Biomedical subjects

L DeLeve

Publications and source records attributed to L DeLeve.

3 recordsLinked to original sources

PubMed1989

Beta-blockade disappearance rate predicts beta-adrenergic hypersensitivity.

We determined whether the beta-blockade disappearance rate would determine the degree of subsequent transient beta-adrenoceptor hyperresponsiveness after abrupt withdrawal of a beta-adrenoceptor drug. In a single-blind randomized study, 10 healthy men took a placebo for 1 week and then took nadolol one time a day (t1/2, 18 to 24 hours) or propranolol three times a day (t1/2, 4 to 6 hours) in doses that were increased weekly for 4 weeks to reach 240 mg per day. beta-Receptor responsiveness was assessed before and repeatedly after abrupt drug withdrawal by infusion of isoproterenol and epinephrine and by ergometer exercise. In the 13 days after drug discontinuation, peak beta-receptor sensitivity correlated (p less than 0.05) with the disappearance rate of beta-blockade as assessed by heart rate responses to isoproterenol (r = 0.68) and to submaximal exercise (r = 0.62) and by diastolic blood pressure responses to isoproterenol (r = 0.86) and epinephrine (r = 0.86). Plasma catecholamine levels and renin activity showed no overshoot. beta-Blockers with long plasma t1/2 values may prevent beta-blocker withdrawal syndromes by means of "self-tapering."

Adult↗

PubMed1984

Nonselective beta-blockade enhances pressor responsiveness to epinephrine, norepinephrine, and angiotensin II in normal man.

Nonselective beta-blockers increase peripheral vascular resistance and, sometimes, blood pressure (BP); increased responsiveness to circulating pressor agents could be one of the underlying mechanisms. Heart rate (HR) and BP responses to graded intravenous infusions of epinephrine, norepinephrine, and angiotensin II were recorded after placebo and then after 4 wk of beta-blocker treatment (nadolol or propranolol, 240 mg/day) in 10 healthy young men. Adequacy of beta-blockade was demonstrated by a mean 31% decrease in HR response to bicycle exercise, with no differences between the two beta-blockers. Under placebo conditions epinephrine lowered diastolic BP and raised HR; these effects were reversed during treatment with beta-blockers. beta-Blockade potentiated BP responses to norepinephrine and angiotensin II: Thirty-five percent less norepinephrine and 52% less angiotensin II were required to increase mean BP by 15 mm Hg. A final study 2 wk after beta-blocker cessation revealed the absence of lasting effect. These results confirm the concept of unopposed alpha-constriction for epinephrine and also demonstrate increased BP responses to norepinephrine and angiotensin II during chronic beta-blockade.

Adult↗

PubMed1983

Nonselective beta-receptor stimulation and blockade and left ventricular function.

The effects of increasing doses of intravenous isoproterenol on left ventricular (LV) size and function were assessed before and after oral propranolol (80 mg). Eleven normal subjects were studied by M-mode echocardiography. The isoproterenol dose was increased until heart rate had risen by 25 to 30 b.p.m. LV end-diastolic (LVED) dimension (46.6 +/- 1.3 mm) was increased by isoproterenol (to 48.8 +/- 1.5 mm) and decreased by propranolol (to 45 +/- 1 mm). LV end-systolic dimension was decreased by isoproterenol and increased by propranolol. Isoproterenol increased LVED dimension despite the opposing effect of the tachycardia, whereas propranolol decreased LVED dimension despite its negative inotropic and chronotropic effects. These results suggest that nonselective beta-receptor stimulation or blockade can affect cardiac output through direct cardiac actions and by influencing venous return.

Adrenergic beta-Antagonists↗