Gregorowicz К., Kosiński S., Traczyk W. Z.: Alteration of brain stem auditory evoked potentials after intracerebroventricular administration of met-enkephalin in rabbits. Acta Physiol. Pol. 1990, 41(1-3): 63-70. Brainstem auditory evoked potentials (BAEPs) were elicited by binaural click stimulation and recorded from the rabbits with chronically implanted electrodes and a cannula for intracerebroventricular injection (i.c.v.). 4000 BAEPs were averaged off line. The registration was carried out before and after i.c.v. injection of met-enkephalin (2.5 or 25 nmol), naloxon (20 μg ), or i.v. injection of morphine (1.0, 2.0, 5.0 mg/kg b.w.). Enkephalin caused shortening of interpeak latency time, naloxon caused its lengthening, while the effect of morphine was not unidirectional. Enkephalin caused increase in the surface area below the negative peaks located in the range of 4.5-7.5 ms from the first positive peak, naloxon caused its decrease while the effect of morphine was also in this respect not unidirectional. It is concluded that opiate receptors are involved in the modulation of the auditory brainstem responses.
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Orexin A influences the central cardiovascular regulation, since after intracerebroventricular (icv) administration it evokes short-lasting increases in mean arterial pressure (MAP) and heart rate (HR) in normotensive animals. The aim of the present study was to examine haemodynamic effects of orexin A in haemorrhage-shocked rats. Experiments were carried out in anaesthetized Wistar rats subjected for a critical irreversible haemorrhagic hypotension of 20-25 mmHg, which resulted in the death of all saline icv-treated control animals within 30 min. Orexin A (0.5-1.5 nmol; icv) administered at 5 min of critical hypotension evoked dose-dependent long-lasting increases in MAP, HR and renal, mesenteric and hindquarters blood flows, with a 100% survival of 2 h after treatment (1.5 nmol; icv). Changes in MAP and peripheral haemodynamics were inhibited by intravenous pretreatment with alpha1- and alpha2-adrenoceptor antagonists prazosin (0.5 mg/kg) and yohimbine (1.0 mg/kg), respectively. Moreover, both antagonists significantly decreased the survival rate to 16.6 and 33.3% (P<0.05 vs. orexin A [1.5 nmol]-treated group). In contrast, ß-adrenoceptor antagonist propranolol (1.0 mg/kg) completely blocked orexin A-induced HR changes, without influence on MAP, peripheral blood flows and the survival rate. Therefore, we conclude that centrally acting orexin A evokes the resuscitating effect in haemorrhage-shocked rats due to the activation of the sympathetic nervous system.