A B S T R A C T Selective autonomic blockade with intravenous propranolol, practolol, atropine, and combined atropine-propranolol was utilized to elucidate the role of the autonomic nervous system in the hemodynamic responses in young adult male volunteers to handgrip sustained at 30% of maximal voluntary contraction for 3 min. The initial 30 s of the tachycardia response was found to be mediated by withdrawal of vagal dominance, as evidenced by blockade of this response by prior atropinization. The mid and late portion of the heart rate response curve was demonstrated to be sympathetic in origin, since it was unaffected by atropine, but was suppressed by combined atropine-propranolol blockade. Sympathetic stimulation appears to be a secondary mechanism for increasing the heart rate, however, as it becomes operative only after the first mechanism of vagal withdrawal has been utilized. This was confirmed by the finding that beta adrenergic receptor blockade alone had little effect on the heart rate response curve.The pressor response to handgrip was accompanied by increased cardiac output and no change in calculated systemic vascular resistance. After propranolol, handgrip resulted in increased peripheral resistance and an equivalent rise in arterial pressure, but no increase in cardiac output. It was concluded that the increase in resistance was the result of sympathetically induced vasoconstriction. This response was shown to be independent of peripheral beta adrenergic receptor blockade by the use of practolol, a cardio-selective beta adrenergic receptor-blocking drug which caused identical hemoPortions of this study were presented previously in abstract form.

Direct correlation of externally measured systolic time intervals with internally measured indices was obtained using catheter-tip micromanometers in six patients who had normal coronary arteriograms. Simultaneous recordings were made of central aorta and left ventricular pressure, maximum rate of rise in left ventricular pressure (dp/dt), external carotid pulse, external and internal sound, and electrocardiogram. Acute interventions were used to vary the indices by a variety of mechanisms including changes in contractility, preload, afterload, and heart rate. The initial values and the changes in these values produced by acute interventions are identical for left ventricular ejection time (LVET) whether measured externally (range 175 to 385 msec) or internally (range 169 to 392), r = 0.99. Although the absolute values differed for internally measured isovolumic contraction time (internal ICT), externally measured ICT, and preejection time (PEP), there was good linear correlation between the changes observed in these values following the interventions. Changes in PEP and internal ICT showed excellent linear correlation (r = 0.94) and were also alike in absolute value following the interventions. The interval from the Q wave of the electrocardiogram to rise in left ventricular pressure (electrical-mechanical delay) did not change significantly during these interventions. During a period of spontaneous isorhythmic dissociation there was close tracking between beat-to-beat changes in PEP and internal ICT and between externally and internally measured LVET. Following acute interventions PEP and left ventricular dp/dt changed inversely. Externally measured systolic time intervals have therefore been shown in man to correlate well with directly measured internal indices, both in steady-state conditions and during a series of acute interventions. This convenient and atraumatic method has been shown to be a valid and sensitive measure of myocardial performance.

Hemodynamic responses to breathing 100% oxygen for an average of 30 min were studied in eight healthy male volunteers. Cardiac output and related determinations were performed with central injections of a radioactive indicator and calculated by the method of Stewart and Hamilton. Arterial blood gas analyses were performed in each phase of the study. Slight but statistically significant decreases in cardiac index and heart rate were observed during oxygen breathing. There was no change in the central blood volume, but a masked increase in pulmonary blood volume may have occurred. Statistically significant increases in peripheral vascular resistance, mean arterial pressure, and both systolic and diastolic arterial pressures occurred during oxygen breathing and persisted at least 40 min after oxygen was discontinued. Submitted on May 1, 1961

Although the circulatory changes in various thyroid states are well known, the alterations of myocardial contractility of hypothyroidism and hyperthyroidism have remained controversial. The changes in the length of the ejection time (ET) and isovolumic contraction time (ICT) are used as indicative of alterations in inotropic state of the myocardium. Isovolumic contraction time, ejection time, and pre-ejection period were measured externally in 10 normal, 13 hyperthyroid, and five hypothyroid subjects. Cardiac outputs, mean rate of left ventricular ejection index, and predicted ejection times were calculated. More shortening of ICT and ET in hyperthyroid and more prolongation of these intervals in hypothyroid subjects than could be attributed to other factors were interpreted as indicative of increased and decreased myocardial contractility, respectively. Catecholamine depletion in hyperthyroid subjects with adequate administration of intramuscular reserpine induced no changes in cardiac output and oxygen consumption and caused no alteration in different phases of ventricular systole; consequently it had no effect on enhancement of hyperthyroid myocardial contractility.

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