To determine whether β-endorphin is involved in the laryngeal chemoreflex. we initially injected 0.01 1 mg of β-endorphin into the cisterna magna (i.c.m.) and registered the respiralory and cardiovascular patterns in 5–10-d-old piglets. From 0.1 to 1 mg of β-cndorphin i.c.m. induced a decrease in the minute volume, hearl rate, and blood pressure within 15 min. Within the next 30 min respiratory pauses accompanied by blood pressure increases and reductions in heart ratc developed, similar to the respiratory and cardiovascular pattern of the induced laryngcal chemoreflex. Based on these initial data, we decided to induce a laryngeal chemoreflex in piglets pretreated with 0.1 mg of β-endorphin i.c.m (n= 6), 0.2 mg of β-endorphin i.c.m. (n= 6), 0.1 mg of β-endorphin i.c.m. and 100 μg/kg naloxone i.v. (n= 6), 100 μg/kg naloxonc i.v. (n- 6). or water i.c.m. (n= 6). Because clevated levels of hypoxanthine in the vitreous humor may indicate hypoxia before death, we therefore measured the postmortem hypoxanthine levels in the vitreous humor. The laryngeal chemoreflex-induced apnea was shortenec in the piglet group pretreated with water i.c.m and naloxone i.v. (p< 0.01) and in the piglet group pictreated with 0.1 mg of β-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 β-endorphin i.c.m. when compared with the piglcts prerreated with water i.c.m. The hypoxanthine levels in the vitreous humor were found increased after death only in piglets prctreated with 0.2 mg of β-endorphin i.c.m. before the laryngeal chemorefltex was induced (p< 0.05). We conclude that β-cndorphin is probably a mediator of apnca induced by the laryngenl chemoreflex in piglets.