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Query: UMLS:C0001127 (respiratory acidosis)
 1,501 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To study the role of carbonic anhydrase in the CSF [HCO3] increase in respiratory acidosis and its effect on brain ammonia, anesthetized rats were subjected to hypercapnia (7% CO2) for 2 hours. The animals received periodic intraventricular injections of either 'mock' CSF or 'mock' CSF and acetazolamide for 45 minutes prior and during hypercapnia when: (a) plasma [HCO3-] was allowed to increase normally and (2) plasma [HCO3] increase was prevented by i.v. HC1 infusion, CSF [HCO3] increased 8.5 mM/L after 2 hours of hypercapnia (delta PCO2 40) in the rats with intraventricular 'mock' CSF injections, and only 6 mM/L in the animals with acetazolamide injections. CSF [HCO3-] increased 7 mM/L during hypercapnia and HCl infusion with intraventricular 'mock' CSF injections, but only 2 mM/L with acetazolamide injections. Changes in total brain CO2 (increase) and brain glutamic acid (decrease) in hypercapnia were not affected by intraventricular acetazolamide and i.v. HCl. The increase of brain NH4+ and glutamine in hypercapnia was reduced in these conditions. It is concluded that there are at least two sources for the CSF [HCO3-] increase in hypercapnia; one formed in the CNS and dependent on carbonic anhydrase, and the other derived from plasma [HCO3-] increase.
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PMID:The CSF HCO3 increase in hypercapnia relationshp to HCO3, glutamate, glutamine and NH3 in brain. 1 66

Hydrochloric acid was instilled into the bronchial tree in anaesthetized dogs. A severe respiratory acidosis resulted. The metabolic component of acid-base balance was little affected.
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PMID:Ventilation and blood-gas studies during experimentally produced Mendelson's syndrome in the dog. 23 46

Serum gastrin concentration and basal acid secretion were studied in normal subjects under the influence of respiratory acidosis induced by CO2 rebreathing. During the intragastric instillation of 100 ml/h 0.5 M bicarbonate a significant increase of gastrinaemia from 133 to 158 pg/ml (p less than 0.01) occurred in ten subjects during respiratory acidosis (pCO2 62 torr, pH 7.25). Under the intragastric instillation of 100 ml/h 0.1 N HCl the rise of gastrin concentration in response to CO2 rebreathing (pCO2 68 torr, pH 7.20) was not significant. The relationship between the decrease of pH and the increase of the gastrin concentration was shifted in the direction of a greater systemic acidosis compared to the results performed in the presence of a neutral intragastric pH. 50 mug/kg propranolol intravenously produced a decrease of gastrin concentrations from 145 to 127 pg/ml (p less than 0.01) and a total suppression of hypergastrinaemia in response to CO2 rebreathing, suggesting activation of beta-cell receptors in respiratory acidosis. The infusion of phentolamine in a dose of 0.6 to 1.8 mg/min. resulted in a rise of gastrin concentration from 140 to 165 pg/ml (p less than 0.01) which was not further elevated during respiratory acidosis. The basal acid secretion showed a significant rise in response to CO2 rebreathing, which was abolished by the administration of propranolol.
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PMID:The effect of propranolol and phentolamine on serum gastrin concentration in response to respiratory acidosis in normal man. 24 51

Although lidocaine HCl is often given to critically ill patients with ventricular tachyarrhythmias, it use is not without hazard. To investigate whether acid-base disturbances and their subsequent effects on molecular ioization influence cardiovascular (CV) response to lidocaine, dogs in normal acid-base balance, metabolic acidosis, respiratory acidosis, and respiratory alkalosis were given 2 or 4 mg/kg lidocaine IV. Heart rate (HR), PR and QT intervals, MAP, LVEDP, LV dp/dt, and LV dp/dt divided by CPIP were measured at intervals. In all groups a slight increase in mean HR occurred after 2 mg/kg. Generally, myocardial contractile force was depressed in direct proportion to dose. Essentially, the CV response to lidocaine was not altered by any clinically remarkable degree by pH disturbances. Responses differing from those observed during normal acid-base conditions could not be significantly correlated with changes in pH or PaCO2. Results suggest that, in the intact animal, the CV effects of lidocaine, administered in therapeutic doses, are not appreciably influenced by clinically encountered states of acid-base imbalance.
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PMID:Crdiovascular effects of lidocaine during acid-base imbalance. 103 6

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.
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PMID:Acid-base status affects gas exchange in canine oleic acid pulmonary edema. 201 14

We studied the effects of metabolic and respiratory acidosis (pH 7.20) and alkalosis (pH 7.60) on pulmonary vascular tone in 32 pentobarbital-anesthetized dogs ventilated with hyperoxia (inspired oxygen fraction, FIO2 0.40) and with hypoxia (FIO2 0.10). Ventilation, pulmonary capillary wedge pressure (Ppw), and cardiac output (3 l.min-1.m-2) were maintained constant to prevent passive changes in pulmonary arterial pressure (Ppa). Metabolic acidosis and alkalosis were induced with HCl (2 mmol.kg-1.h-1) and NaHCO3-Na2CO3 (5 mmol.kg-1.h-1) infusions, respectively, and respiratory acidosis and alkalosis by modifying the inspiratory CO2 fraction. The hypoxia-induced rise in Ppa-Ppw gradient increased from 5 to 9 mmHg in metabolic acidosis (P less than 0.001), decreased from 6 to 1 mmHg in metabolic alkalosis (P less than 0.001), remained unchanged in respiratory acidosis, and decreased from 5 to 2 mmHg in respiratory alkalosis (P less than 0.001). Linear relationships were found between pH and Ppa-Ppw gradients. These data indicate that in intact anesthetized dogs, metabolic acidosis and alkalosis, respectively, enhance and reverse hypoxic pulmonary vasoconstriction (HPV). Respiratory acidosis did not affect HPV and respiratory alkalosis blunted HPV, which suggests an pH-independent vasodilating effect of CO2.
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PMID:Effects of acidosis and alkalosis on hypoxic pulmonary vasoconstriction in dogs. 230 2

The present study examines the involvement of acidosis in stress ulceration in rat stomachs. Cold restraint stress for 2 hr did not affect the blood lactate level; however, it produced respiratory acidosis, as reflected by the depressed respiratory rate which was associated with increased CO2 tension and a lowered blood pH. Severe hemorrhagic ulceration was found in the glandular mucosa. The effects of stress on blood pH and the stomach were reversed by IV infusion of NaHCO3. Infusion of HCl IV decreased the blood pH and HCO-3 level and produced gastric ulceration. It is concluded that respiratory acidosis could be involved in stress ulceration. The metabolic acidosis evoked by HCl also induced gastric damage, but the effect was much less.
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PMID:Does acidosis contribute to stress-induced ulceration in rat stomachs? 255 22

Respiratory acid-base disorders elicit physiological responses that alter O2 delivery to various tissues. We have used a near infrared (NIR) optical technique to monitor cytochrome a,a3 oxidation state, tissue O2 store (relative hemoglobin plus myoglobin oxygenation), and regional blood volume in intact resting skeletal muscle during respiratory acid-base disturbances in anesthetized cats. Hypercapnic acidosis and hypocapnic alkalosis were produced in separate groups of animals by ventilation with increasing concentrations of CO2 (n = 13) or hyperventilation (n = 8). Respiratory acidosis decreased oxygen availability to hindlimb muscle while respiratory alkalosis did not change tissue oxygenation. Inspired CO2 progressively decreased muscle blood volume, cytochrome a,a3 oxidation level, and muscle oxygen store. These optical responses were greatly attenuated both by pre-treatment with bretylium and by hemorrhagic hypotension, suggesting mediation through sympathetic vasoconstriction. Metabolic acidosis, produced by intravenous HCl infusion (n = 8), did not reproduce the hindlimb optical responses mediated by CO2. These experiments demonstrate that hypercapnic acidosis significantly decreases oxygen supply to resting skeletal muscle in the anesthetized cat, probably via neuroregulatory responses to CO2 which do not depend on changes in arterial [H+] in the tested pH range.
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PMID:Skeletal muscle oxygen availability during respiratory acid-base disturbances in cats. 282 60

This study examined the ability of bullfrogs to correct a non-respiratory acidosis by renal and cutaneous mechanisms. Acidosis was induced by intravascular infusions of HCl (3 mmole/kg) or NH4Cl (4 mmole/kg). The acid load was removed primarily by increased renal excretion of NH4+, while urine pH and titratable buffer acid excretion changed little. Acid loading resulted in an increase in cutaneous permeability, shown by large ion losses and elevated water uptake across the skin. It is concluded that infused mineral acids were immediately buffered by the extracellular fluids, moved rapidly into the intracellular fluid compartment, and only later were slowly cleared.
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PMID:Cutaneous and renal responses to intravascular infusions of HCl and NH4Cl in the bullfrog (Rana catesbiana). 287 65

The role of skeletal muscle thermogenesis (increases in skeletal muscle tone) in the hyperthermic responses of conscious, unrestrained rats given acute or repeated i.p. or i.c.v. injections of morphine sulfate (MS) or beta-endorphin was investigated. Initial blood gas experiments showed that rats given acute i.p. injections of MS caused PO2 and pH to decrease by 60 min postadministration in a dose-related fashion whereas PCO2 increased; with repeated MS administration the respiratory acidosis seen with acute injections was reduced. Acute i.p. injections of MS (1, 10 or 20 mg/kg) caused catalepsy scores, plasma lactate levels and electromyographic (EMG) amplitude to be elevated in a dose-related fashion along with a rise in rectal temperatures (TRS). Surface (tail) temperatures also rose after the acute MS injections but only after the increase in TR. Significant increases in EMG amplitude after acute injections of MS occurred even before TRS increased and, with subsequent naloxone HCl administration (10 mg/kg i.p.), a rapid and marked fall in EMG amplitude occurred before TRS fell back to saline control levels. Acute i.c.v. injections of 1.1 nmol of either MS or beta-endorphin also caused EMG amplitudes to rise significantly before TRS began to increase. Tail temperatures again increased passively after i.c.v. injection of either drug. Subsequent naloxone injections (10 mg/kg i.p.) to these groups also caused EMG amplitudes to decrease before TRS decreased back to control TRS. Repeated i.p. injections of MS (10 mg/kg i.p. daily for 5 days) caused TRS to be higher than those seen after the initial injection but catalepsy scores, plasma lactates and EMG amplitudes were below those respective levels seen upon acute MS administration. Similar chronic findings occurred in other groups of rats given 1.1 nmol of either MS or beta-endorphin i.c.v., when they had been previously given repeated i.p. injections of MS (5 mg/kg i.p. twice daily for 2 days). The results indicate that acute peripheral or central injections of MS or beta-endorphin to conscious rats cause skeletal muscle to be activated, resulting in nonlocomotor, catatonic behavior. This skeletal muscle activation occurs before the rise in TR and is thought to be an important and possibly the primary cause of the resultant hyperthermia seen in rats after acute central or peripheral administration of MS or beta-endorphin. Repeated injections of morphine cause TRS to escalate higher, compared to that seen with acute MS administration, yet catalepsy scores, plasma lactate levels and EMG amplitude changes did not increase likewise.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Skeletal muscle thermogenesis: its role in the hyperthermia of conscious rats given morphine or beta-endorphin. 295 69


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