Rectal temperature and prostaglandin E-2 increase in cerebrospinal fluid of conscious rabbits after intracerebroventricular injection of hemoglobin

Fever accompanies subarachnoid hemorrhage (SAH) in the majority of patients . In a previous study, hemoglobin (Mb) was shown to catalyze in vitro, unde r aerobic conditions, the conversion of arachidonic acid to prostaglandin E -2 (PGE(2)) and prostaglandin F-2 alpha. The aim of the present work was to assess whether this pathway also operates in vivo and to provide a mechani sm to explain post-SAM fever. To this end, PGE(2) concentration was determi ned in cerebrospinal fluid (CSF) of conscious rabbits chronically cannulate d in the lateral ventricle and cisterna magna, following intracerebroventri cular (i.c.v.) injection of 10 mu g or 100 mu g of commercial rabbit bicrys tallized Hb as a model of SAH. Before i.c.v. injection, Mb solutions were f iltered on a polimixin-B column to remove substantially, by over 90%, endot oxin-like substances. Results show that in nine rabbits injection of 10 mu g Mb did not significantly modify body temperature or significantly alter C SF PGE(2) content. On the contrary, in nine rabbits, injection of 100 mu g Hb produced a significant increase in core temperature which was accompanie d by a significant increase in CSF PGE(2). When data related to these two p arameters from the 9 control and 18 Mb-treated rabbits were analyzed as a s ingle group, a linear, positive, and highly significant correlation was fou nd. These findings indicate that, once Mb is released into the subarachnoid space during SAH, it enhances CSF PGE(2) content and elicits hyperthermia, thus offering an explanation for the fever that is an aggravating conditio n in most SAH patients.