Circulatory markers of nervous activation during myocardial ischemia.

In man, electrocardiographic changes typical of transient myocardial ischemic episodes can be accompanied by increases in arterial pressure and heart rate or, at the opposite side of the spectrum, by decreases in arterial pressure and heart rate. It has been clearly proved that all of these changes can occur independently of the perception of pain. Transient ischemic episodes associated with hypotension and bradycardia or hypotension without the tachycardia that could be expected from a baroreceptive mechanism, are likely to reflect a depressor reflex mediated by cardiac vagal afferent fibers. It is a clinical and experimental working hypothesis that these depressor reflexes would characterise more severe episodes of ischemia: in clinics, those accompanied by signs of acute ventricular failure; in the laboratory, those induced by "global" ischemia. On the other hand, ischemic episodes associated with hypertension and tachycardia, usually thought to depend on a pain mechanism, are likely to reflect a pressor reflex mediated by cardiac sympathetic afferent fibers. It is our hypothesis that these pressor reflexes from the heart are the most frequent companions of less severe ischemic episodes, whether or not signalled by anginal pain. In the laboratory, a pressor reflex can be constantly obtained with a limited "regional" ischemia. These neural mechanisms, that should be analyzed independently of any teleologic reasoning, may be of paramount importance not only in determining the hemodynamic profile accompanying ischemic episodes, but in inducing those local changes in visceral neural activity that an increasing evidence indicates as crucial factors in arrhythmias and coronary death.