 7 and 9% at pH 7.09. At pH 7.44, 0.7-2.1% HAL produced no change in APD; but 2.1% increased ERP, while 3.5% HAL decreased ERP. At pH 8.08, the decrease in ERP induced with alkalosis alone was converted to an increase with 1.4 and 2.1% HAL. At pH 7.09, 0.7-1.4% HAL had no additional effect on the acidosis-induced increases in APD and ERP, but 2.1 and 2.8% HAL greatly reduced these responses. At HAL fractions greater than 1.4% the marked inverse changes in APD and ERP, induced alone by acidosis and alkalosis, were no longer significantly different from control. This study shows that the opposing effects of alkalosis to shorten and of acidosis to lengthen APD and ERP were attenuated at low levels and abolished at high levels of HAL.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis↗
PubMed2006

Hyponatremic dehydration as a presentation of cystic fibrosis.

BACKGROUND: The purpose of this study is to present a case report of a child with hyponatremic dehydration diagnosed after CF and to review the cases of 13 patients with CF who had the same initial presentation in our hospital. METHODS: This report reviewed the clinical records of children diagnosed with CF to ascertain the prevalence of metabolic alkalosis with electrolyte depletion as the presentation of CF. It also used sweat tests to diagnose a child with CF. RESULTS: The laboratory tests of a 12-month-old girl presented 3 times to the ;pediatric emergency department with vomiting and weight loss showed hyponatremia, hypochloremia, and metabolic alkalosis. The patient was subsequently diagnosed with CF by means of 2 positive sweat tests. Meanwhile, the review of the clinical records of all children diagnosed with CF from 1985 to 2004 (N = 77) showed that the prevalence of metabolic alkalosis with electrolyte depletion as the presentation of CF was 16.8%. The age of the infants ranged from 3 to 14 months. All episodes took place during summer. CONCLUSIONS: There are not many causes of metabolic alkalosis with hyponatremic dehydration, and one of them is CF. This report emphasizes sodium depletion as a common sign of CF presentation. This is most important in countries where the neonatal screening test for CF is not available because the disease may be asymptomatic or oligosymptomatic for several months or even years. Cystic fibrosis should be considered in differential diagnosis of any child presenting with unexplained hyponatremic dehydration.

Alkalosis↗
PubMed1989

Effect of magnesium depletion and potassium depletion and chlorothiazide on intracellular pH in the rat, studied by 31P NMR.

1. Both dietary magnesium depletion and potassium depletion (confirmed by tissue analysis) were induced in rats which were then compared with rats treated with chlorothiazide (250 mg/kg diet) and rats on a control synthetic diet. 2. Brain and muscle intracellular pH was measured by using a surface coil and [31P]-NMR to measure the chemical shift of inorganic phosphate. pH was also measured in isolated perfused hearts from control and magnesium-deficient rats. Intracellular magnesium status was assessed by measuring the chemical shift of beta-ATP in brain. 3. There was no evidence for magnesium deficiency in the chlorothiazide-treated rats on tissue analysis or on chemical shift of beta-ATP in brain. Both magnesium and potassium deficiency, but not chlorothiazide treatment, were associated with an extracellular alkalosis. 4. Magnesium deficiency led to an intracellular alkalosis in brain, muscle and heart. Chlorothiazide treatment led to an alkalosis in brain. Potassium deficiency was associated with a normal intracellular pH in brain and muscle. 5. Magnesium depletion and chlorothiazide treatment produce intracellular alkalosis by unknown mechanism(s).

Acid-Base Equilibrium↗
PubMed1994

Hypocarbia and cystic periventricular leukomalacia in premature infants.

One hundred sixty seven survivors among very low birthweight infants with a gestational age of less than 35 weeks have been studied prospectively. The purpose of this study was to clarify the relationship of severe prenatal and perinatal complications and hypocarbic alkalosis, defined as a carbon dioxide tension (PaCO2) of less than or equal to 2.67 kPa and a pH of 7.50 or greater during the first 24 hours of life, to cystic periventricular leukomalacia (PVL) depicted by serial cranial ultrasonographic examinations. Complications occurred in 16 infants, five of whom presented with PVL, while eight of 151 infants without complications had PVL. Twenty six of the infants had hypocarbic alkalosis, six with evidence of PVL, and seven of the 136 infants without hypocarbic alkalosis had PVL. These results suggest a significant relationship of complications and hypocarbic alkalosis to PVL. Mechanical ventilation should be managed carefully in premature infants to avoid PaCO2 of lower than 2.67 kPa.

Alkalosis↗
PubMed1991

Acid-base status affects gas exchange in canine oleic acid pulmonary edema.

The effects of acidosis and alkalosis on pulmonary gas exchange were studied in 32 pentobarbital sodium-anesthetized intact dogs after induction of oleic acid (0.06 ml/kg) pulmonary edema. Gas exchange was assessed at constant ventilation and constant cardiac output, by venous admixture calculations and by intrapulmonary shunt measurements using the sulfur hexafluoride (SF6) method. Metabolic acidosis (pH 7.20) and alkalosis (pH 7.60) were induced with HCl and Carbicarb (isosmolar Na2CO3 and NaHCO3), respectively. Hypercapnia was induced by adding inspiratory CO2, whereas pH was allowed to change (respiratory acidosis, pH 7.20) or maintained constant (isolated hypercapnia). Mean intrapulmonary shunt and pulmonary arterial minus wedge pressure difference, respectively, changed from 44 to 33% (P less than 0.05) and from 9 to 10 mmHg (P greater than 0.05) in metabolic acidosis, from 44 to 62% (P less than 0.001) and from 12 to 8 mmHg (P less than 0.01) in metabolic alkalosis, from 40 to 42% (P greater than 0.05) and from 13 to 16 mmHg (P less than 0.05) in respiratory acidosis, from 42 to 52% (P less than 0.05) and from 8 to 12 mmHg (P less than 0.01) in isolated hypercapnia. These results indicate that acidosis, alkalosis, and hypercapnia markedly influence pulmonary gas exchange and/or pulmonary hemodynamics in dogs with oleic acid pulmonary edema.

Acidosis↗
PubMed1975

Carbohydrate metabolism and its response to catecholamines as modified in alkalotic rat.

Metabolic activities and their responses to catecholamines were studied in fasted rats exposed to simulated altitudes. Analysis of hepatic levels of gluconeogenic intermediates revealed the inhibition of gluconeogenesis between glyceric acid 3-P and fructose 6-P associated with a rise of the ratios of redox pairs such as lactate to pyruvate in livers of alkalotic rats. Inhibition of gluconeogenesis was indicated also by the suppressed incorporation of glutamate 14C into blood glucose. Since no activation was detected on glycolytic pathway of skeletal muscles, marked hyperlactacidemia during alkalosis appeared to result from the suppression of hepatic gluconeogenesis. Most of metabolic actions of epinephrine and isoproterenal known to be mediated via the beta receptor were significantly reduced but not completely abolished during alkalosis. Exceptionally, hyperinsulinemia induced by isoproterenol was completely reversed and replaced by hypoinsulinemia during alkalosis. Despite hypoinsulinemia, hyperglycemia induced by glucose load decreased more rapidly in alkalotic than in normal rats. In view of the fact that the adrenergic alpha receptor is involved in theinhibition of insulin secretion, the observed irregular modifications of catecholamine actions could be explained on the basis of a postulate that the adrenergic alpha-receptor functions are potentiated in alkalosis.

Alkalosis, Respiratory↗
PubMed1978

Changes in the plasma anion gap during chronic metabolic acid-base disturbances.

A basic premise in the utilization of the plasma anion gap in the assessment of acid-base disorders is that this parameter remains constant during hyperchloremic metabolic acidosis and metabolic alkalosis. Experimental data under in vitro conditions, however, cast serious doubt on this premise. The purpose of the present study was to characterize the plasma anion gap, estimated as (Na + K) - Cl + HCO3), in two large groups of dogs with graded degrees of chronic, HCl-induced metabolic acidosis or chronic, diuretic-induced metabolic alkalosis. The data indicate that the plasma anion gap decreases significantly in HCl acidosis and increases significantly in metabolic alkalosis; the predicted mean anion gap in animals with a plasma bicarbonate concentration of 10, 21 (normal), and 40 meq/liter approximated 13, 18, and 26 meq/liter, respectively. The observed variation in the plasma anion gap is interpreted as originating mainly from directional changes in the net negative charge of plasma proteins; these changes result from the titration process secondary to the altered plasma acidity and, in the case of metabolic alkalosis, from the additional effect of an increased plasma protein concentration.

Acidosis↗