Control of left ventricular function during acceleration-induced blood volume shifts

Peripheral pooling of blood was produced in chronically instrumented, sedated dogs (n = 7) by subjecting them to a +2 Gz force (along their spinal axis) for 3 min. The acceleratory force was then quickly removed, thereby mobilizing blood toward the thoracic cavity. Left ventricular volume, calculated from ultrasound measurements of major and minor axes and wall thickness, increased (p less than 0.05) from 21.7 +/- 3.6 ml (diastolic, mean +/- S.E.M.) and 14.1 +/- 3.3 ml (systolic) during the peripheral pooling of blood to 28.2 +/- 4.1 ml (diastolic) and 16.0 +/- 2.9 ml (systolic) as measured at 2 min after release of the acceleratory force. The d(LVP)/dt was essentially unchanged (i.e., from 3415 +/- 482 mm Hg.s-1 to 3536 +/- 249 mm Hg.s-1). The experiment was repeated after total pharmacologic autonomic blockade (propranolol, atropine, phenoxybenzamine). Left ventricular volumes during +2 Gz after blockade were 27.7 +/- 2.5 ml (diastolic) and 21.2 +/- 2.9 (systolic). The acceleration-induced changes in cardiovascular function, including the changes in ventricular volume, were not significantly different from those of the reflexive state. These results, therefore, do not reveal a substantial role for the autonomic nervous system in the regulation of left ventricular volume responses to the sudden cessation of G-induced peripheral blood pooling. Since the cessation of the G force induced essentially identical increases in left ventricular volumes and stroke volumes both before and after the autonomic blockade, it is concluded that the heart relied mainly upon the Frank-Starling mechanism to adapt to the changes in load.