Naloxone or TRH fails to improve neurologic deficits in gerbil models of "stroke".
The effects of naloxone or thyrotropin releasing hormone (TRH) upon neurologic outcome were evaluated in gerbil models of cerebral ischemia. Following temporary bilateral carotid occlusion, hypotension was transiently reversed by these endorphin antagonists. However, neither drug altered time to awaken, time to death, or the severity of neurologic signs (ptosis, movement, retracted paws, circling, righting reflexes, seizures, or opisthotonus) when evaluated by a blinded rater. Hot plate escape and roto-rod performance were also unaltered by naloxone or TRH; TRH, but not naloxone, increased respiratory rates. Thus, the transient improvement of cardiorespiratory function produced by these drugs is unrelated to the morbidity and mortality associated with temporary cerebral ischemia in the gerbil. Additional studies evaluating the effects of naloxone or TRH upon neurologic outcome following permanent unilateral carotid occlusion also failed to show any therapeutic effects of these drugs. Both morphine and TRH exacerbated the effects of ischemia. Of gerbils which developed neurologic impairment, the deficit was usually ipsilateral to the occluded carotid. Collectively, these results indicate that neither naloxone nor TRH prevents ischemic deficits in the gerbil. Further studies with different cerebral ischemia models in other species are required to clarify the possible therapeutic effects of these drugs in experimental stroke.
D000818:Animals; D001157:Arterial Occlusive Diseases / Q000188:drug therapy; D002545:Brain Ischemia / Q000188:drug therapy*; D002340:Carotid Artery Diseases / Q000188:drug therapy; D004195:Disease Models, Animal; D005849:Gerbillinae; D008297:Male; D009043:Motor Activity / Q000187:drug effects; D009270:Naloxone / Q000494:pharmacology / Q000627:therapeutic use*; D013973:Thyrotropin-Releasing Hormone / Q000494:pharmacology / Q000627:therapeutic use*
D009270:Naloxone; D013973:Thyrotropin-Releasing Hormone