Background: Previous data suggest that preoperative myocardial dysfunction is associated with an altered cardiac response to infra-renal aortic cross-clamping (AXC). This study was designed to further explore how acute reductions in stroke volume and cardiac output influence the systemic, preportal and renal circulatory responses to AXC.
Methods: In chloralose-anesthetized normoventilated pigs, graded increases in pericardial pressure (PPERICARD) were obtained by local infusions of dextran. Measurements included cardiac output (CO, thermodilution), mean blood pressure proximal to the aortic clamping site (MAPPROX) and ultrasonic flowmetry for portal (QPORT) and renal (QREN) blood flows. In all animals, measurements were made a) prior to AXC, b) at the end of a 5 min AXC period and, c) 5 min following declamping. These recordings were repeated during control (PPERICARD 0 cmH2O) and during stages with increased PPERICARD (4 and 8 cmH2O, respectively).
Results: Pericardial infusions of dextran produced hemodynamic responses that in magnitude were proportional to PPERICARD levels. Stroke volume, CO and mean arterial pressure decreased, while systemic vascular resistance (SVR) increased. In the preportal tissues, vascular resistance increased and QPORT decreased. Similarly, in the kidney, vascular resistance and QREN decreased, but only at a PPERICARD of 8 cmH2O. At control, AXC increased SVR, MAPPROX, QPORT and both renal and preportal vascular resistances. When PPERICARD was increased to 4 cm H2O, the responses to AXC concerning SVR and MAPPROX were not significantly altered, while renal and preportal circulatory responses were blunted. At stages with a PPERICARD of 8 cmH2O, we could not demonstrate any circulatory responses to AXC.
Conclusions: AXC-induced systemic, preportal and renal circulatory responses are inhibited during a condition of acutely lowered cardiac output.