1. Capsaicin prevents the adrenocorticotropin-induced improvement of cardiovascular function and survival in hemorrhage-shocked rats.
- Author
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Guarini S, Bazzani C, Tagliavini S, Bertolini A, and Ferrari W
- Subjects
- Adrenocorticotropic Hormone therapeutic use, Afferent Pathways drug effects, Animals, Capsaicin toxicity, Cosyntropin therapeutic use, Endorphins physiology, Female, Male, Neurons, Afferent drug effects, Rats, Rats, Wistar, Shock, Hemorrhagic drug therapy, Substance P antagonists & inhibitors, Substance P pharmacology, Substance P therapeutic use, Survival Rate, Adrenocorticotropic Hormone antagonists & inhibitors, Capsaicin pharmacology, Cosyntropin antagonists & inhibitors, Hemodynamics drug effects, Neurons, Afferent physiology, Recombinant Proteins, Shock, Hemorrhagic physiopathology, Substance P analogs & derivatives, Substance P physiology
- Abstract
A volume-controlled hemorrhagic shock was produced in anesthetized rats by intermittent bleeding from an iliac vein over a period of 20-30 min, until the carotid mean arterial pressure (MAP) stabilized around 20-24 mmHg. In this condition, which caused the death of all saline-treated animals within 25-30 min, the intravenous (i.v.) bolus injection of the adrenocorticotropin fragment 1-24 (ACTH(1-24)) at a dose of 160 micrograms/kg promptly restored MAP, as well as pulse pressure, heart rate and respiratory function, and greatly prolonged the survival time. Capsaicin (125 mg/kg cumulatively, s.c., 1 week before) completely prevented the anti-shock effect of ACTH(1-24), which, on the other hand, was shared by i.v. [Nle11]-substance P (SP) (200-300 micrograms/kg). Finally the SP-antagonist [D-Arg1,D-Pro2,D-Trp7,9,Leu11]-SP prevented the effect of ACTH(1-24). These results suggest that SP-containing nerve fibers are required for the effect of ACTH in hemorrhagic shock.
- Published
- 1992
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