1992
DOI: 10.1161/01.res.71.4.912
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Microvascular sites and mechanisms responsible for reactive hyperemia in the coronary circulation of the beating canine heart.

Abstract: Our aim was to elucidate the site and mechanism responsible for reactive hyperemia in coronary circulation. In in vivo beating canine hearts, microvessels of the left anterior descending coronary artery (LAD) were observed through a microscope equipped with a floating objective. Flow velocity of the LAD was measured with a suction-type Doppler probe. The LAD was occluded for 20 or 30 seconds and then released, and reactive hyperemia was observed before and after 8-phenyltheophylline (7.5 mg/kg i.v.) or glibenc… Show more

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Cited by 76 publications
(46 citation statements)
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“…19 This triggers a number of mechanisms, some of which involve endothelium-derived nitric oxide, adenosine, K + ATP channels, and certain cyclooxygenase-derived metabolites to maintain the elevated flow velocity during the period of reactive hyperaemia. [20][21][22][23][24] Peak hyperaemic blood flow is only partially regulated by the release of endotheliumderived nitric oxide. 25 On the other hand, among the various vasodilators, such as prostaglandins and endotheliumderived hyperpolarizing factor, released from the endothelium, nitric oxide is the primary mediator of FMD.…”
Section: Discussionmentioning
confidence: 99%
“…19 This triggers a number of mechanisms, some of which involve endothelium-derived nitric oxide, adenosine, K + ATP channels, and certain cyclooxygenase-derived metabolites to maintain the elevated flow velocity during the period of reactive hyperaemia. [20][21][22][23][24] Peak hyperaemic blood flow is only partially regulated by the release of endotheliumderived nitric oxide. 25 On the other hand, among the various vasodilators, such as prostaglandins and endotheliumderived hyperpolarizing factor, released from the endothelium, nitric oxide is the primary mediator of FMD.…”
Section: Discussionmentioning
confidence: 99%
“…The precise mechanisms involved and their interactions and roles at different times in the response are, however, still not clearly understood. Vasodilation of downstream vessels during occlusion has been attributed to the myogenic response (20), extracellular (22,23) and potentially intracellular (25) changes in metabolite concentration, release of vasodilators from endothelial cells (24), and viscoelastic wall properties (16).…”
Section: Discussionmentioning
confidence: 99%
“…Therefore, in the present study, flow distributions during maximal vasodilation were approximated by those measured during the peak plateau of the reactive hyperemia. Although region-to-region or microvascular site-to-site asynchronous vasodilation during reactive hyperemia (13,24) prohibits the complete removal of coronary tone effects on regional flows, coronary tone could not be involved in causing the differences of flow distributions under Tyrode and blood perfusion. Future experiments should, however, be designed to elucidate more clearly the role of corpuscular mechanistic factors in the determination of regional flows.…”
Section: Discussionmentioning
confidence: 99%