No abstract

In this study, we examined autonomic influences on pulse transit time measured from the R-wave of the electrocardiogram (R-PTT). Six subjects received three doses each of isoproterenol and atropine. Isoproterenol produced a significant linear decrease in R-PTT, a significant linear increase in heart rate (HR), and a significant linear decrease in diastolic blood pressure (DBP). Atropine produced a significant linear decrease in R-PTT and significant linear increases in HR and DBP. The R-PTT shortening effect of isoproterenol may reflect positive inotropic effects of beta-sympathetic myocardial stimulation. The R-PTT shortening effect of atropine may reflect reduction of parasympathetic inhibition of ventricular myocardial activity. However, possible vascular contributions to these effects remain to be determined. Nonetheless, the results encourage further examination of R-PTT in research concerning autonomic regulation of cardiovascular activity.

The purpose of this study was the development of a simple method for assessing autonomic nervous system (ANS) effects on the cardiovascular system. Pulse transit time (PTT) is the interval between ventricular electrical activity and the peripheral appearance of the pulse (here measured by ear densitography). Six normal subjects were studied with six drugs which either enhanced or blocked activity of one of the three major divisions of the ANS: parasympathetic, beta‐sympathetic, alpha‐sympathetic. Data analysis revealed characteristic patterns of change in PTT and heart rate (HR) which permitted differentiation of five of the six drugs' effects. Vagal enhancement (edrophonium) and alpha‐sympathetic enhancement (phenylephrine)—which reflexly also increases vagal tone to the heart—could not be distinguished from one another unless blood pressure also was monitored. Monitoring of PTT and HR offers a simple, non‐invasive method which can be used on‐line to evaluate ANS effects on the cardiovascular system.

Comparison of mild-to-moderate essential hypertension patients treated for 6 weeks by antihypertensive medication versus metronome-conditioned relaxation versus biofeedback versus a mild exercise control procedure showed that those on medication achieved the greatest decrease in blood pressure. The relaxation and biofeedback groups decreased more than the mild exercise group, as predicted, but not significantly more. The differences in benefits of the groups were not a function of group differences in initial blood pressure levels nor in compliance. Nor did the groups differ in the side effects that are usually associated with medications. A second phase of 6 weeks with another treatment or combination of treatments did not add significantly. Some characteristics of patients moderately predicted treatment benefits, for example, high scores on the Jenkins Activity Survey Scales (1) [Type A, S or H], for the relaxation and biofeedback treated patients predicted which patients received greater benefits.

This study addresses the hypothesis that electrocardiographic T-wave amplitude is influenced by beta-adrenergic stimulation of the heart. Beta-adrenergic activity was manipulated both pharmacologically and through behavioral challenge. Under resting conditions, 12 healthy men underwent infusion of placebo and then the beta-agonist, isoproterenol, and the beta-blocker, propranolol, in a counterbalanced, crossover design. During infusion of placebo, subjects also underwent two behavioral challenges, a structured interview and mental arithmetic. Analysis of the resting data indicated that propranolol produced a significant increase in T-wave amplitude, and isoproterenol produced significant T-wave amplitude attenuation. As previously reported, drug effects were also in evidence for heart rate. Behaviorally-induced reduction of T-wave amplitude was observed for mental arithmetic but not structured interview, which again paralleled heart rate data. Both pharmacological and behavioral data reported in this study support the hypothesis that the T-wave is significantly affected by beta-sympathetic influence on the heart. However, a nonspecific effect of heart rate change on T-wave amplitude would also account for these results. The findings are discussed in terms of their implications for the utility of T-wave amplitude in psychophysiological research.