[Left ventricular functional capacity in patients with chronic ischemic heart disease, with special reference to severity and extent of coronary artery lesions].
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Biomedical subjects
Publications and source records attributed to M Oguma.
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The effects of intracerebroventricular (i.c.v.) injection of guanfacine, a new antihypertensive agent, on blood pressure and heart rate were investigated and compared with those of clonidine in anaesthetized rabbits. The i.c.v. injection of guanfacine or clonidine induced a decrease in blood pressure and heart rate in doses which were ineffective by an intravenous route. The depressive effect of guanfacine was less than that of clonidine, but the duration of this action was obviously longer than that of clonidine. A fall in heart rate caused by guanfacine was always less conspicuous than that by clonidine in equipotent hypertensive doses. Decrease in blood pressure and heart rate caused by the two drugs were inhibited by i.c.v. pretreatment with phentolamine and 6-hydroxydopamine, respectively. These findings suggest that presynaptic and/or postsynaptic alpha-adrenoceptors in the brain may play an important role in the hypotension and bradycardia produced by guanfacine as well as clonidine. Furthermore, the uptake mechanism at the presynaptic sites of central noradrenergic neurons may be involved in the mode of hypotensive and bradycardic actions of these two drugs since these effects were abolished by pretreatment with desipramine, an inhibitor of noradrenaline uptake into the presynaptic nerve terminals.
The effect of diltiazem, a calcium antagonist, was examined in eight male patients with stable effort angina pectoris by means of multistage treadmill testing using body surface mapping. The area and severity of exercise-induced ST depression after 90 mg of diltiazem administered orally three hours before exercise were compared with those without diltiazem. Although the same workload was performed, the area and severity of exercise-induced ST depression were significantly diminished (P less than 0.005) after diltiazem. The reproducibility of these observations was confirmed in two of the eight patients studied and in three other patients. Because exercise-induced ST depression in patients with coronary artery disease is generally believed to reflect myocardial ischemia, our results provide objective evidence that diltiazem is able to reduce the exercise-induced myocardial ischemia in effort angina pectoris.
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