Naloxone and haemorrhagic hypotension in rats. Evidence against sympathetic nervous system as the primary mediator of improved cardiovascular haemodynamics.

Release of endogenous opiate-like substances seem to occur in different forms of stress. Earlier studies have shown that the opiate antagonist, naloxone, has a positive effect on cardiac performance and blood pressure in animals with haemorrhagic shock. In the present study, we have examined the involvement of the sympathetic nervous system in this response. Two groups of anaesthetized normotensive Wistar-Kyoto rats were studied. Both groups were bled rapidly (about 5 min) down to an arterial pressure of 50 mmHg and were kept at that level for 30 min. At the end of the 30-min bleeding period, naloxone 1, 2, or 5 mg kg-1 was injected i.v. in a small volume of saline. In the first group of rats (n = 6), the aortic pressure was kept constant at 50 mmHg by further bleedings after naloxone. In the other group (n = 7), the arterial pressure was allowed to rise after naloxone. As reported earlier, haemorrhagic hypotension caused a pronounced inhibition of renal sympathetic nerve activity. Naloxone injected after 30 min of hypotension caused an immediate rise in blood pressure, followed 1-2 min later by a rise in sympathetic nerve activity (SNA). In animals in which pressure was held constant by further bleeding after naloxone, only small and insignificant changes in SNA were observed. The conclusions are the following: injection of naloxone increases blood pressure in rats exposed to severe haemorrhage (Faden & Holiday 1979). The rise in aortic pressure is followed 1-2 min later by a rise in SNA.(ABSTRACT TRUNCATED AT 250 WORDS)