Effects of Alpha Adrenergic Blockade upon Coronary Hemodynamics

Orlick, Arthur E.; Ricci, Donald R.; Alderman, Edwin L.; Stinson, Edward B.; Harrison, Donald C.

doi:10.1172/jci109147

Cited by 82 publications

(13 citation statements)

References 36 publications

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“…The impact of alpha adrenergic activity on coronary vascular resistance has been demonstrated in experimental myocardial infarction (47)(48)(49) and recently in a clinical study. In patients with stable ischemic heart disease, increase in coronary vascular resistance and chest pain, provoked by cold pressure test, were abolished by alpha adrenergic blockade (50).…”

Section: Methodsmentioning

confidence: 97%

Propranolol decreases sympathetic nervous activity reflected by plasma catecholamines during evolution of myocardial infarction in man.

Mueller¹,

Ayres²

1980

J. Clin. Invest.

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Section: Methodsmentioning

confidence: 97%

Propranolol decreases sympathetic nervous activity reflected by plasma catecholamines during evolution of myocardial infarction in man.

Mueller¹,

Ayres²

1980

J. Clin. Invest.

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“…52, No. 1, January 1983 benzamine (Mohrman and Feigl, 1978;Orlick et al, 1978;Murray and Vatner, 1979;Gwirtz and Stone, 1981;Heyndrickx et al, 1982). Even in left circumflex artery where postjunctional a-adrenergic responses occur, the prejunctional action of phentolamine during low frequency stimulation may be solely responsible for the augmented relaxation of coronary vascular smooth muscle observed in the presence of the a-adrenergic antagonist.…”

Section: Prejunctional Actions Of Endogenous Norepinephrinementioning

confidence: 99%

“…/8-Adrenergic coronary vasodilation accompanies sympathetic activation resulting from hypothalamic stimulation in conscious dogs (Von Restorff and Bassenge, 1976), but the prevailing opinion is that cardiac sympathetic nerves exert a tonic a-adrenergic constrictor influence on coronary resistance which persists even during severe exercise (Berne et al, 1965;Feigel, 1968;Vatner et al, 1970;Mohrman and Feigl, 1978;Orlick et al, 1978;Berne and Rubio, 1979;Murray and Vatner, 1979;Gwirtz and Stone, 1981;Heyndrickx et al, 1982). This conclusion is based largely on the characterization of coronary vascular responses using nonselective a-adrenergic antagonists (e.g., phentolamine or phenoxybenzamine) which, by augmenting norepinephrine release (Stjarne, 1975;Starke and Docherty, 1980;Langer, 1981), could significantly alter the response to nerve stimulation.…”

mentioning

confidence: 99%

Prejunctional and postjunctional actions of endogenous norepinephrine at the sympathetic neuroeffector junction in canine coronary arteries.

Cohen¹,

Shepherd²,

Vanhoutte³

1983

Circulation Research

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SUMMARY. The effects of endogenous and of exogenous norepinephrine were studied in isolated rings of canine left circumflex coronary artery and its first ventricular branch. Norepinephrine was released from adrenergic nerve endings by transmural electrical stimulation and by tyramine. In rings contracted with prostaglandin ¥20, transmural electrical stimulation resulted in frequencydependent relaxations which were blocked by propranolol or tetrodotoxin; tyramine and exogenous norepinephrine caused concentration-dependent relaxations which were blocked by propranolol. The tyramine-induced relaxations also were inhibited by cocaine. The left circumflex artery was less sensitive than its branch to /S-adrenergic activation; this difference was significant even between rings of the two vessels immediately adjacent to the branching point and was abolished by phentolamine. In the presence of propranolol, transmural electrical stimulation, tyramine and phenylephrine, produced contractions of the left circumflex artery, but not the branch; these contractions were prevented by phentolamine. Phentolamine, but not prazosin, augmented the /?-adrenergic response of left circumflex artery to low frequency stimulation; in arteries preincubated with 3 H-norepinephrine, this was accompanied by an increased overflow of tritiated neurotransmitter. The prejunctional effect of phentolamine was also evident in branch coronary arteries which exhibit no postjunctional a-adrenergic responses. With high frequency stimulation, both a-adrenergic antagonists equally augmented the relaxation of left circumflex artery; the efflux of tritiated norepinephrine was not different from untreated arteries. These experiments demonstrate, in isolated coronary arteries, that the primary adrenergic response to released endogenous norepinephrine is /S-adrenergic relaxation. The prejunctional effects of nonspecific a-adrenergic antagonists preclude their use in determining the importance of postjunctional coronary a-adrenergic receptor activation caused by sympathetic nerve stimulation. (Circ Res 52: 16-25, 1983)

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“…7 8 The mechanism of such variation in coronary artery vasomotion is unknown, but several studies have implicated a central role for the adrenergic nervous system. [9][10][11][12][13][14][15][16] Studies in animals have shown that coronary artery vasoconstriction and increases in coronary vascular resistance can be elicited by sympathetic stimulation after 13-adrenergic blockade. '2'2 1'1 Clinical studies of patients with variant angina have shown exacerbation of coronary spasm after subcutaneous administration of epinephrine in patients receiving propranolol.…”

mentioning

confidence: 99%

Potentiation of coronary vasoconstriction by beta-adrenergic blockade in patients with coronary artery disease.

Kern¹,

Ganz²,

Horowitz³

et al. 1983

Circulation

172

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SUMMARY Although ,t-adrenergic blocking agents reduce myocardial oxygen consumption and symptoms of myocardial ischemia in patients with coronary artery disease (CAD), propranolol has been reported to exacerbate coronary artery spasm in some patients with variant angina. To determine whether increased coronary vasomotor tone can be induced by 3-adrenergic blockade, we measured the changes in coronary vascular resistance (CVR) during cold pressor testing (CPT) in 15 patients, nine with severe CAD and six with normal left coronary anatomy, before and after i.v. propranolol (0.1 mg/kg). Coronary blood flow was measured by coronary sinus thermodilution. CVR was calculated as mean arterial pressure divided by coronary sinus blood flow. Heart rate was maintained constant at a paced subanginal rate of 95 + 5 beats/min.Before propranolol, CPT induced significant increases in coronary vascular resistance in patients with CAD (15.0 ± 2.2%, p < 0.02), but no increase in CVR in the normal patients. After propranolol, the CVR change during CPT was augmented for patients with CAD (29 ± 6%, p < 0.01) and for the normal population (9 ± 5%, NS). The potentiated increase in CVR occurred without significant changes in resting CVR or in the magnitude of the hypertensive response to CPT.We conclude that ,B-adrenergic blockade with propranolol can potentiate coronary artery vasoconstriction in some patients with CAD, possibly mediated by unopposed ct-adrenergic vasomotor tone. These changes may be important in patients in whom intense adrenergic stimulation may increase coronary artery tone and adversely influence the balance between myocardial oxygen supply and demand.COMPELLING EVIDENCE suggests that myocardial ischemia may be induced by a reduction in myocardial oxygen supply due to coronary artery spasm. Primary decreases in coronary blood flow associated with abnormal coronary vasomotor reactivity have been found to occur not only in variant angina, I but also in classic and unstable angina,2 3 cold-induced angina,4 exercise-induced angina5 6 and myocardial infarction.7 8 The mechanism of such variation in coronary artery vasomotion is unknown, but several studies have implicated a central role for the adrenergic nervous system. ProtocolThe investigational protocol and consent form were approved by the Human Subjects Committee of the Brigham and Women's Hospital. After the patients gave informed consent, treatment with 3-adrenergic blocking agents was withheld for at least 12-24 hours before cardiac catheterization, and long-acting nitrate preparations were withheld for at least 6 hours before catheterization. Before coronary arteriography, all patients received 0.4 mg of sublingual nitroglycerin and six also received 0.5 mg of i.v. atropine.Fifteen minutes after completion of the diagnostic cardiac catheterization and coronary angiography, a #8F coronary sinus thermodilution pacing catheter (Wilton Webster Laboratories) was inserted into an antecubital vein and advanced under fluoroscopic guidance to the coronary sinus. The lo...

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Effects of Alpha Adrenergic Blockade upon Coronary Hemodynamics

Cited by 82 publications

References 36 publications

Propranolol decreases sympathetic nervous activity reflected by plasma catecholamines during evolution of myocardial infarction in man.

Propranolol decreases sympathetic nervous activity reflected by plasma catecholamines during evolution of myocardial infarction in man.

Prejunctional and postjunctional actions of endogenous norepinephrine at the sympathetic neuroeffector junction in canine coronary arteries.

Potentiation of coronary vasoconstriction by beta-adrenergic blockade in patients with coronary artery disease.

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