beta-Endorphin central depression of respiration and circulation

Abstract

.beta.-Endorphin was injected into CSF of lightly anesthetized dogs. Its effects on ventilation (V), tidal volume (VT), respiratory frequency (f), preinspiratory occlusion pressure (P500) and respiratory timing of unoccluded and occluded breaths were studied during CO2 rebreathing. Blood pressure and heart rate (HR) were monitored throughout the study. .beta.-Endorphin produced early (.apprx. 15 min), but temporary depression of VT-PCO2 and P500-PCO2 responses; progression hypoventilation during spontaneous breathing and progressive depression of .ovrhdot.V-PCO2 and f-PCO2 responses, which were maximal at about 7 min, followed by gradual recovery; and progressive hypotension and bradycardia starting at .apprx. 15 min and reaching maximal effect at about 105 min. Increased expiratory (TE) accounted for the changes in f. TE increased in unoccluded breaths and during preinspiratory and inflation occlusion. After vagotomy .beta.-endorphin produced insignificant effect on f, TE and HR. Naloxone itself increased P500-PCO2 response; when given during .beta.-endorphin effect, it reversed the hypotension, bradycardia, .ovrhdot.V-PCO2 and f-PCO2 responses and facilitated the P500-PCO2 and VT-PCO2 responses. .beta.-Endorphin effect is evidently produced by depression of specific central cardiovascular and respiratory control units and facilitation of central vagal projections.