Variations of arterial PCO2 and pH are known to influence myocardial blood flow (MBF) in that
hypercapnia results in a coronary vasodilatation, while
hypocapnia possibly decreases MBF. The present study was performed to examine if
hypocapnia and
hypercapnia might influence the sensitivity to exogenous administration of
adenosine.
Aminophylline, an
adenosine receptor blocking agent, was administered to rule out the effect of endogenously liberated
adenosine during variations of PCO2 and pH. In the last part of the study, it was examined whether
verapamil, a
calcium-channel blocker, might influence the MBF response to variations in PCO2 and pH. Closed-chest dogs were anaesthetized with
pentobarbital, and
hypocapnia induced by
hyperventilation.
Carbon dioxide was added to the inspiratory gas to create normocapnia and
hypercapnia. In the control group
hypocapnia did not significantly reduce MBF although a decrease in coronary sinus (CS) SO2 indicated a coronary vasoconstriction. During continuous
adenosine infusion (7.5 +/- 0.3 mg/kg/h) which increased MBF 116% during normocapnia, creating
hypocapnia caused a 40% decrease in MBF.
Hypercapnia seemed to potentiate the vasodilating effect of
adenosine. During administration of
aminophylline hypocapnia did not cause any decrease in MBF, while
hypercapnia increased MBF by 39%, and these results are in harmony with the results obtained in the control group without
aminophylline.
Verapamil did not result in any altered MBF response to
hypocapnia and
hypercapnia when compared to the unblocked control group. These observations do not support the idea of any major influence of the Ca2+ fluxes blocked by
verapamil as the cause of MBF changes during variations in PCO2 and pH.(ABSTRACT TRUNCATED AT 250 WORDS)