Compensatory cardiac mechanisms evoked by septal ischemia in dogs.
To examine the cardiac responses to selective septal ischemia, the septal artery was occluded intermittently in anesthetized open-chest dogs. Myocardial segment length was recorded continuously by an ultrasonic technique in the interventricular septum and the right and left ventricular free walls. At left ventricular end-diastolic pressure of 3.0 +/- 0.6 mm Hg, occlusion of the septal artery increased left ventricular end-diastolic segment length by 3.9 +/- 0.9% and stroke volume was maintained. After blood volume expansion to a left ventricular end-diastolic pressure of 7.2 +/- 1.4 mm Hg, occlusion of the septal artery did not increase end-diastolic dimensions and stroke volume decreased significantly but by less than 10%. At all levels of blood volume expansion, occlusion of the septal artery did not alter significantly the end-systolic segment length of the free wall of the left ventricle and the dimensions of the free wall of the right ventricle. The distance between the septum and the right ventricular free wall was unchanged in end-diastole and reduced in end-systole after occlusion of the septal artery. These observations indicate paradoxical movement of the ischemic septum. The ischemic septum seems to act as a passive diaphragm pump on the right ventricle without activation of the Frank-Starling mechanism in uninjured areas. In the left ventricle, the Frank-Starling mechanism is fully exploited with unaltered end-systolic dimensions of the uninjured myocardium because of the systolic bulging of the ischemia septum.
D000818:Animals; D001157:Arterial Occlusive Diseases / Q000150:complications / Q000503:physiopathology; D001794:Blood Pressure; D003327:Coronary Disease / Q000150:complications / Q000503:physiopathology; D004285:Dogs; D005260:Female; D006346:Heart Septum / Q000503:physiopathology*; D007511:Ischemia / Q000209:etiology / Q000503:physiopathology*; D008297:Male; D009200:Myocardial Contraction; D013318:Stroke Volume; D013599:Systole