EFFECTS OF ACID ASPIRATION-INDUCED LUNG INJURY ON LEFT-VENTRICULAR FUNCTION

Background. Acid aspiration-induced acute lung injury (AALI) leads to myocardial leukosequestration and edema in rats and hemodynamic depres sion in dogs, but the effects of AALI on left ventricular (LV) functio n have not been carefully studied. Methods. We examined the effects of 0.1 N HCl administration into the lung on LV function, leukosequestra tion, and edema in pentobarbital-anesthetized, atropinized (n = 8), or autonomically blocked (n = 7) dogs. Saline solution was administered into the lungs of a control group of autonomically blocked dogs (n = 6 ). LV contractility was assessed by end-systolic elastance (E(ES)) and preload recruitable stroke work (PRSW). Active relaxation was assesse d by the time constant of LV pressure decline (tau). Results. AALI res ulted in significant (p < 0.05) decreased in mean arterial pressure an d cardiac output and increases in pulmonary artery pressure and system ic vascular resistance in atropinized and autonomically blocked dogs b ut not in saline control group. In atropinized dogs tau did not change after injury, but E(ES) and PRSW were increased significantly at 2 or 3 hours after injury, despite significant myeloperoxidase activity an d extravascular fluid wet-dry weight ratios. E(ES), PRSW, and tau did not change in the autonomically blocked dogs in response to AALI or in the saline control group. Conclusions. We concluded that AALI results in a baroreflex mediated enhancement of LV contractility in dogs, des pite mild myocardial leukosequestration and edema formation.