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PubMed1994

Intracellular pH recovery during respiratory acidosis in perfused hearts.

Na(+)-H+ exchange and Na(+)-dependent HCO3- influx both contribute to recovery of intracellular pH (pHi) after an acidosis induced by using the NH4Cl prepulse technique in mammalian and avian cardiac tissue. We have investigated the relative contributions of these mechanisms to pHi recovery during respiratory acidosis in the Langendorff-perfused ferret heart with and without correction of extracellular pH (pHo). pHi was measured from the chemical shift of the exogenous 31P nuclear magnetic resonance pH indicator 2-deoxy-D-glucose 6-phosphate. Intrinsic intracellular buffering capacity, calculated from the change in intracellular HCO3- concentration after a change in CO2, was reduced from approximately 33 (no inhibitors of acid extrusion present) to 19 +/- 5 mM when H+ extrusion during the acid loading phase was inhibited. During respiratory acidosis (pHo approximately 6.95), the proton efflux rate (JH) calculated at pHi 6.85 was 0.30 +/- 0.04 mmol.l-1.min-1 (n = 9). When pHo was corrected by increasing external HCO3- concentration to 60 mM during respiratory acidosis (pHo approximately 7.33), JH was 1.11 +/- 0.11 mmol.l-1.min-1 (n = 7), and when pHo was partially corrected by the addition of 50 mM N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid to the perfusion solution (pHo approximately 7.1), JH was 0.64 +/- 0.08 mmol.l-1.min-1 (n = 6). In all three groups Na(+)-H+ exchange and HCO3- influx each contributed approximately 50% to acid-equivalent efflux.(ABSTRACT TRUNCATED AT 250 WORDS)

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗

PubMed1985

Intracellular pH in hibernation and respiratory acidosis in the European hamster.

Intracellular pH was determined (DMO method) in European hamsters, in the spontaneously-occurring respiratory acidosis of hibernation, in hypercapnia due to breathing 12% CO2 in air in euthermy in spring, and in euthermicnormocapnic controls. From euthermy to hibernation, the temperature coefficient of pH was lowest in blood plasma and brain, intermediate in striated muscles (thigh muscles and diaphragm), and highest in heart and liver (Fig. 1). Correspondingly, the estimated dissociation ratio of the protein imidazole buffer groups, alpha Im, decreased markedly in plasma and brain, denoting an acid titration, but varied little in liver and heart. Striated muscles were intermediate (Fig. 2). Like in other mammals, intracellular responses to short-term euthermic respiratory acidosis were characterized by a partial metabolic compensation in the brain and a small metabolic acidification in striated muscles. In hibernation, a powerful metabolic compensation took place in liver and heart, nearly restoring alpha Im, but none occurred in brain (Figs. 3 to 5). The existence of an intracellular acidosis in brain and striated muscles during hibernation is in keeping with an inhibitory role of acidosis, whereas the homeostasis of intracellular alpha Im in liver and heart would subserve the eurythermal functioning of metabolic regulations in these organs, like in most organs of ectotherms.

Acidosis, Respiratory↗

PubMed1983

Effect of respiratory acidosis on acidification by the medullary collecting duct.

The effect of acute respiratory acidosis (ARA) on inner medullary collecting duct (IMCD) acidification was studied and the results were compared with previously obtained data by our laboratory in rats with acute metabolic acidosis (AMA). We employed the microcatheterization technique to directly measure pH and PCO2 with glass-membrane electrodes, and fluid samples were obtained for measurement of bicarbonate, phosphate, and ammonium. Arterial pH was 7.18 +/- 0.01 and PCO2 was 88 +/- 2 mmHg. The IMCD data were analyzed as a function of IMCD length (approximately 6 mm). pH decreased from 5.78 +/- 0.07 to 5.27 +/- 0.03 and PCO2 increased from 55 +/- 4 to 75 +/- 2 mmHg between origin and tip. Bicarbonate delivery decreased from 154 +/- 34 to 25 +/- 3 nmol/min but no change was noted in acid phosphate, ammonium, or net acid addition along the IMCD. However, net acid excretion was not different from that found previously in AMA. We conclude that during ARA acidification is augmented prior to, but not along, the IMCD. In contrast, during AMA we previously found that IMCD plays a major regulatory role in urinary acidification, accounting for about 50% of the excreted hydrogen ion.

Acidosis↗

PubMed1992

Changes in high-energy phosphates in rat skeletal muscle during acute respiratory acidosis.

We used 31P magnetic resonance spectroscopy to study changes in phosphorus metabolite concentrations in rat skeletal muscle during respiratory acidosis (14 and 20% inspired CO2) and recovery. As intracellular pH fell (from 7.05 to 6.75 after 20 min of 20% CO2), intracellular [P(i)] increased by up to 50% while phosphocreatine concentration decreased by up to 8%. The sum of all intracellular phosphates remained constant. [ADP] decreased by up to 40% in accordance with the creatine kinase equilibrium but the phosphorylation potential [ATP]/([ADP][P(i)]) was preserved as a result of increased [P(i)]. This adjustment may be a mechanism for maintaining mitochondrial ATP synthesis despite low pH. Eventually this increase in cellular [P(i)] could lead to slow efflux of P(i) from the skeletal muscle cell contributing to the hyperphosphataemia of acute respiratory acidosis.

Acidosis, Respiratory↗

PubMed2002

Respiratory acidosis prolongs, while alkalosis shortens, the duration and recovery time of vecuronium in humans.

STUDY OBJECTIVE: To determine the effects of respiratory acidosis and alkalosis by mechanical ventilation on the onset, duration, and recovery times of vecuronium. DESIGN: Randomized, prospective study. SETTING: Operating rooms in the Sapporo Medical University Hospital and Kitami Red Cross Hospital. PATIENTS: 90 ASA physical status I and II patients undergoing lower abdominal surgery. INTERVENTIONS: Patients were randomly allocated to one of three groups by arterial carbon dioxide tension level (PaCO2; mmHg) after induction: hyperventilation group (PaCO2 = 25-35), normoventilation group (PaCO2 = 35-45), and hypoventilation group (PaCO2 = 45-55). Anesthesia was maintained by spinal block with inhalation of 50% to 66% nitrous oxide in oxygen and intermittent intravenous administration of fentanyl and midazolam with tracheal intubation. MEASUREMENTS AND MAIN RESULTS: After vecuronium 0.08 mg/kg was given, onset, duration, and recovery time were measured by mechanomyography (Biometer Myograph 2,000, Odense, Denmark). There were significant differences in the duration and recovery time of vecuronium among the normoventilation group (12.7 +/- 3.3 min and 11.8 +/- 2.8 min, respectively), the hyperventilation group (10.6 +/- 3.5 min and 9.2 +/- 2.7 min, respectively; p < 0.01), and the hypoventilation group (14.4 +/- 3.1 min and 15.0 +/- 3.7 min, respectively; p < 0.01) (mean SD). The closest significant correlation in this study was observed between recovery time and arterial blood pH (r = 0.57; p < 0.05). CONCLUSION: In humans, duration and recovery times of vecuronium are prolonged in respiratory acidosis and shortened in respiratory alkalosis.

Abdomen↗

PubMed1978

Cooperation of peripheral and central chemosensitive mechanisms in the control of the extracellular pH in brain in non-respiratory acidosis.

The mathematical model of the respiratory control system in man of Middendorf and Loeschcke (1976 a, b) opens the possibility to stimulate the constellation of parameters in non-respiratory acidosis. Several investigators agree that the pH in CSF or in the extracellular fluid of the brain stays remarkably constant in this situation and it can be shown that this is a result of a precise control rather than the consequence of a sluggishly reacting system. Application of the model assuming constant extracellular brain pH allowed to calculate the relative sensitivities to pH changes of the central and the peripheral sensory mechanisms generating respiratory drive. Assuming air breathing and a normal critical arterial O2-pressure and otherwise normal parameters of respiration, circulation and blood composition (except diminished buffer base) the central chemosensitivity to a pH change turned out to be 25 times the peripheral. This factor is critically dependent on the ratio of the bicarbonate change in extracellular brain fluid to that in arterial blood. The coinciding data of Fencl (1971) and of Kronenberg and Cain (1968) were used for the calculation.

Acidosis↗

PubMed1986

Effect of respiratory acidosis on glucose homeostasis in experimental intrauterine growth retardation in rats.

Hypoglycemia and asphyxia account for a significant proportion of morbidity in the infant with intrauterine growth retardation (IUGR). The purpose of this study was to evaluate changes in glucose homeostasis in IUGR rats during acute respiratory acidosis. IUGR was produced by bilateral uterine artery ligation at 17 days of gestation in 14 pregnant rats with 23 successfully delivered pups. The normal pups (n = 31) were those whose mothers were sham operated at the same gestational period. The IUGR and normal pups were studied at 2 days of age. One group of pups was studied under room air while another was subjected to 20 min of exposure to a gas mixture of 10% O2/15% CO2, balanced with N2. Gluconeogenesis in the liver and carcass, as well as plasma glucose and catecholamines were determined before and after the exposure to the gas mixture. The results showed that the 2-day-old IUGR rats have lower body weight (P less than 0.001), liver weight (P less than 0.001), plasma glucose (P less than 0.001), and rate of gluconeogenesis (P less than 0.01) when compared with the normally grown rats. During respiratory acidosis, the normally grown rats showed an increase in plasma epinephrine (P less than 0.005) without significant change in plasma glucose and rate of gluconeogenesis. The IUGR rats on the other hand, demonstrated a decrease in rate of gluconeogenesis (P less than 0.02), an increase in plasma glucose (P less than 0.001) while the plasma epinephrine level remained unchanged. We speculate that respiratory acidosis blunted cellular metabolism in the IUGR rat resulting in decreased peripheral glucose utilization.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis, Respiratory↗

PubMed1994

[The effect of beta-adrenergic blockade on the plasma potassium elevation induced by acute respiratory acidosis during halothane or fentanyl anesthesia].

The effect of beta-adrenergic blockade on the plasma potassium elevation induced by acute respiratory acidosis (CO2 inhalation) was studied in adult mongrel dogs during halothane or fentanyl anesthesia. Twenty-two dogs were divided into 4 groups: halothane-control (HC, n = 15), halothane-beta-blockade (H beta, n = 8), fentanyl-control (FC, n = 15) and fentanyl-beta-blockade (F beta, n = 10). Beta-blockade was achieved by continuous infusion of propranolol. The maximum levels of plasma potassium after 14% CO2 inhalation were 5.0 +/- 0.7 mM (mean +/- SD) in HC, 6.1 +/- 0.8 mM in H beta, 4.3 +/- 0.4 mM in FC and 4.8 +/- 0.5 mM in F beta. With halothane anesthesia more prominent elevation was observed in the beta-blockade group (P < 0.05), but with fentanyl anesthesia this elevation was not significantly different between the two groups. In acute respiratory acidosis, pH-induced plasma potassium elevation is suppressed by simultaneously increased catecholamines, especially epinephrine. Beta-adrenergic blockade, therefore, may cause severe hyperkalemia due to inhibition of adrenergic potassium disposal. During fentanyl anesthesia plasma potassium elevation was less marked than during halothane. This indicates that fentanyl has less suppressing action on the secretion of stress hormones, including epinephrine, under similarly stressful conditions as halothane anesthesia.

Acidosis, Respiratory↗

PubMed1975

CSF bicarbonate regulation in respiratory acidosis and alkalosis.

CSF bicarbonate regulation was studied in respiratory acidosis and alkalosis of 4h duration in antsthetized dogs. PCO2, pH, HCO3, ammonia, and lactate in CSF and arterial and safittal sinus bloof were measured when equal volumes of saline or acetazolamide (8 mg) were injected into lateral cerebral ventricles. The brain CO2 dissociation curve was determined at the end of all experiments. CSF and arterial bicarbonate increased 11.8 and 5.9 meg/l, respectively, in acidosis. Acetazolamide limited the rise in CSF bicarbonate to 4.2 meg/l, and prevented the CSF bicarbonate increase associated with hyperammonemia. During alkalosis CSF bicarbonate fell 6.5 meg/l and CSF lactate increased almost 2 meg/l while arterial bicarbonate fell 5.7 meg/l and lactate remained unchanged. Thus plasma bicarbonate changes account for some of the CSF unchanged. Thus plasma bicarbonate changes account for some of the CSF bicarbonate alterations in respiratory acid-base-disturbances. In acidosis additional CSF bicarbonate is formed by the choroid plexus and glial cells on the inner and outer surfaces of the brain--a reaction catalyzed by the locally present carbonic anhydrase. In alkalosis the greater fall in CSF bicarbonate than blood is due to selective brain and CSF lactic acidosis.

Acetazolamide↗

PubMed2002

Secondary chronic respiratory acidosis in a dog following the cervical cord compression by an intradural glioma.

An intradural tumor in the upper cervical region was found in a dog with quadriparesis and chronic respiratory acidosis. Surgical removal of the tumor in the atlas and intraoperative radiotherapy were attempted. The tumor was histologically diagnosed as a neural glioma. A preoperative acid-base disturbance was dramatically improved after surgery. The clinical changes appeared in this case suggest that compression of the spinal cord at this region may cause paralysis of the respiratory muscles and secondarily result in chronic respiratory acidosis following the respiratory insufficiency.

Acidosis, Respiratory↗

PubMed1990

Effect of alkalinization and fluids on survival in acute, non-hypoxic respiratory acidosis.

Effects of intravenous normal saline, sodium bicarbonate, hypertonic saline, and Tromethamine were studied in 21 pigs and 60 rats subjected to acute, severe respiratory acidosis. Transient multiphasic alterations of systemic arterial pressures were seen with boluses of each agent-especially sodium bicarbonate and hypertonic saline-but any improvements in hemodynamic variables were transient. At the dose given, sodium bicarbonate significantly increased PaCO2 while decreasing hydrogen ion (H+) accumulation, whereas tromethamine buffered pH without significantly increasing PaCO2. However, no change of either arterial or venous H+ or PCO2 could be identified which rapidly produced death. Survival times were statistically equivalent among all groups. Therefore, intravenous treatment of respiratory acidosis with fluids or alkalinizing agents appears neither helpful nor harmful.

Acid-Base Equilibrium↗

PubMed1997

The effects of bupivacaine and ropivacaine on baroreflex sensitivity with or without respiratory acidosis and alkalosis in rats.

Systemic toxicity of local anesthetics causes cardiac and central nervous system (CNS) depression that could be enhanced in the presence of respiratory acidosis. We examined a potential suppression of baroreflex function with bupivacaine and ropivacaine during hypercapnic acidosis or hypocapnic alkalosis. Baroreflex sensitivity (BRS) was randomly tested in rats with one of 13 conditions during intravenous administration of saline (control), bupivacaine 1, 2, or 3 mg/kg, or ropivacaine 2, 4, or 6 mg/kg. The effects of bupivacaine (3 mg/kg) or ropivacaine (6 mg/kg) on BRS were also examined during hypercapnic acidosis or hypocapnic alkalosis. The BRS was assessed using a value of delta heart rate/ delta mean arterial pressure after infusion of phenylephrine (3 micrograms/kg). Both bupivacaine and ropivacaine (at the largest dose) significantly suppressed BRS. Acute respiratory acidosis (pHa 7.24 +/- 0.04, Paco2 63 +/- 4 mm Hg) enhanced BRS. The BRS enhanced during acidosis was also suppressed with bupivacaine and ropivacaine, but less so than in the absence of acidosis. The presence of hypocapnic alkalosis (pHa 7.55 +/- 0.03, Paco2 25 +/- 2 mm Hg) did not affect BRS and reversed BRS suppression caused by both drugs. Thus, bupivacaine and ropivacaine affect neuronal control mechanisms for maintaining cardiovascular stability, and acute changes of respiration could significantly modify such suppression.

Acidosis, Respiratory↗

PubMed2002

Direct effect of acute metabolic and respiratory acidosis on parathyroid hormone secretion in the dog.

Because both metabolic (Met Acid) and respiratory acidosis (Resp Acid) have diverse effects on mineral metabolism, it has been difficult to establish whether acidosis directly affects parathyroid hormone (PTH) secretion. Our goal was to determine whether acute Met Acid and Resp Acid directly affected PTH secretion. Three groups of dogs were studied: control, acute Met Acid induced by HCl infusion, and acute Resp Acid induced by hypoventilation. EDTA was infused to prevent acidosis-induced increases in ionized calcium, but more EDTA was needed in Met Acid than in Resp Acid. The PTH response to EDTA-induced hypocalcemia was evaluated also. Magnesium needed to be infused in groups receiving EDTA to prevent hypomagnesemia. The half-life of intact PTH (iPTH) was determined during hypocalcemia when PTH was measured after parathyroidectomy. During normocalcemia, PTH values were greater (p < 0.05) in Met Acid (92 +/- 19 pg/ml) and Resp Acid (77 +/- 22 pg/ml) than in controls (27 +/- 5 pg/ml); the respective pH values were 7.23 +/- 0.01, 7.24 +/- 0.01, and 7.39 +/- 0.02. The maximal PTH response to hypocalcemia was greater (p < 0.05) in Met Acid (443 +/- 54 pg/ml) than in Resp Acid (267 +/- 37 pg/ml) and controls (262 +/- 48 pg/ml). The half-life of PTH was greater (p < 0.05) in Met Acid than in controls, but the PTH secretion rate also was greater (p < 0.05) in Met Acid than in the other two groups. In conclusion, (1) both acute Met Acid and Resp Acid increase PTH secretion when the ionized calcium concentration is normal; (2) acute Met Acid may increase the bone efflux of calcium more than Resp Acid; (3) acute Met Acid acts as a secretogogue for PTH secretion because it enhances the maximal PTH response to hypocalcemia.

Acidosis↗

PubMed1985

Influence of hypoxemia and respiratory acidosis on the plasma kinetics and tissue distribution of digoxin in the conscious dog.

The aim of the present study was to investigate the influence of hypoxemia combined with respiratory acidosis on the kinetics of digoxin in conscious dogs. One group of three beagles was exposed to air and 7 days later to 10% O2, 10% CO2, and 80% N2. In a second group of three dogs, the order of exposure to the two atmospheric conditions was reversed. The dogs received 25 micrograms/kg digoxin and blood and urine samples were collected over the next 29 h. At the conclusion of the second treatment, the dogs were sacrificed to determine digoxin concentrations in the left ventricle, liver, renal cortex, and skeletal muscle. Digoxin total body clearance increased from 6.2 +/- 0.9 in control to 9.0 +/- 1.0 mL X min-1 X kg-1 in hypoxemic and hypercapnic dogs (p less than 0.05). The digoxin apparent volume of distribution at steady state (Vss) was increased in the dogs with hypoxemia and hypercapnia (11.63 +/- 1.11 vs. 8.62 +/- 0.41 L/kg in the controls, p less than 0.05). As a consequence the digoxin plasma half-life remained unchanged (18.6 +/- 1.5 h in hypoxemic and hypercapnic dogs versus 20.1 +/- 2.8 h in the controls). In dogs with hypoxemia and hypercapnia, the ratio of tissue to plasma digoxin concentrations tended to increase in the liver, in the renal cortex, and in the left ventricle and remained unchanged in the left hind leg muscle. In vitro studies showed that the digoxin total binding to erythrocyte membranes was slightly increased in the dogs with hypoxemia and hypercapnia, resulting from an increase in the apparent intrinsic association constant for digoxin (p less than 0.003). It is concluded that hypoxemia combined with respiratory acidosis changes digoxin disposition in the conscious dog and is the cause of a digoxin redistribution into the tissues.

Acidosis, Respiratory↗

PubMed1984

Severe hypophosphataemia during recovery from acute respiratory acidosis.

Three elderly patients with established chronic obstructive airways disease were admitted with a short history of increasing dyspnoea and tiredness and (in two cases) a deterioration in mental state. Acute respiratory acidosis was diagnosed and mechanical ventilation instituted. Two hours after beginning mechanical ventilation the mean arterial pH had risen to 7.40, but all patients showed a dramatic fall in the serum phosphate concentration (lowest value 0.3 mmol/l (0.9 mg/100 ml] accompanied by a low urinary excretion of phosphate. No patient could tolerate withdrawal of mechanical ventilation until the serum and urinary concentrations of phosphate had returned to normal. Recovery from acute respiratory acidosis should be added to the list of conditions associated with severe hypophosphataemia.

Acidosis, Respiratory↗

PubMed1984

Effect of amiloride on cisternal fluid [HCO3-] in acute respiratory acidosis.

In the present study we investigated if an amiloride inhibitable Na+ -H+ exchange mechanism may also be involved in the regulation of cisternal cerebrospinal fluid (CSF) [HCO3-] during acute respiratory acidosis (ARA). In anesthetized, paralyzed and ventilated dogs either mock CSF (group I, control) or mock CSF containing amiloride (group II) was injected into the cerebral lateral ventricles and ARA was induced by 8-10% CO2 breathing during 4 1/2 hours. During hypercapnia arterial PCO2 and plasma [HCO3-] rose respectively by about 35 mm Hg and 3 mmol/L in both groups. The rise in cisternal CSF PCO2 (about 40 mm Hg) was similar. However, changes in CSF [HCO3-] were significantly different between the two groups; in the control group, mean CSF [HCO3-] rose by 2.4, 4.1 and 4.4 mmol/L respectively, 1 1/2, 3 and 4 1/2 h after induction of ARA. In the amiloride group the respective rise was only 1.1, 2.5 and 2.5 mmol/L. The differences in CSF [HCO3-] could not be ascribed to differences in CSF lactate concentration. We conclude that an amiloride inhibitable Na+ -H+ exchange may play a role in the regulation of CSF [HCO3-] during acute respiratory acidosis in dogs.

Acidosis, Respiratory↗

PubMed2001

Acute respiratory acidosis does not increase plasma potassium in normokalaemic anaesthetized patients. A controlled randomized trial.

BACKGROUND AND OBJECTIVE: Few and conflicting data are available regarding the changes of plasma potassium concentration during acute respiratory acidosis in human beings. This study compares the acute changes in plasma potassium concentration in acutely hypercapnic patients and in non-hypercapnic patients during general anaesthesia. METHODS: Thirty-three patients undergoing interventional rigid bronchoscopy were studied. Ventilation of the lungs was randomly conducted using either spontaneous-assisted ventilation or intermittent negative-pressure ventilation. All patients received the same anaesthetic protocol. Arterial blood gases and osmolality, and plasma concentrations of glucose, sodium, potassium and chloride were measured. RESULTS: Intraoperatively, PaCO2 was higher during spontaneous-assisted ventilation than during intermittent negative-pressure ventilation (9 +/- 1.8 vs. 5.4 +/- 1.2 kPa, P < 0.001) and the pH was also lower during spontaneous-assisted ventilation than during intermittent negative-pressure ventilation (7.24 +/- 0.07 vs. 7.4 +/- 0.08, P < 0.001). Plasma potassium concentration remained similar in both groups (3.8 +/- 0.2 mmol L(-1) with spontaneous-assisted ventilation vs. 3.7 +/- 0.4 mmol L(-1) with intermittent negative-pressure ventilation). CONCLUSION: Acute respiratory acidosis does not affect plasma potassium concentration.

Acidosis, Respiratory↗

PubMed1975

Distribution of H+ and HCO3 minus between CSF and blood during respiratory acidosis in dogs.

To evaluate the regulation of (H+) and (HCO3 minus) in brain extracellular fluid during respiratory acidosis, the changes in cisternal and lumbar CSF acid-base state were assessed in six anteshetized, paralyzed, mechanically ventilated dogs rendered hypercapnic by increase in FIco2. Arterial (HCO3 minus) was held constant. The electrochemical potential difference (mu) between CSF and blood for H+ and HCO3 minus was calculated from values for (H+) and (HCO3 minus) in CSF and arterial plasma and the simultaneously measured CSF/plasma DC potential difference. Measurements were made at pHa equal to 7.40, after stable arterial values of pHa of about 7.2 were attained and 3, 4.5, and 6 h thereafter. A steady state for ion distribution was attained by 4.5 h. Values of mu for H+ and HCO3 minus at 6 h had returned to +0.7 and minus 0.7 mV of control for cisternal CSF and +1.3 and minus 0.6 mV of control for lumbar CSF. The attainment of steady-state values for mu close to control is comparable with passive distribution of these ions between CSF and blood.

Acid-Base Equilibrium↗