Myhre H O
Acta Chir Scand. 1975;141(4):265-71.
The effect on reactive hyperaemia of variations in oxygen content of the inspired air and in tissue temperature, was studied by electromagnetic flowmetry in the hind limbs of rabbits. Flowmetry was used together with oxygen polarography to compare recovery time of blood flow and recovery time of oxygen tension in muscle tissue during reactive hyperaemia. After occlusions lasting more than 10 seconds; recovery time of oxygen tension was much shorter than recovery time of blood flow. Breathing of different oxygen concentrations induced relatively small changes of reactive hyperaemia. After increasing tissue temperature all variables of reactive hyperaemia were reduced following 10-60 seconds' occlusion. On the other hand, after 5 minutes' occlusion percentual repayment and recovery time increased significantly. During hypothermia, percentual repayment and recovery time were reduced significantly after 5 minutes' occlusion. Thus, the time-response curves for percentual repayment and recovery time during hyper-and hypothermia crossed each other when occlusion time was extended beyond 60 seconds. Normalization of oxygen tension when blood flow was still increased seems to exclude that oxygen deficiency per se is the only cause of reactive hyperaemia. Oxygen deficiency may be a contributory factor in the initiation of vasodilation during circulatory arrest and may possibly be of importance in the first part of reactive hyperaemia. The results of changing the tissue temperature suggested that metabolites which are accumulated during circulatory arrest, maintain the increased blood flow, at least after release of longer occlusions.
