The influence of adenosine triphosphate on left ventricular function and blood flow distribution during aortic crossclamping in dogs.

To evaluate the influence of adenosine triphosphate (ATP)-induced vasodilation on myocardial performance and blood flow during aortic crossclamping (XC), ten dogs were instrumented to measure left ventricular (LV) pressure and dimensions. Regional LV function was assessed from the percentage of systolic shortening, whereas the slope of the linear regression of the LV end-systolic pressure-diameter relationship was used as an index of overall contractility. The regional blood flow distribution was measured from sequential injections of radioactive microspheres. Following XC, systemic arterial pressure proximal to the clamp (SAPa), LV end-diastolic pressure (LVEDP), LV end-systolic meridional wall stress (WS), and central venous pressure (CVP) increased significantly, whereas the cardiac index (CI) and heart rate did not change. After 30 minutes of ATP infusion (1 mg/kg/min) SAPa, LVEDP, WS, and CVP returned to control levels, CI increased significantly compared with XC alone, and vascular resistance fell below the control level. ATP produced a threefold increase in myocardial blood flow and shifted the intramural distribution in favor of the endocardial layer. In conclusion, our investigation of the effect of ATP on aortic XC in a canine model showed the drug to produce a smooth, predictable, and rapid reduction in left ventricular preload and afterload. This was accomplished with minimal changes in distal organ perfusion, some improvement in measured cardiac performance, and a large increase in myocardial blood flow.