Accession Number : ADA181882
Title : Neuropeptides in Experimental Head Injury.
Descriptive Note : Annual rept. 1 Mar 85-28 Feb 86,
Corporate Author : VETERANS ADMINISTRATION MEDICAL CENTER SAN FRANCISCO CA
Personal Author(s) : Faden,Alan I ; McIntosh end,Tracy K
PDF Url : ADA181882
Report Date : 28 Feb 1986
Pagination or Media Count : 34
Abstract : Much of the damage resulting from ischemic or traumatic insults to the central nervous system (CNS) appears to result from secondary injury mechanisms relating to the release of endogenous factors. Endogenous opioids may represent one such class of pathophysiological factors. The studies covered under the present contract examine the potential pathophysiological role endogenous opioids and their mediated changes following traumatic brain injury in both cats and rats. Utilizing a fluid-percussion device manufactured for us by Medical College of Virginia, we have evaluate the effects of graded levels of injury on outcome measures, including mean arterial pressure, intracranial pressure, electroencephalographic (EEG) activity (including the Fast-Fourier transformed EEG), and regional cerebral blood flow in the cat. In studies conducted during the present Army contract we have compared the effectiveness of the opiate antagonist WIN44, 441-3, which has enhanced activity at the kappa-opiate receptor, with its inactive stereoisomer WIN44, 441-2 and saline. The results suggest that endogenous opioids contribute to the pathophysiology of head injury and indicate that opiate antagonists with increased activity at Kappa sites may be effective in the treatment of low flow states associated with acute head injury.
Descriptors : *HEAD(ANATOMY), *WOUNDS AND INJURIES, *BRAIN, *OPIUM ALKALOIDS, *PHARMACOLOGICAL ANTAGONISTS, CATS, PATHOLOGY, PHYSIOLOGY, INTERNAL, PRESSURE, SKULL, ARMY, CONTRACTS, CENTRAL NERVOUS SYSTEM, ELECTROENCEPHALOGRAPHY, MEAN, NERVES, PEPTIDES, NEUROCHEMISTRY, BLOOD CIRCULATION, CEREBRUM, RATS, SECONDARY
Subject Categories : Biochemistry
Medicine and Medical Research
Distribution Statement : APPROVED FOR PUBLIC RELEASE