1. Role of neuronal and vascular Ca(2+)-channels in the ACTH-induced reversal of haemorrhagic shock
- Author
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Alfio Bertolini, Carla Bazzani, and Salvatore Guarini
- Subjects
Male ,medicine.medical_specialty ,Nicardipine ,Blood Pressure ,Shock, Hemorrhagic ,Muscle, Smooth, Vascular ,nicardipine ,Adrenocorticotropic Hormone ,omega-Conotoxin GVIA ,Internal medicine ,medicine ,Animals ,Channel blocker ,Respiratory function ,Rats, Wistar ,Injections, Intraventricular ,Pharmacology ,Ca2+-channel blockers ,Neurons ,Voltage-dependent calcium channel ,Dose-Response Relationship, Drug ,business.industry ,omega-conotoxin ,Respiration ,Shock ,Omega-Conotoxins ,Calcium Channel Blockers ,Pulse pressure ,ACTH ,Rats ,Blood pressure ,Endocrinology ,Shock (circulatory) ,Injections, Intravenous ,haemorrhagic shock ,haemorrhage ,Ca2+-channels ,Female ,Calcium Channels ,medicine.symptom ,business ,Peptides ,medicine.drug ,Research Article - Abstract
1. In a rat model of volume-controlled haemorrhagic shock causing the death of all control (saline-treated) animals within 30 min, the intravenous (i.v.) bolus injection of ACTH-(1-24) at a dose of 160 micrograms kg-1 produced an impressive and sustained restoration of arterial pressure, pulse pressure and respiratory function, with 100% survival at the end of the observation period (2 h). 2. Both intracerebroventricular (i.c.v., 0.015-0.06 microgram kg-1) and i.v. (5 micrograms kg-1) pretreatment with the N-calcium channel blocker, omega-conotoxin GVIA, and i.v. (but not i.c.v.) pretreatment with the L-calcium channel blocker, nicardipine (125-500 micrograms kg-1) dose-dependently prevented the ACTH-induced shock reversal. 3. These results further indicate that the effect of ACTH in haemorrhagic shock may involve a neuronal link and the eventual restoration of vascular tone mediated by N- and L-type calcium channels, respectively.
- Published
- 1993