Canine hindlimb muscles were perfused with arterial blood from a donor at a constant pressure or at a constant flow rate. Blood samples were analyzed for adenosine, oxygen and potassium during load-free twitch contractions (2 cps) and/or after 3-min ischemia. (1) During exercise hyperemia A-V oxygen (
p<0.001) and V-A potassium (
p<0.001) differences increased in both perfusion systems. Under the constant pressure
total amount of adenosine and/or AMP released (TAAR) remained constant at 34.4±7.8 (mean±s. D. ) nmoles/ml of blood compared with 31.0±5.6 at rest, whereas under the constant flow rate the value increased from 32.8±9.4 to 74.6±5.7 (
p<0.001). (2) In reactive hyperemia A-V difference of oxygen increased (
p<0.001) and TAAR remained at 33.0±8.3 under the constant pressure. Under the constant flow rate TAAR increased from 32.8±9.4 to 48.1±2.6 (
p<0.001). (3) After ischemic contractions TAAR remained constant under the constant pressure perfusion. Under the constant flow rate, however, TAAR showed definite decrease compared with that during exercise hyperemia with intact flow (
p<0.001). (4) The authors think that adenosine and/or AMP is the mediator of exercise hyperemia, supported by potassium ions and local hypoxia. Adenosine and/or AMP, and local hypoxia are responsible for reactive hyperemia. In ischemic contractions, no special circulatory mediator was found.
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