Journal of Okayama Medical Association
Published by Okayama Medical Association

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急性虚血心における虚血部収縮曲線と循環諸量の関係―Strain gauge archによる虚血部心筋の収縮異常の検討

Tawara, Rituya
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Abstract
The animal experiments of Tennant, Wiggers and the subsequent clinical observations of Harrison had stimulated interests in abnormal ventricular wall motion in coronary artery disease. It was well known that an ischemic arec of ventricular myocardium might bulge or balloon out during systole. Herman et al. showed that there were four distinct local types of asynergy, and employed the term "dyskynesis" to express the paradoxical systolic expansion of part of the wall. Recently the strain gauge arches had been used generally for measurement of the contractility of the local ventricular myocardium. There had been many experimental studies on myocardial contractility and hemodynamic changes following the coronary occlusion. However, few had been reported on relationship between hemodynamic changes and paradoxical bulging. The purpose of the present study is to investigate effects of ischemic myocardial contractility on hemodynamic changes. Adult mongrel dogs weightening 10-25kg anesthetized with intravenous pentobarbital sodium (25mg/kg) were subjected to thracotomy under artificial respiration. The following tracings were simultaneously recorded; and left anterior descending branch was occluded completely for one minute (group Ⅰ) and for 30 minutes (group Ⅱ). (1) aortic blood flow and blood flow in circumflex branch. (2) rate of left ventricular pressure rise (LV dp/dt). (3) myocardial contractility obtained with strain gauge arch (in the ischemic and in the non-ischemic areas). By the experiments, following results were obtained. (A) Myocardial contractility The time relations which existed among simultaneous recordings of left ventricular pressure, aortic pressure, aortic blood flow, electrocardiogram and myocardial contractilities were studied. Five seconds after the coronary occlusion, shortening of the myocardial segment did not continue to the end of systole, and in late systole actual lengthening of the myocardial segment occurred. The late systolic bulge rapidly increased in early systole after 20 seconds of the occlusion. Within 50 seconds, paradoxical movement was observed in all cases. In a half of cases, myocardial contractility increased in the nonischemic area in contrast with diminution of the contractility in the ischemic area. (B) Changes in hemodynamics Heart rate unchanged during and after coronary occlusion. Shortening of ejection time began immediately after the coronary occlusion, and reached maximum at 85% of control level after 10-20 seconds. Thirty seconds after ocronary occlusion, ejection time recovered in spite of continuing the occlusion. Aortic blood pressure and peak left ventricular pressure were lowered in the both group. Mamimum aortic flow rate and stroke volume were reduced. Left ventricular end-diastolic pressure was elevated from a mean control value of 4.8 mmHg to average 5.8 mmHg, but not significant statistically. LVmaxdp/dt increased in 4 out of 8 cases immediately after the coronary occlusion followed by decrease in all cases after 40 seconds. LVmin. dp/dt was lowered in all cases immediately after the coronary occlusion. It was averaged 69% of control value. Blood flow in circumflex branch was averaged 112% of control mean value. Peak systolic coronary blood flow was reduced slightly, but not significant statistically. Peak diastolic coron ary blood flow increased. Mean coronary vascular resistance decreased and was averaged 85% of mean control value. (C) Relationship between changes of myocardial contractility and hemodynamics. Late systolic left ventricular pressure was lowered, ejection time was shortend and LVmindp/dt was reduced with late systolic bulge formation in myocardial tension curve. Maximum aortic flow rate and peak left ventricular pressure were decreased by pansystolic bulge. It may be concluded that hemodynamic findings had a close relation with myocardial contractility in the ischemic ares.
ISSN
0030-1558
NCID
AN00032489