Competition between sympathetic vasoconstriction and metabolic vasodilation in the canine coronary circulation.

Mohrman, David E.; Feigl, Eric O.

doi:10.1161/01.res.42.1.79

Cited by 248 publications

(93 citation statements)

References 38 publications

(18 reference statements)

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“…Even when under normal conditions a substantial coronary dilator reserve is present, a-adrenergic constriction acts to limit metabolic coronary dilation by about 30%, such that myocardial oxygen extraction increases together with coronary blood flow during sympathetic activation to match oxygen supply to the increased myocardial oxygen demand. [2][3][4] Whether a-adrenergic coronary constriction is powerful enough to limit coronary blood flow also under ischemic conditions when endogenous coronary dilator reserve is exhausted is highly controversial. It is also controversial whether a-adrenergic coronary constriction, if effective during myocardial ischemia, exerts a beneficial or deleterious influence on the ischemic myocardium.…”

mentioning

confidence: 99%

Alpha-adrenergic mechanisms in myocardial ischemia.

Heusch¹

1990

Circulation

239

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Dedicated to Prof Dr. Franz Loogen on the occasion of his 70th birthday c-Adrenoceptor-mediated effects of sympathetic activation on the heart and coronary circulation are reviewed with emphasis on the pathophysiology of myocardial ischemia. A classification of a-adrenoceptor subtypes is presented, and the effects of a-adrenoceptor activation on presynaptic sympathetic nerve terminals, cardiomyocytes, endothelium, platelets, and coronary smooth muscle cells are discussed. av-Adrenergic coronary vasoconstriction at rest and during situations of sympathetic activation such as exercise and excitement is analyzed for the segmental, transmural, and regional distribution of coronary blood flow. Evidence for a significant contribution of av-adrenergic coronary vasoconstriction to experimental and clinical myocardial ischemia is provided. Cardiomyocyte a-adrenoceptor activation may be involved in ischemic and reperfusion arrhythmias. The participation of presynaptic and postsynaptic aadrenoceptors, as well as of ael-and a2-adrenoceptors, in experimental and clinical myocardial ischemia will require further investigation. (Circulation 1990;81:1-13) D uring the sympathetic activation induced by exercise or excitement, the activity of cardiac sympathetic nerves, as well as the release of circulating catecholamines, is enhanced. The resultant activation of cardiac 83-adrenoceptors by neuronal and humoral catecholamines mediates an increase in heart rate and myocardial inotropic state, thereby increasing myocardial oxygen demand. Increased oxygen demand is adequately matched by an augmented oxygen supply after metabolic dilation of the coronary vasculature under normal conditions.' However, the direct effect of the sympathetic neurotransmitter norepinephrine on coronary vascular smooth muscle cells is vasoconstriction through activation of a-adrenoceptors. Even when under normal conditions a substantial coronary dilator reserve is present, a-adrenergic constriction acts to limit metabolic coronary dilation by about 30%, such that myocardial oxygen extraction increases together with coronary blood flow during sympathetic activation to match oxygen supply to the increased myocardial oxygen demand.2-4

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mentioning

confidence: 99%

Alpha-adrenergic mechanisms in myocardial ischemia.

Heusch¹

1990

Circulation

239

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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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“…Coronary blood flow is determined by several factors such as perfusion pressure, coronary vascular resistance, metabolic demands and vasomotor tone' 6 '. In normal coronary arteries, blood flow increases three to five times during physical exercise, whereas in stenotic coronary arteries the increase in blood flow is strongly dependent on the severity of the stenosis.…”

Section: Discussionmentioning

confidence: 99%

“…The actual regional blood flow is, however, not solely determined by the luminal area but is the result of the complex interplay of the aforementioned haemodynamic, metabolic and neural factors. Several studies' 6 ' 71 have established the presence of both alpha-and beta-adrenergic receptors in animal and human coronary arteries. An increase in alpha-adrenergic tone has been associated with coronary artery vasoconstriction, whereas an increase in beta-receptor tone is accompanied by coronary artery vasodilation' 5 '.…”

Section: Discussionmentioning

confidence: 99%

Coronary stenosis vasomotion during dynamic exercise before and after PTCA

Suter¹,

Hess²,

Bortone³

et al. 1989

European Heart Journal

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KEY WORDS: Coronary artery disease, coronary vasomotion, percutaneous transluminal coronary angioplasty, supine bicycle exercise. Normal coronary arteries showed a minimal increase in mean luminal area before (+2%; NS) as well as after (+ 6%; NS) PTCA. Nitroglycerin produced dilation of the normal vessel segment to a similar extent pre-(+27%; P < 0-001) and post-(+31%; P < 0-001) PTCA. In contrast, stenotic vessel segments showed coronary vasoconstriction during exercise before PTCA (-28%; P < 0-01); after PTCA, exercise-induced vasoconstriction of the diseased segment was minimal (-4%; NS). Nitroglycerin was associated with vasodi

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Competition between sympathetic vasoconstriction and metabolic vasodilation in the canine coronary circulation.

Cited by 248 publications

References 38 publications

Alpha-adrenergic mechanisms in myocardial ischemia.

Alpha-adrenergic mechanisms in myocardial ischemia.

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

Coronary stenosis vasomotion during dynamic exercise before and after PTCA

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