Temperature and hemodynamic changes associated with increased neural damage to global hemispheric hypoxic ischemia by prior prostaglandin E2,D2and F2αadministration

Abstract

Experiments compared the hemispheric neural damage resulting from global hemispheric hypoxic ischemia (GHHI, ligation of right common carotid artery plus 35min of 12% O2) in groups of anesthetized, male Long Evans rats, 9–10 weeks of age, kept at 37°C, and previously given an intracerebroventricular (i.c.v., 2.5μl) injection of 28 or 70 pmoles of PGE2, PGF2αor PGD2or sterile saline (SS) 30 min beforehand. Mean arterial pressure (MAP), ipsilateral cortical capillary blood flow (CBF), colonic (Tc), ipsilateral (Tipsi) and contralateral (Tcontra), temporalis muscle temperatures were measured before, during and for 15 min after GHHI. Necrotic neural damage was assessed 7 days post-GHHI. All groups given GHHI + PGs showed increased ipsilateral hemispheric damage to GHHI especially due to enhanced neocortical damage, compared to the saline control group given the same insult. PGD2was the most potent PG to cause further damage to the global insult. Tc, Tipsi, Tcontraand MAP increased following the i.c.v. injection of PGE2. Icv PGF2αtransiently decreased MAP, PGD2tended to decrease cerebral blood flow and neither evoked changes in temperature compared to respective pre-injection control values. Results demonstrate increased neural damage to GHHI with prior icv PGE2, PGF2αor PGD2administration.