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  • Title: Respiratory control of sympathetic nerve activity during naloxone-precipitated morphine withdrawal in rats.
    Author: Baraban SC, Stornetta RL, Guyenet PG.
    Journal: J Pharmacol Exp Ther; 1993 Apr; 265(1):89-95. PubMed ID: 8474034.
    Abstract:
    In this study, we describe and compare the changes in phrenic nerve discharge and vasomotor sympathetic output produced by 1) acute administration of morphine in naive rats and 2) naloxone-precipitated withdrawal in morphine-dependent rats. Lumbar or splanchnic sympathetic nerve discharge and phrenic nerve discharge were recorded along with mean arterial pressure and end-expiratory CO2 in vagotomized, urethane-anesthetized, paralyzed and artificially ventilated rats. Acute injection of morphine (1 and 5 mg/kg, i.v.) reduced resting mean arterial pressure, resting phrenic nerve discharge amplitude, the sympathetic baroreflex and the central respiratory drive of sympathetic nerve discharge. Subsequent administration of naloxone (1 mg/kg) reversed all cardiorespiratory effects of morphine and produced an overshoot, suggesting acute withdrawal. Morphine-dependent rats displayed a prolonged central inspiratory phase and a higher threshold for apnea. Naloxone-induced withdrawal was associated with an increase of mean arterial pressure and phrenic nerve discharge amplitude and a large reduction in the inspiratory phase. Withdrawal produced three distinct effects on sympathetic nerve discharge: 1) sensitization of the baroreflex, 2) large increase in the central respiratory drive and 3) selective increase in a respiratory-independent component of the splanchnic sympathetic outflow. It is concluded that the increase in central respiratory drive is a significant component of the sympathoactivation associated with naloxone-induced withdrawal.
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