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

Abstract

The study determined if head cooling would reduce the augmented increase in neural damage of global hemispheric hypoxic ischemia (GHHI) of prostaglandin E 2 (PGE 2) treated rats. Halothane anesthetized, male, Long–Evans rats (9–11 weeks of age), kept at 37°C colonically ( T c) had (a) systemic core (colonic, T c), temporalis muscle temperatures ipsilateral ( T ipsi) and contralateral ( T contra) to the side of right common carotid artery (RCCA) ligation, (b) mean arterial pressure (MAP) and (c) ipsilateral cortical capillary blood flow (CBF) measured simultaneously after intracerebroventricular (i.c.v.) injection (2.5 μl) 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°C cool air over the head region) occurred in one PGE 2 subgroup 10 min post-injection until the end of the hypoxic period. Icv-PGE 2 treated rats, maintained at 37°C (no head cooling) had increased T c, T ipsi, T contras and MAPs from respective pre-injection control values; this group showed increased ipsilateral 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 region of rats previously given PGE 2 decreased T ipsi and T contras from respective control temperatures but did not change MAP or CBF from respective pre-injection values. Hemispheric damage of the PGE 2 cooled group was reduced 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 fever induction) play a significant role in escalating the neural damage to global ischemia.