The effect of head cooling on the physiological responses and resultant neural damage to global hemispheric hypoxic ischemia in prostaglandin E-2 treated rats

The study determined if head cooling would reduce the augmented increase in neural damage of global hemispheric hypoxic ischemia (GHHI) of prostagland in E-2 (PGE(2)) treated rats. Halothane anesthetized, male, Long-Evans rats (9-11 weeks of age), kept at 37 degrees C colonically (T-c) had (a) system ic core (colonic, T-c), temporalis muscle temperatures ipsilateral (T-ipsi) and contralateral (T-contra) to the side of right common carotid artery (R CCA) ligation, (b) mean arterial pressure (MAP) and (c) ipsilateral cortica l capillary blood flow (CBF) measured simultaneously after intracerebrovent ricular (i.c.v.) injection (2.5 mu l) of sterile (SS) or 25 ng PGE(2) then GHHI (35 min of 12% O-2, balance N-2 after RCCA ligation) followed by a 10 min normoxic recovery period. Head cooling (10 degrees C cool air over the head region) occurred in one PGE(2) subgroup 10 min post-injection until th e end of the hypoxic period. IcV-PGE(2) treated rats, maintained at 37 degr ees C (no head cooling) had increased T-c, T-ipsi, T(contra)s and MAPs from respective pre-injection control values; this group showed increased ipsil ateral hemispheric neural damage to GHHI assessed 7 days later, compared to i.c.v.-SS treated group given the same GHHI insult. Cooling the head regio n of rats previously given PGE(2) decreased T-ipsi and T(contra)s from resp ective control temperatures but did not change MAP or CBF from respective p re-injection values. Hemispheric damage of the PGE(2) cooled group was redu ced from damage of non-cooled PGE(2) treated rats and was similar to i.c.v. -SS treated rats. Results demonstrate that the heightened core temperatures induced by PGE(2) administration (major endogenous mediator of bacterial f ever induction) play a significant role in escalating the neural damage to global ischemia. (C) 1999 Elsevier Science B.V. All rights reserved.