Effects of Adrenergic Receptor Activation and Blockade on the Systolic Preejection Period, Heart Rate, and Arterial Pressure in Man

Abstract

Summary. We have investigated the possibility that alterations in -the duration of the systolic preejection period can be used to estimate adrenergic influences on the human left ventricle. The preejection period was determined from high speed, simultaneous recordings of the phonocardiogram, carotid pulse tracing, and electrocardiogram. The preejection period was shortened by isoproterenol, epinephrine, and moderate doses of norepinephrine-all of which activate beta adrenergic receptors-and by cedilanid-D. It was unaltered by changes in heart rate induced by atropine and right atrial electrical pacing. Beta adrenergic receptor blockade by propranolol abolished the shortening effects of the three catecholamines but did not inhibit that due to cedilanid-D. Vasoconstriction, both alpha adrenergic (epinephrine and norepinephrine after propranolol) and nonadrenergic (angiotensin), prolonged the preejection period. Most of the shortening of the preejection period by beta adrenergic receptor activating agents and cedilanid-D and all of the prolongation accompanying pharmacologic vasoconstriction occurred after the onset of the first heart sound, thereby excluding changes in eiectrical-mechanical delay as a major factor in the observed preejection period responses. Shortening of the preejection period by beta adrenergic activity induced with isoproterenol was dose-related. Increasing doses of propranolol produced parallel shifts to the right in the isoproterenol dose-response curve.In 37 normal resting subjects intravenous propranolol (10 mg) prolonged the preejection period an average of 10 (SE + 1) msec. In six patients with psychogenic sinus tachycardia and a patient with a pheochromocytoma the presence of excessive beta adrenergic influences on the left ventricle was demonstrated by the finding of an initially short preejection period which responded with an abnormally great prolongation to beta adrenergic receptor blockade. IntroductionThe duration of the preejection period of left ventricular systole can be determined easily and

Effects of Antidepressants, but not Psychopathology, on Cardiac Sympathetic Control: A Longitudinal Study

“…To measure cardiac sympathetic activity, we use non-invasive thoracic impedance cardiography to derive the PEP as the time interval between the onset of ventricular depolarization and the opening of the semilunar valves (Sherwood et al, 1990). Changes in PEP reliably index changes in b-adrenergic inotropic drive to the left ventricle as shown in laboratory studies manipulating b-adrenergic tone by EPI infusion (Mezzacappa et al, 1999;Schachinger et al, 2001;Svedenhag et al, 1986), amyl nitrite inhalation (Nelesen et al, 1999), adrenoceptor blockade (Harris et al, 1967;Schachinger et al, 2001;Winzer et al, 1999;Cacioppo et al, 1994), exercise (Krzeminski et al, 2000;Miyamoto et al, 1983;Smith et al, 1989), or emotional stress Newlin and Levenson, 1979;Sherwood et al, 1986). PEP is an indirect measure of cardiac sympathetic activity as the sympathetic effects on the left ventricle are not just determined by changes in cardiac NE release but also by adrenoceptor status and circulating catecholamines.…”

Shortening of Electromechanical Systole as a Manifestation of Excessive Adrenergic Stimulation in Acute Myocardial Infarction

“…[9][10][11][12][13][14] Patients with acute myocardial infarction frequently exhibit excessive adrenergic activity as evidenced by an elevation of plasma and 24-hour urinary catecholamines. [15][16][17][18][19][20][21][22][23] It was therefore hypothesized that the abbreviated electromechanical systole characteristic of patients with myocardial infarction is a direct reflection of increased sympathetic nervous system activity.…”

Cardiovascular haemodynamic response to repeated mental stress in normotensive subjects at genetic risk of hypertension: evidence of enhanced reactivity, blunted adaptation, and delayed recovery

“…The haemodynamic measures included cardiac index (CI), peripheral resistance index (PRI), heart rate (HR), mean successive difference in heart period (MSD), a measure of parasympathetic tone, 25 stroke volume index (SI), systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial blood pressure (MAP), and pre-ejection period (PEP), a betaadrenergic measure. 26 …”