Circulation, Vol 79, 797-809, Copyright © 1989 by American Heart Association
JM Hodgson, MD Cohen, S Szentpetery and MD Thames
Our purpose was to determine if there are basal adrenergic influences on
the coronary circulation in humans. We studied 56 patients with denervated
hearts after cardiac transplantation and 19 normally innervated patients
with angiographically normal coronary arteries. Coronary blood flow
velocity was measured during cardiac catheterization with a subselective 3F
intracoronary Doppler catheter. Heart rate was controlled by atrial pacing.
Epicardial coronary artery diameter was measured by automated analysis of
digital coronary angiograms. Coronary flow reserve was assessed by
intracoronary papaverine hydrochloride (12 mg) injections. Regional
sympathetic blockade was produced by intracoronary injections of
phentolamine (3 mg, alpha) and propranolol (2 mg, beta) or metoprolol (3
mg, beta 1). After alpha-blockade, mean arterial pressure fell
significantly (p less than 0.05) in both the denervated transplant (-5.8
+/- 1.5%) (mean +/- SEM) and normally innervated patients (-12.6 +/- 3.2%).
Reductions in coronary flow velocity also were observed in these groups
(-8.2 +/- 2.3% and -9.2 +/- 5.8%, respectively). Calculated coronary
vascular resistance was unchanged. Similar changes were seen when patients
were pretreated with beta-blockade before alpha-blockade. Nonspecific beta-
blockade did not affect mean arterial pressure but decreased coronary
velocity (innervated, -11.6 +/- 3.9%; denervated, -9.3 +/- 2.4%) and
increased coronary vascular resistance (innervated, 15.4 +/- 6.7%;
denervated, 10.2 +/- 3.7%). Coronary vascular resistance did not rise in
either group after selective beta 1-blockade with metoprolol. Coronary flow
reserve did not change in either patient group after either alpha- or
beta-blockade. Changes in epicardial coronary artery diameter were small
and generally not significant. These data suggest that
alpha-receptor-mediated vascular tone is negligible in both denervated
transplant patients and normally innervated patients. Additionally, the
increase in vascular resistance after nonselective beta-blockade is the
result of direct beta 2 vascular effects. Our data further suggest that
there is little adrenergically mediated epicardial artery tone (either
humoral or neural) at rest and that maximal vasodilator responses are not
limited by adrenergically mediated vasomotor tone.
ARTICLES
Effects of regional alpha- and beta-blockade on resting and hyperemic coronary blood flow in conscious, unstressed humans
Department of Internal Medicine (Cardiology), Medical College of Virginia, Richmond.
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