Conditions for increased cardiac output during occlusion of the descending thoracic aorta.

Previous studies have demonstrated that occlusion of the descending thoracic aorta (AO) at constant heart rate induces a rise in stroke volume during a continuous intravenous (i.v.) isoproterenol infusion, but no change in stroke volume during a selective inotropic stimulation of the left ventricle as achieved by an intracoronary (i.c.) isoproterenol infusion. To determine the mechanism for this difference in stroke volume response, the haemodynamic adjustments of both the right and the left ventricle to AO during continuous i.v. and i.c. isoproterenol infusion in anesthetized open-chest pigs were compared. The AO induced a similar rise in left ventricular systolic pressure and end-systolic segment length (measured by an ultrasonic technique) in both ventricles whether isoproterenol was infused i.v. or i.c., but stroke volume rose by 26.3 (11.9-38.1%) (median and 95% confidence interval) (P less than 0.01) during i.v., compared with 3.8 (-7.4-14.7)% (n.s.) during i.c. isoproterenol infusion (difference in response: P less than 0.01). End-diastolic segment length increased more by AO during i.v. than i.c. isoproterenol infusion; 7.8 (5.1-16.9)% vs. 5.7 (3.1-8.5)% (difference in response: P less than 0.01) in the left ventricle, and 5.9 (3.5-8.1)% vs. 1.0 (-1.5-3.3)% (difference in response: P less than 0.01) in the right ventricle. Redistribution of blood through the inferior caval vein measured immediately after AO, amounted to 130 (110-172) ml during i.v. and to 77 (52-89) ml during i.c. isoproterenol infusion (n = 3).(ABSTRACT TRUNCATED AT 250 WORDS)