摘要
Objective: To study the effect of intracerebroventricular administration of interferon (IFN-α) on the splenic sympathetic nerve activity. Methods: IFN-α (3×104 U/rat ) was microinjected into the third cerebroven-tricle of urethane and α-chloralose anesthetized rats. Electrical activity of the splenic nerve. body temperature and blood pressure were determined simultaneously. Results: Intracerebroventricular administration of IFN-α caused amarked and long term (>120 min) increase in the splenic nerve activity, which could be reversed by naloxonetreatment. No changes in blood pressure and body temperature. which could alter the sympathetic nerve actlvity by reflex. were observed during IFN-α and naloxone treatment. Naloxone intravenous injection alone had no effecton the splenic nerve activity. Conclusion: IFN-α in the brain can activate the splenic sympathetic nerve, and thisaction is, in some way, mediated by the opioid receptor.
Objective: To study the effect of intracerebroventricular administration of interferon (IFN-α) on the splenic sympathetic nerve activity. Methods: IFN-α (3×104 U/rat ) was microinjected into the third cerebroven-tricle of urethane and α-chloralose anesthetized rats. Electrical activity of the splenic nerve. body temperature and blood pressure were determined simultaneously. Results: Intracerebroventricular administration of IFN-α caused amarked and long term (>120 min) increase in the splenic nerve activity, which could be reversed by naloxonetreatment. No changes in blood pressure and body temperature. which could alter the sympathetic nerve actlvity by reflex. were observed during IFN-α and naloxone treatment. Naloxone intravenous injection alone had no effecton the splenic nerve activity. Conclusion: IFN-α in the brain can activate the splenic sympathetic nerve, and thisaction is, in some way, mediated by the opioid receptor.
