title: The effect of head cooling on the physiological responses and resultant neural damage to global hemispheric hypoxic ischemia in prostaglandin E2 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 E2 (PGE2) treated rats. Halothane anesthetized, male, Long-Evans rats (9-11 weeks of age), kept at 37 degrees C colonically (Tc) had (a) systemic core (colonic, Tc), temporalis muscle temperatures ipsilateral (Tipsi) and contralateral (Tcontra) 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 microl) of sterile (SS) or 25 ng PGE2 then GHHI (35 min of 12% O2, balance N2 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 PGE2 subgroup 10 min post-injection until the end of the hypoxic period. Icv-PGE2 treated rats, maintained at 37 degrees C (no head cooling) had increased Tc, Tipsi, Tcontras 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 PGE2 decreased Tipsi and Tcontras from respective control temperatures but did not change MAP or CBF from respective pre-injection values. Hemispheric damage of the PGE2 cooled group was reduced from damage of non-cooled PGE2 treated rats and was similar to i.c.v.-SS treated rats. Results demonstrate that the heightened core temperatures induced by PGE2 administration (major endogenous mediator of bacterial fever induction) play a significant role in escalating the neural damage to global ischemia.
authors.affiliation: Department of Physiology and Saskatchewan Stroke Research Centre, University of Saskatchewan, Saskatoon, Saskatchewan, Canada. thornhill@sask.usask.ca
authors.forename: J
authors.initials: J
authors.lastname: Thornhill
authors.forename: J
authors.initials: J
authors.lastname: Asselin
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D001833:Body Temperature Regulation / Q000502:physiology*; D002560:Cerebrovascular Circulation / Q000502:physiology; D003080:Cold Temperature; D003342:Corpus Striatum / Q000098:blood supply / Q000502:physiology; D015232:Dinoprostone / Q000494:pharmacology*; D006257:Head / Q000502:physiology; D006624:Hippocampus / Q000098:blood supply / Q000502:physiology; D007036:Hypothermia, Induced; D000860:Hypoxia / Q000503:physiopathology / Q000628:therapy; D002534:Hypoxia, Brain / Q000503:physiopathology* / Q000628:therapy; D002546:Ischemic Attack, Transient / Q000503:physiopathology* / Q000628:therapy; D008297:Male; D008833:Microcirculation / Q000502:physiology; D019579:Neocortex / Q000098:blood supply / Q000502:physiology; D009474:Neurons / Q000187:drug effects / Q000502:physiology; D051381:Rats; D020318:Rats, Long-Evans; D013047:Specific Pathogen-Free Organisms; D013788:Thalamus / Q000098:blood supply / Q000502:physiology
chemical_list: D015232:Dinoprostone