To determine the essential mechanism of increased systolic wall motion, i.e., hyperkinesis, in a nonischemic region (NIR) during acute ischemia, we simultaneously evaluated global and regional function ofthe excised, cross-circulated canine left ventricle connected to a volume servo pump before and after coronary occlusion. Regional areas were determined with pairs of orthogonal subendocardial sonomicrometers in the ischemic region (IR) and NIR.
468increased systolic segment shortening in a nonischemic region that correlated well with an increase in enddiastolic segment length and interpreted the increased shortening as a manifestation of a compensatory operation of the Frank-Starling mechanism. Thereafter, an increase in systolic segment shortening or wall thickening in a nonischemic region has been shown by many others5 8i and has been ascribed to either compensatory operation of the Frank-Starling mechanism or increased sympathetic activity. More recent studies by Lew et al.9 14 and Smalling et al. 15 have attributed the increased segment shortening to a combination of the Frank-Starling mechanism and mechanical unloading due to an intraventricular interaction between the ischemic and nonischemic regions. However, all these studies were performed in hearts in situ in which acute ischemia is usually accompanied by compensatory operation of the Frank-Starling mechanism and myocardial function is regulated by various neurohumoral mechanisms. This has made it difficult to separate the effects of the Frank-Starling mechanism and neurohumoral factors from other CIRCULATION by guest on