Spath J A, Blum P S
Adv Shock Res. 1983;10:111-20.
Anesthetized cats were subjected to hemorrhage to a mean arterial blood pressure of 40 +/- 1 mmHg. After 60 min of oligemia pressure regulation was stopped, and naloxone hydrochloride or an equivalent volume of 0.9% saline was given intravenously as a bolus (2 mg x kg-1) followed by a continuous infusion (2 mg x kg-1 x hr-1). In other cats supraspinal systems were ablated by functional decapitation (FD) or serotonergic systems were ablated by IP injection of parachlorophenylalanine (pCPA, 300 mg/kg, 48 h prior to hemorrhage). Cats subjected to ablation of supraspinal or serotonergic neurons showed a distinct pressor response after naloxone. Although cats with intact neuronal systems failed to show a distinct pressor response to naloxone, the arterial pressures of these cats were significantly greater than hemorrhaged cats given saline (P less than 0.05, unpaired t). Our results suggest that a supraspinal system and a serotonergic system can interact to limit the pressor response to naloxone in hemorrhagic shock.