It has been postulated that a coronary vasoconstriction during
hypocapnia might be opposed by a compensating coronary vasodilatation due to impaired myocardial
oxygen supply. The present study was performed first to examine whether a maximal decline in coronary sinus (CS)
oxygen content was reached during
hypocapnia. During
hypercapnia a myocardial "over perfusion" has been demonstrated. The second purpose of the present study was to examine whether a myocardial "over perfusion" is essential to maintain a sufficient myocardial tissue
oxygen supply during
hypercapnia. Closed-chest dogs were anesthetized with
pentobarbital and
hypocapnia was induced by
hyperventilation.
Nitrogen gas and
carbon dioxide could both be added to the inspiratory gas to create arterial
hypoxemia (arterial SO2 65%) and
hypercapnia, respectively. Arterial
hypoxemia during
hypocapnia increased myocardial blood flow (MBF) by 50%, while CS SO2 decreased significantly. The decrease in CS SO2 demonstrates a reserve capacity of myocardial
oxygen extraction during
hypocapnia, thereby ruling out any major coronary vasoconstriction during
hypocapnia.
Hypercapnia during normoxemia increased MBF, myocardial
oxygen delivery, and CS SO2 substantially, but this was not observed when
hypercapnia was created during arterial
hypoxemia. From the present results we conclude that
hypocapnia does not cause any major coronary vasoconstriction, while
hypercapnia results in a myocardial "over perfusion," which is a luxury perfusion not essential to maintain sufficient myocardial
oxygen supply during
hypercapnia.