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Cardiopulmonary dysfunction in a feline septic shock model: possible role of leukotrienes.

The aim of the present study was to explore the possible involvement of leukotrienes (LTs) in the development of cardiopulmonary dysfunction in experimental septic shock. Sepsis was induced in anesthetized cats by infusion of liver Escherichia coli bacteria. One series (N = 6) was pretreated with diethylcarbamazine (DEC), a 5-lipooxygenase inhibitor; another series (N = 7) was pretreated with FPL 55712, a LTC4-D4 antagonist; and a third series (N = 8) served as septic controls. After 2 hr of bacteremia, there were no differences in cardiac function in the three series. By subjecting the heart to volume load, two points on a Starling curve were obtained, indicating the limits of the functional cardiac reserve. This loading procedure disclosed a significantly better preserved left ventricular function in the DEC-pretreated group as compared with the other two groups. Pretreatment with DEC and FPL 55712 had no effects on early pulmonary vascular reactions. However, the tracheal pressure response was less pronounced after pretreatment compared with septic controls. Calculated airway resistance was less increased and pulmonary compliance less decreased in the two pretreated groups. Furthermore, arterial hypoxia was prevented by pretreatment. It is concluded that this study suggests that LTs are involved in the development of myocardial insufficiency in experimental bacteremic septic shock. Moreover, the results strongly indicate that LTs may be of importance in compromising pulmonary gas exchange, partly by effects on the smaller airways.