Circulation, Vol 79, 836-844, Copyright © 1989 by American Heart Association
JE Brush Jr, G Eisenhofer, M Garty, R Stull, BJ Maron, RO Cannon 3d, JA Panza, SE Epstein and DS Goldstein
We examined the uptake and release of norepinephrine in the cardiac
circulation and other regional vascular beds in 11 patients with
hypertrophic cardiomyopathy (HCM) and in 10 control subjects during
simultaneous infusion of tracer-labeled norepinephrine and isoproterenol.
Cardiac neuronal uptake of norepinephrine was assessed by comparing
regional removal of tracer-labeled norepinephrine with that of
tracer-labeled isoproterenol (which is not a substrate for neuronal uptake)
and by the relation between production of dihydroxyphenylglycol (DHPG), an
exclusively intraneuronal metabolite of norepinephrine, and regional
spillover of norepinephrine. Cardiac extraction of norepinephrine averaged
59 +/- 17% in the patients with HCM, significantly less than in the control
subjects (79 +/- 13%, p less than 0.05), whereas cardiac extraction of
isoproterenol was similar in the two groups (13 +/- 23% versus 13 +/- 14%),
indicating that neuronal uptake of norepinephrine was decreased in the
patients with HCM. The cardiac arteriovenous difference in norepinephrine
was significantly larger in the patients with HCM than in the control
subjects (73 +/- 77 versus 13 +/- 50 pg/ml, p less than 0.05), as was the
product of the arteriovenous difference in norepinephrine and coronary
blood flow (7.3 +/- 7.3 versus 0.8 +/- 3.0 ng/min, p less than
0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
ARTICLES
Cardiac norepinephrine kinetics in hypertrophic cardiomyopathy
Cardiology Branch, National Heart, Lung, and Blood Institute, Bethesda, Maryland.
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