Systemic inflammation is a leading cause of mortality and morbidity in both human and equine intensive care patients. This systemic inflammatory response may be due to insult from bacterial, viral, fungal or parasitic invasion or from trauma or hypoxemia. Local and systemic release of a wide variety of endogenous pro-inflammatory mediators results in activation of the innate immune system in order to resolve the insult. In sepsis this initial appropriate host response becomes amplified and deregulated leading to refractory hypotension and multiple organ dysfunction. The exact incidence of sepsis (SIRS due to bacterial infection) has not been reported in the equine literature (Roy 2004). Since early recognition and treatment of sepsis are associated with improved outcome the search for markers to accurately predict presence of sepsis and likelihood of survival continues. The serum concentration of both procalcitonin and its related molecule CGRP have been documented to increase in humans with SIRS, yet no literature exists as to the production or role of CGRP in equine patients with SIRS.

This study showed that equine CGRP was produced in detectable quantities by healthy adult horses and neonatal foals less than two weeks of age using a rat á-CGRP ELISA. The low percentage recovery of CGRP from samples and the high lower limit of detection for the assay prevented establishment of a normal concentration range of CGRP in healthy horses. In both adult horses and foals with documented SIRS, CGRP concentrations were significantly increased at time of presentation to the hospital (p<0.0002, p<0.003 respectively). A trend towards increased serum CGRP concentration was present in anaesethized horses exposed to endotoxin, but this was not statistically significant (p< 0.067).