A model for the study of coronary spasm induced changes in cardiac metabolism

Burger, Wolfram; Jm, Chemnitius; Mz, Metz; Rj, Bing

doi:10.1016/s0022-2828(85)80105-x

Cited by 7 publications

(4 citation statements)

References 22 publications

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“…Localized coronary artery obstruction of the obtuse marginal coronary artery induced by histamine administration severely alters the redox potentials lactate/pyruvate and a-glyceryl phosphate/dihydroxyacetone phos phate [17]. The mechanism of coronary vas cular spasm remains largely unclear: a defect in parasympathetic [21] and/or sympathetic control [22], local damage of the intima of the vascular wall [23] or hypersensitivity of the coronary smooth muscle to vasoactive agents may be responsible [24].…”

Section: Discussionmentioning

confidence: 99%

“…Histamine in the rabbit is a powerful coronary vasoconstrictor [17,23]. Topical administration of 40 jiM to a large coronary artery produces marked localized coronary vasoconstriction [13,17], Intraartrial injection of histamine causes more severe disturbances [ 17], such as a decline in myocardial oxygen consumption, and an in crease in total vascular coronary resistance. Removal of endothelium further increases coronary vascular constriction [12,16].…”

Section: Discussionmentioning

confidence: 99%

“…Histamine (1 ml of 10-2 M) was injected into the left atrium as a coronary vasoconstrictor. Previous expe rience from this laboratory has shown that its action on coronary arteries is dose-dependent [ 13,17],…”

Section: Measurement O F the Internal Diameter O F Large Epicardial Cmentioning

confidence: 95%

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Effect of Nisoldipine on De-Endothelialized Large Coronary Artery in Isolated Working Rabbit Hearts

1987

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The effect of nisoldipine on coronary vascular resistances, cardiac performance and myocardial oxygen consumption was determined. Rabbit hearts were perfused with a perfluorochemical (FC-43) emulsion. Endothelium was removed from the obtuse marginal and the upper portion of the anterior descending coronary artery. Changes in the internal diameter of these arteries were visualized using injection of Patent Blue Dye (color arteriography). Mean internal diameter of coronary arteries and surface area/unit length were computer calculated. Nisoldipine reduced the constriction of coronary arteries and the decrease on coronary flow induced by histamine. Nisoldipine abolished or reduced the decrease in cardiac output, LVESP, dP/dt and myocardial oxygen consumption. The results demonstrate that in the supported rabbit heart preparation, nisoldipine is an effective dilator of large subepicardial coronary arteries, deprived of endothelial lining, and counteracts constriction of coronary resistance vessels. As a consequence nisoldipine improves performance of the ischemic myocardium.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Effect of Nisoldipine on De-Endothelialized Large Coronary Artery in Isolated Working Rabbit Hearts

1987

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“…20 -21 Furthermore, histamine infusion has been shown to induce coronary artery vasospasm in patients being evaluated for variant angina, 3 -22 in the in vivo porcine preparation, 23 and in the isolated rabbit heart preparation. 24 Plasma histamine levels have also been shown to be increased by experimental acute coronary thrombosis in the conscious dog. 23 Thus, while a pathophysiologic role for histamine in the mediation of coronary vessel responses has not been definitively established, current data suggest the potential for histamine involvement in epicardial coronary artery spasm.…”

Section: Discussionmentioning

confidence: 99%

Differential H1- and H2-receptor-mediated histamine responses of canine epicardial conductance and distal resistance coronary vessels.

Miller

Bové

1988

Circulation Research

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The contributions of histamine (H1 or H2) receptor-mediated responses and, therefore, the effects of histamine blocking agents are unclear with regard to regulation of proximal epicardial and distal resistance coronary arteries. This study was designed to evaluate the effects of selective H1- and H2-receptor antagonists on epicardial and resistance vessels in the closed chest dog model. Histamine, diphenhydramine (H1 blocker), and cimetidine (H2 blocker) were infused into the left anterior descending coronary artery (LAD), and responses were studied by quantitative coronary angiography and flow measurements (133Xe washout). Histamine infusion alone produced a significant dilation of the proximal LAD (13% above control) only at the highest dose (45 micrograms/min), while LAD flow was increased by 128%. In the presence of H1 blocker, histamine produced significantly greater epicardial dilation (55% above control). The flow response curve was shifted to the right in the presence of H1 blocker, but the flow attenuation was overcome by the highest histamine dose. In contrast, the H2 blocker attenuated both epicardial dilation (6% below control) and flow response (31% above control) to the highest histamine dose. Results support a differential regulation of proximal epicardial and distal resistance vessels to histamine with epicardial arteries demonstrating H1-mediated vasoconstriction and H2-mediated vasodilation and distal resistance vessels showing H1- and H2-mediated vasodilation. In addition, these findings suggest that H1 blockade may antagonize histamine-related vasoconstriction and vasospasm, while H2 blockers may permit unopposed H1-mediated vasoconstriction of epicardial arteries and also limit resistance vessel vasodilatory responsiveness in the presence of elevated tissue histamine, as may occur in atherosclerotic coronary artery disease.

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