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At least 127 records · Page 7Linked to original sources
PubMed1982

Effect of supramaximal vagal stimulation in combination with hypoxia, respiratory acidosis and deep halothane anaesthesia on cardiovascular function in dogs.

Vagal reflexes are generally recognized as a possible cause of cardiac arrest during anaesthesia. Studies were performed to determine whether hypoxia, respiratory acidosis or deep halothane anaesthesia modify the cardiovascular effect of vagal stimulation (VS) in dogs. The animals were anaesthetized with intravenous urethane and chloralose, and paralysed with metocurine. Normal temperature and arterial blood gas variables were maintained and supramaximal VS was applied to the distal end of both vagus nerves for 5 min. No differences were found in any of the variables measured among the time periods when VS was repeated five times in six control dogs receiving urethane-chloralose basal narcosis only to determine the effects of time. VS resulted in 15 +/- 3 s (mean +/- s.e. mean) of asystole. Heart rate, cardiac output (CO) and mean arterial pressure (MAP) were still significantly decreased (P less than 0.001) and central venous pressure, right atrial pressure, pulmonary capillary wedge pressure (PCW), systemic (SVR) and pulmonary vascular resistance significantly increased (P less than 0.01--P less than 0.001) at the end of stimulation when compared to values before VS in all 24 dogs. Neither hypoxia [PaO2 5.3 kPa (40 mmHg)] nor respiratory acidosis [pH 7.00, PaCO2 10.6 kPa (80 mmHg)] modified these effects of VS. VS during halothane anaesthesia (1.6% end-tidal concentration) resulted in further significant decreases (P less than 0.05--P less than 0.001) in CO, MAP, mean pulmonary arterial pressure, PCW and SVR when compared to VS under basal narcosis. VS under halothane anaesthesia combined with hypoxia or respiratory acidosis did not decrease the cardiovascular parameters as much as VS under halothane anaesthesia alone. VS alone, or in combination with hypoxia or respiratory acidosis, failed to cause persistent asystole.

Acidosis↗
PubMed1983

Cellular response to acute respiratory acidosis in rat medullary collecting duct.

The collecting duct of the mammalian kidney is involved in urine acidification. Recent studies in the turtle bladder suggest that hydrogen ion secretion in response to elevated CO2 is regulated by insertion of hydrogen pumps into the luminal membrane of the mitochondria-rich cells. Because intercalated cells of the collecting duct are structurally similar to mitochondria-rich cells of the amphibian bladder, we studied the rat outer medullary collecting duct (OMCD) during respiratory acidosis to determine whether changes compatible with hydrogen ion secretion occur in the intercalated cells. Rats were studied during normal acid-base conditions and after 4-5 h of respiratory acidosis. After collection of physiologic data, the kidneys were fixed by in vivo perfusion and processed for electron microscopy. No changes were observed in the principal cells of the OMCD. Morphometric analysis revealed a significant increase in the surface density of the apical plasma membrane and a decrease in the number of tubulovesicular profiles in the apical region of the intercalated cells throughout the OMCD with respiratory acidosis. There were no changes in surface density of the basolateral membrane. These findings suggest that in response to respiratory acidosis there is transport of membrane from the tubulovesicular membrane compartment to the apical plasma membrane of the intercalated cells.

Acidosis, Respiratory↗