Sepsis and septic shock represent the most common cause of death in ICU patients. It is very likely that much of the morbidity and mortality associated with sepsis results from endogenous mediators released by host defense systems in response to bacterial invasion. One such host defense system include the endogenous cytokines. Interleukin-1, one such cytokine, has been speculated to play an important role in sepsis induced tissue injury and organ dysfunction. We have evaluated the effects of interleukin-1 on cardiopulmonary function in a chronically tracheotomized canine model. Purpose bred beagles were instrumented under local anesthesia with femoral and pulmonary arterial catheters. Measurements of pulmonary gas exchange and systemic and pulmonary hemodynamics, as well as bronchoalveolar lavage, were performed for seven days before, on the day of, and 1,3 6,8, and 21 days after IL-1 infusion. Although IL-1 was associated with a marked alveoli neutrophil influx, this influx was not associated with abnormalities of gas exchange or of pulmonary hemodynamics. L-1 was also not associated with any significant changes in systemic hemodynamics. Other mediators, possibly acting with IL-1 appear necessary for the full expression of sepsis induced cardiopulmonary dysfunction.
