This study examined the effects of cardiomyoplasty with vascular delay on canine normal and depressed left ventricular (LV) function. To improve viability of the latissimus dorsi muscle (LDM), vascular delay was performed 2 weeks before cardiomyoplasty in 10 mongrel dogs. Two weeks after cardio-myoplasty, LV function was evaluated by simultaneously measuring LV and aortic pressure, and aortic flow. The LDM was stimulated at a ratio of 1:4–1:7 synchronously with ventricular systole. Microspheres (90 μ) were sequentially injected into the left coronary artery to depress LV function. Data were acquired and analyzed on a beat to beat basis. Results were as follows: LDM stimulation significantly augmented LV systolic pressure (LVSP) from 138 ± 2 to 161 ± 2*mmHg, the peak rate of change of LV pressure (+dP/dt) from 1888 ± 46 to 2584 ± 43*mmHg/sec, aortic systolic pressure (AoSP) from 140 ± 2 to 159 ± 2*mmHg, stroke volume (SV) from 11.2 ± 0.3 to 133 ± 0.3*ml, stroke work (SW) from 19 ± 1 to 26 ± 1*gm. m, peak aortic flow (P Qa) from 5542 ± 142 to 7190 ± 161*ml/mm, and decreased -dP/dt from −1683 ± 31 to −1689 ± 49*mmHg/sec (* = p < 0.05). Microsphere injections depressed LV function, but did not affect the magnitude of the net changes between stimulated and nonstimulated beats. However, the percent changes significantly increased. Preconditioning of LDM with vascular delay augments cardiac function in LDM assisted beats. This improved performance was, present in both normal as well as depressed I.V function groups. Thus, investigations of cardiomyoplasty may not necessarily require a model of severe myocardial dysfunction. Vascular delay offers an important preconditioning method of LDM to augment cardiac function in cardiomyoplasty. ASAIO Journal 1997; 43:M786-M790.
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