Systemic and local surfactant protein a is altered in a model of multiple organ dysfunction syndrome (MODS)

Introduction: MODS is a leading cause of morbidity and mortality in ICU patients. A disturbance in the body's inflammatory/ antiinflammatory balance is thought to be at the root of the pathogenesis of MODS. Recently we have modified an established model of MODS by decreasing the dose of intraperitoneal (IP zymosan and have demonstrated decreased renal and mesenteric blood flow without the mortality of higher doses (CCM, 26, 1S, 1999). Inflammatory changes that accompany this new model are unknown. The collecting [including surfactant proteins A (SP-A) and D (SP-D) and mannose binding protein] are involved in innate immunity. Their role has not been explored in MODS. We hypothesized that the collectin production would be altered during the development of MODS. Methods: On day #0, rats (n=18) received either zymosan (0.25mg/g of body weight)or saline IP. They also received saline (20 cc/kg) to counter zymosan's hypovolemic effects. Serum, peritoneal fluid, and whole organs were collected from 3 rats in each group at days #1,#5, and #12. SP-A was determined by ELISA, Results: Serum and peritoneal SP-A was significantly higher in zymosan-treated rats on day #12 (p=0.03) when compared to controls. Peritoneal SP-A was significantly lower on days #1 (p=0.02) and #5 (p=0.02), and greater on day #12 (p>0.01) when compared with controls. Conclusions: SP-A is altered both early and late in serum and peritoneum in this animal model of MODS. The collecting may be central to the late onset development of MODS. Further Study is ongoing to more completely define the kinetics of these alterations in SP-A, as well as changes in SP-A and other collectin expression in whole organs.