[Mediators of reactive hyperemia].
Reactive hyperemia is a protective adaptive phenomenon, which quickly restores blood flow distal to a transient arterial occlusion. It involves the vascular tone regulation mechanisms of the ischaemic distal territory as a whole, but also its proximal control (flow-mediated dilation). The resulting vasodilatation differs from one vascular bed to another, and also between the large proximal arteries and the distal arterioles in the microcirculation. Thus, although both are elicited by a similar transient occlusion of brachial blood flow, non-invasive investigation of reactive hyperemia in the humeral circulation differs from assessment of endothelial function with the flow-mediated arterial dilation. Indeed, whereas nitric oxide (NO) plays the key-role in the later, several mediators are involved in the former, including myogenic and metabolic factors, prostaglandins, K + ATP channels, adenosine and NO which is only one of the many components of this complex regulation mechanism.
Monsuez
J J
JJ
Service de médecine interne, hôpital Paul-Brousse, 12-14, avenue Paul-Vaillant-Couturier, F-94804 Villejuif.
D000222:Adaptation, Physiological; D000241:Adenosine / Q000494:pharmacology; D000255:Adenosine Triphosphate / Q000494:pharmacology; D001157:Arterial Occlusive Diseases / Q000150:complications*; D003327:Coronary Disease; D006801:Humans; D006940:Hyperemia / Q000503:physiopathology*; D008833:Microcirculation / Q000502:physiology; D009569:Nitric Oxide / Q000494:pharmacology*; D011188:Potassium; D011453:Prostaglandins / Q000494:pharmacology; D012039:Regional Blood Flow
D011453:Prostaglandins; D009569:Nitric Oxide; D000255:Adenosine Triphosphate; D000241:Adenosine; D011188:Potassium