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September 7, 1984

Opiate Antagonists and Thyrotropin-Releasing Hormone: I. Potential Role in the Treatment of Shock

Author Affiliations

From the Neurobiology Research Unit, Uniformed Services University of the Health Sciences, Bethesda, Md. Dr Faden is now with the Department of Neurology, Veterans Administration Medical Center, San Francisco.

JAMA. 1984;252(9):1177-1180. doi:10.1001/jama.1984.03350090053022

DURING the past decade, a large number of peptides have been found in the brain and spinal cord. These neuropeptides appear to act as transmitters or modulators and, in many cases, have been found to be colocalized in synaptic terminals with "classic" neurotransmitters. More specific physiological and pathophysiological roles for these substances have been suggested, ie, endogenous opioids (endorphins) in pain transmission and autonomic regulation. In 1978, J. W. Holaday and I proposed that endorphins were major factors contributing to the pathophysiology of shock and subsequently demonstrated that administration of opiate receptor antagonists, like naloxone hydrochloride, significantly improved physiological variables and survival in a variety of experimental shock models.1-3 In 1981, we showed that large pharmacologic doses of thyrotropin-releasing hormone (TRH), possibly by acting as a "physiological" antagonist of endorphin systems, also significantly improved cardiovascular function and survival in experimental shock.4 Since these initial reports, a large body of