Myocardial Metabolism in Reactive Hyperemia
Yoshio Yazaki, Kizuku Kuramoto, SHlN-ICHI Kimata, Masao Ikeda, K Nakao
Abstract
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Yoshio Yazaki, Kizuku Kuramoto, SHlN-ICHI Kimata, Masao Ikeda, K Nakao
Abstract
Open-access reader
Myocardial metabolism in reactive hyperemia was studied in anesthetized open-chest dogs. To produce reactive hyperemia the cessation of left coronary blood flow was carried out for 20 sec. During reactive hyperemia the myocardial extraction of glucose did not change significantly, but that of lactate was slightly decreased. On the other hand the. marked increase in the myocardial extraction of FFA was demonstrated during reactive hyperemia. The concentration of pyruvate in coronary sinus blood elevated over the control level 20 to 40 sec after the release of coronary occlusion and returned to the control level in two or three minutes. However the concentration of lactate revealed little change in this period. The increase in the myocardial oxygen consumption was remarkable in the first 20 sec after the release and calculated oxygen debt was already repaid in this period. These results confirmed that the anoxic metabolism in myocardium returned to the control level in a very short time during reactive hyperemia. A possible role of FFA in the mechanism of reactive hyperemia was indicated.
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Myocardial metabolism in reactive hyperemia was studied in anesthetized open-chest dogs. To produce reactive hyperemia the cessation of left coronary blood flow was carried out for 20 sec. During reactive hyperemia the myocardial extraction of glucose did not change significantly, but that of lactate was slightly decreased. On the other hand the. marked increase in the myocardial extraction of FFA was demonstrated during reactive hyperemia. The concentration of pyruvate in coronary sinus blood elevated over the control level 20 to 40 sec after the release of coronary occlusion and returned to the control level in two or three minutes. However the concentration of lactate revealed little change in this period. The increase in the myocardial oxygen consumption was remarkable in the first 20 sec after the release and calculated oxygen debt was already repaid in this period. These results confirmed that the anoxic metabolism in myocardium returned to the control level in a very short time during reactive hyperemia. A possible role of FFA in the mechanism of reactive hyperemia was indicated.
Key concepts: Reactive hyperemia, Blood flow, Coronary sinus, Cardiology, Internal medicine, Coronary circulation, Coronary occlusion, Occlusion