The Pathophysiology of Myocardial Stunning : Reversibility, Accumulation and Continuity of the Ischemic Myocardial Damage after Reperfusion : 54th Annual Scientific Session of the Japanese Circulation Society

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In order to understand the pathophysiology of myocardial stunning, reversibility, accumulation and continuity of ischemic myocardial damage after reperfusion should be studied. Then, to analyze these three factors, myocardial function, metabolism and morphology under ischemia and reperfusion were studied in anesthetized, open-chest dogs. When myocardial ischemia was induced by occlusion of the left anterior descending coronary artery, percentage regional systolic shortening (%SS) of ischemic myocardium sharply decreased and became stable 10min after occlusion. After reperfusion, ischemic myocardium showed active shortening after within 30-min occlusion, but did not after more than 60-min occlusion. During 90-min of ischemia, extracellular K^+ concentration (Ke) steeply increased for first 10min and was almost stable for next 10min. Then, Ke straighthy in-creased till 90min. Metabolic rates, calculated from myocardial tissue CO_2 and pH, steeply increased for first 20min and sharply decreased for next 10min. After 30min, these two variables were almost stable, near zero. By electron-microscopy with cytochemistry, distribution of Na/K ATPase to myocardial cell membrane was observed to be almost after 15-min occlusion but distinctly sparse with destruction of cell membrane after 30-min occlusion. Therefore, irreversible myocardial damage appears after about 20-min ischemia and is almost complete after 60min. Reversibility of damage to ischemic myocardium after reperfusion may mainly occur within 60-min ischemia. Although stunned myocardium in a narrow sense is may appear after reperfusion within less than 20-min of ischemia, stunned myocardium in a broad sense may appear within less than 60-min ischemia. When reversible myocardial ischemia (4- or 15-min occlusion) was repeated after short time intervals (20-min reperfusion), %SS of ischemic myocardium was gradually decreased with each ischemic episode. Active shortening of ischemic myocardium disappeared after more than two episodes of 15-min occlusion. Fluctuation of PCO_2, pH and Ke of ischemic myocardium was gradually depressed with each occlusion. Metabolic viability of ischemic myocardium was cumulatively depressed by repeated brief occlusion. Naturally, myocardial damage was more severe after repeated 15-min occlusion than after 4-min occlusion. Accumulation of ischemic myocardial damage may arise as brief ischemia, which only induces reversible damage, is repeated. At last, continuity of ischemic myocardial damage was studied. The effect of 5-min occlusion to %SS of ischemic myocardium was apparently reversed after 90-min reperfusion. Early contractile failure was advanced even after very short duration of ischemia. Thus, myocardial function will be latently damaged. Fluctuation of PCO_2, pH and Ke was still depressed, thus, metabolic viability of ischemic myocardium will be latently depressed. This phenomenon, continuity of latent myocardial damage, is very important condition preceding myocardial stunning.
社団法人日本循環器学会の論文
1991-09-20

The Pathophysiology of Myocardial Stunning : Reversibility, Accumulation and Continuity of the Ischemic Myocardial Damage after Reperfusion : 54th Annual Scientific Session of the Japanese Circulation Society

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