Reactive Hyperemia in Legs of Dogs:

Abstract

1. In normal dogs 5- and 10-minute occlusions of the femoral artery were followed by periods of reactive hyperemia (RH) whose duration closely approximated the length of occlusion. The resulting vasodilatation repaid about 50% of the blood flow debt, which was calculated from the flow rate measured just prior to occlusion. 2. When the animal's body temperature was lowered to 32°C, the duration and percentage blood flow debt repaid decreased to about one-half and one-third, respectively, of that found at 40°C. Observations of RH during rewarming revealed progressive increases in debt repayment and duration of the hyperemic period. The temperature characteristics of RH suggested that thermolabile factors were responsible for the vasodilatation that resulted from arterial occlusion. 3. Venous occlusion was followed by RH that was considerably reduced, resulting in a debt repayment of about one-fourth of that attained after arterial occlusion. The possibility that high transmural pressure might be a factor in reducing the intensity of RH that followed venous blockage was investigated. However, when a pressure equivalent to that in the carotid artery was maintained in the vasculature by pumping venous blood into the leg with its artery and vein clamped, the RH following restoration of blood flow closely resembled that induced by arterial clamping only. When arterial blood was infused, RH was reduced to the level seen after simple venous occlusion. It was concluded from these results that during venous occlusion some arterial blood entered the vascular bed, and brought with it chemical factors that reduced the degree of vasodilatation. Since total absence of arterial blood inflow was required to cause maximal dilatation, it may be that oxygen lack was involved in relaxation of the vascular wall, as has been implied by the work of investigators using other techniques.