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 depression in dogs, but the effects of AALI on left ventricular (LV) function have not been carefully studied. Methods We examined the effects of 0.1 N HCl administration into the lung on LV function, leukosequestration, 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 assessed by the time constant of LV pressure decline (τ). Results AALI resulted in significant (p ES and PRSW were increased significantly at 2 and 3 hours after injury, despite significant myeloperoxidase activity and extravascular fluid wet-dry weight ratios. E ES , PRSW, and τ 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, despite mild myocardial leukosequestration and edema formation.