Indexed on: 09 Mar '99Published on: 09 Mar '99Published in: Journal of Surgical Research
Acute respiratory distress syndrome (ARDS) is seen in a variety of clinical settings in critically ill patients. ARDS has been defined as a clinical syndrome characterized by progressive hypoxemia, tachypnea, and generalized patchy bilateral pulmonary infiltrates in the absence of cardiac failure. Furosemide has been shown to improve pulmonary gas exchange and intrapulmonary shunt in animal models of ARDS by preferential perfusion of nonedematous lung units. We hypothesized that continuous dose furosemide would improve lung injury during resuscitation from oleic acid-induced lung injury in canines.Ten mongrel dogs were anesthetized and given intravenous oleic acid (0.1 mg/kg) to induce lung injury. Once lung injury was established (2 h) the control animals (n = 6) were continued on standard supportive therapy, and the study animals (n = 4) were started on continuous dose furosemide at 0.2 mg/kg/h. Cardiac filling pressures were maintained in all animals by infusion of isotonic saline solution. Data collected included lung injury score (LIS), cardiac index (CI), stroke volume index (SVI), pulmonary capillary wedge pressure (PCWP), urine output (UO), volume of resuscitation (VR), and pulmonary shunt fraction (Qs/Qt). Data were collected at baseline, established lung injury (2 h), and end of protocol (6 h). Data were compared between groups at various stages of the model using one-way analysis of variance with repeated measures.All 10 animals survived the protocol. There was no difference between the experimental and control groups at baseline or established lung injury (2 h) for CI, SVI, PCWP, or VR. There was a significant improvement in PO2/FIO2 and reduction of PEEP values in the furosemide group. There was also a statistically significant difference between experimental and control groups in LIS, Qs/Qt, and urine volumes.Continuous dose furosemide therapy improves LIS, PO2/FIO2, and Qs/Qt and decreases PEEP requirements in this oleic acid model of ARDS.