Mechanism of reactive hyperemia in limbs of anesthetized dogs

• Published in: The American journal of physiology Vol. 209; no. 6; pp. 1106 - 1114
• Main Authors: Kontos, Hermes A, Mauck, H. Page, JR, Patterson, John L., JR
• Format: Journal Article
• Language: English
• Published: United States 01-12-1965
• Subjects: Acetazolamide - pharmacology; Animals; Blood Gas Analysis; Carbon Dioxide - toxicity; Dogs; Femoral Artery; Hyperemia - etiology; Ischemia - physiopathology
• ISSN: 0002-9513; 2163-5773
• DOI: 10.1152/ajplegacy.1965.209.6.1106

1 Department of Medicine, Medical College of Virginia, Richmond, Virginia
Reactive hyperemia was studied in the hindlimb and forelimb of 81 anesthetized dogs. Reactive hyperemia volume in response to 5-sec arterial occlusions correlated moderately well with the decrease in intravascular pressure. This correlation was poor for 30-sec arterial occlusions. Venous congestion induced by venous occlusion decreased or abolished the vasodilator response to 5-sec arterial occlusions and decreased the response to 30-sec occlusions. Evidence is presented supporting the view that this effect of venous congestion was related to reduction in the fall in intravascular pressure during arterial occlusion. The response to 30-sec occlusions was decreased during acutely induced hypocapnia and increased following acetazolamide administration. The data support the view that both physical and metabolic factors contribute to the production of reactive hyperemia. They further suggest that the accumulation of CO 2 in the ischemic tissues contributes to the production of reactive hyperemia. Key Words: vasodilatation • effects of hypocapnia on limb blood vessels • role of CO 2 in reactive hyperemia • role of myogenic factors in reactive hyperemia • vascular response to ischemia
Submitted on March 26, 1964