1. The effects of hypoxaemia, hyperoxaemia,
alkalosis,
acidosis, hypocarbia with
alkalosis or hypercarbia with
acidosis on the blood pressure and pulse rate responses to
verapamil were studied in
chloralose-anaesthetized rats. 2. At a fixed stroke volume (10 mL/kg) and rate (80
strokes/min; except for the hypocarbic group at 160
strokes/min), hypoxaemia, hyperoxaemia, hypercarbia with
acidosis, or hypocarbia with
alkalosis was induced by artificial ventilation with gas mixtures containing 17% O2, 28% O2, 23% O2, with 5% CO2, or 17% O2, without CO2 respectively.
Acidosis or
alkalosis was produced by
intravenous infusion of 1 mol/L HCl or 1 mol/L NaHCO3 respectively, in animals artificially ventilated with room air. 3. Changes in individual blood gas/pH parameters had no significant effect on blood pressure except for
acidosis which caused a significant decrease. Effects on pulse rate were significant increases in the
alkalosis and hypercarbia groups, decrease in the
acidosis group, while in other conditions no significant changes were recorded. 4. In the controls,
intravenous injections of
verapamil 20-320 micrograms/kg caused dose-dependent increases in mean blood pressure, while effects on pulse rate were not marked. 5. The hypotensive responses to
verapamil were significantly alleviated or enhanced in the presence of
alkalosis or
acidosis respectively.
Verapamil also caused greater falls in pulse rate during
acidosis. Effects of Po2 changes were not statistically significant. The influence of PCO2 changes remained unclear. 6. The present findings suggest that changes in blood pH may play a more important role than Po2 alterations in affecting the cardiovascular responses to
verapamil in the presence of blood gas abnormalities.