BETA-ENDORPHIN MAY BE A MEDIATOR OF APNEA INDUCED BY THE LARYNGEAL CHEMOREFLEX IN PIGLETS

To determine whether beta-endorphin is involved in the laryngeal chemo reflex, we initially injected 0.01-1 mg of beta-endorphin into the cis terna magna (i.c.m.) and registered the respiratory and cardiovascular patterns in 5-10-d-old piglets. From 0.1 to 1 mg of beta-endorphin i. c.m. induced a decrease in the minute volume, heart rate, and blood pr essure within 15 min. Within the next 30 min respiratory pauses accomp anied by blood pressure increases and reductions in heart rate develop ed, similar to the respiratory and cardiovascular pattern of the induc ed laryngeal chemoreflex. Based on these initial data, we decided to i nduce a laryngeal chemoreflex in piglets pretreated with 0.1 mg of bet a-endorphin i.c.m (n = 6), 0.2 mg of beta-endorphin i.c.m. (n = 6), 0. 1 mg of beta-endorphin i.c.m. and 100 mu g/kg naloxone i.v. (n = 6), 1 00 mu g/kg naloxone i.v. (n = 6), or water i.c.m. (n = 6). Because ele vated levels of hypoxanthine in the vitreous humor may indicate hypoxi a before death, we therefore measured the postmortem hypoxanthine leve ls in the vitreous humor. The laryngeal chemoreflex-induced apnea was shortened in the piglet group pretreated with water i.c.m and naloxone i.v. (p < 0.01) and in the piglet group pretreated with 0.1 mg of bet a-endorphin i.c.m and naloxone i.v. (p < 0.05), but not significantly prolonged in the piglet groups pretreated with 0.1 or 0.2 mg of beta-e ndorphin i.c.m. when compared with the piglets pretreated with water i .c.m. The hypoxanthine levels in the vitreous humor were found increas ed after death only in piglets pretreated with 0.2 mg of beta-endorphi n i.c.m. before the laryngeal chemoreflex was induced (p < 0.05). We c onclude that beta-endorphin is probably a mediator of apnea induced by the laryngeal chemoreflex in piglets.