Co-Authors:
Feuerstein, G., Neurobiology Research Unit, Uniformed Services, University of the Health Sciences, Bethesda, MD 20814, United States
Lux Jr., W.E., Neurobiology Research Unit, Uniformed Services, University of the Health Sciences, Bethesda, MD 20814, United States
Snyder, F., Neurobiology Research Unit, Uniformed Services, University of the Health Sciences, Bethesda, MD 20814, United States
Ezra, D.
Faden, A.I.
Abstract:
Platelet-activating factor (PAF), a vasoactive phospholipid implicated in anaphylactic reactions, causes severe hypotension in experimental animals that is highly resistant to pharmacological therapy. In the present studies, we showed that PAF (1 nmol/600 g body weight, IV) produced profound hypotension in unanesthetized guinea pigs that was promptly and completely reversed by thyrotropin-releasing hormone (TRH) (2 mg/kg, IV) or by the synthetic TRH analog MK771 (2 mg/kg, IV). TRH also reversed this hypotension when administered intracerebroventricularly (ICV) at a dose (0.02 mg/kg) that was systemically ineffective. The opiate receptor antagonist naloxone (5 mg/kg) was less effective than TRH in reversing the cardiovascular consequences of PAF administration. These data suggest that TRH reverses PAF-induced shock through central receptor-mediated mechanisms. This therapeutic action of TRH may partially account for the beneficial cardiovascular effects of this peptide in anaphylactic shock.
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