No abstract

In the first part of the study, the influence of changes in preload and afterload on mean circumferential fiber shortening velocity, Vcf, was investigated in the absence of any extrinsic cause for change in the contractile state of the left ventricle (LV) of seven dogs. In five of seven dogs in which afterload was controlled and contractility was unchanged, there was a significant negative correlation between LV end-diastolic pressure and mean Vcf expressed in circumferences per second ( r = –.88 to –.97). In one dog there was a positive correlation ( r = +0.847) and in another dog there was no significant correlation. Correlation as a group was poor. In five of the above seven dogs in which afterload was decreased from a control level while preload was controlled and contractility was not extrinsically altered, mean Vcf increased in all instances. Because of the influence of afterload on Vcf increased in all instances. Because of the influence of afterload on Vcf and the inconsistent relation between Vcf and preload, we controlled preload and afterload during assessment of Vcf in reflecting a change of LV contractility. Since mean left ventricular hydraulic output power, MLVP, quantitates practically all of the mechanical power of the left ventricular musculature, MLVP was utilized to represent the contractile state of the left ventricle under conditions in which preload and afterload were controlled. Mean and peak Vcf, Vcf at peak tension, extent of circumferential fiber shortening, and peak tension were compared with MLVP to test their usefulness in reflecting a change in the contractile state of the LV. Twenty dogs were divided into four groups of five each. Group I was exposed to cardiopulmonary bypass alone. Dogs of groups II, III, and IV were exposed to a total of 45 minutes of myocardial ischemia during bypass. After bypass, groups I, II, III and IV retained an average of 89.3, 79.9, 82.5 and 69.2% of the control or original mean Vcf, and 87.1, 63.9, 53.4 and 33.5% of the control MLVP, respectively. Although an effect of ischemia was detected by changes of peak tension and extent of fiber shortening, the statistical evidence was less satisfactory than observed for MLVP. It was concluded that mean Vcf, peak Vcf, and Vcf at peak tension are inadequate indices to detect acute changes in the contractile state of the LV produced by prior myocardial ischemia. These same changes in contractility are readily determined by MLVP.