Adrenocorticotropin release is not involved in the nicotine-induced reversal of hemorrhagic shock in anesthetized rats.

In a model of volume-controlled hemorrhagic shock causing the death of all control animals within 30 min, the intravenous injection of nicotine produced a rapid, sustained and dose-dependent restoration of cardiovascular and respiratory functions, with 60 and 100% survival 2 h after the administration of 3 and 12 micrograms/kg, respectively. An effect similar to that of the highest dose of nicotine were obtained with the intravenous bolus injection of ACTH(1-24) at the dose of 160 micrograms/kg. However, the ACTH plasma levels of hemorrhage-shocked rats treated with nicotine was not different from that of hemorrhage-shocked rats treated with saline, thus excluding the possibility that nicotine-induced shock reversal may be due to the massive release of ACTH. Since in rats pretreated with cycloheximide at a dose (20 mg/kg intraperitoneally) causing an 82% inhibition of protein synthesis, and then bled to hemorrhagic shock, the effect of nicotine was greatly reduced (only the dose of 50 micrograms/kg producing 100% survival 2 h after treatment), protein synthesis, however, seems to be important for the effect of nicotine in hemorrhagic shock, at least at the lowest doses.