OF LABORATORIES became interested in the role of endogenous opioids in circulatory shock soon after their initial discovery in 1975. This was based on the very attractive hypothesis that the accumulation of opioids during circulatory distress would suppress cardiovascular function contribute to the progressive circulatory collapse that often accompanies shock. Although do accumulate during hypotension (4, 11, 12, 14, 18, 22, 31), the strongest support for the hypothesis arose from the dramatic recovery of circulatory function in experimental circulatory shock following opiate receptor blockade (9, 19, 26, 30). Although cardiovascular indexes usually improved after administration of naloxone during shock, comparable improvements in survival were less consistent therapeutic interest in this approach diminished. Some of the effects of naloxone may be mediated by nonopioid mechanisms (16) . A NUMBER HZ082 0363-6135/95 $3.00 Copyright o 1995 The cardiovascular role of the opioids, including that in shock, remains unresolved. When they accumulate, may impair peripheral vascular compensations by opposing reflex vasomotor traffic through peripheral sympathetic ganglia (5, 8). Additional mechanisms may include reduced cardiac function through the prejunctional inhibition of norepinephrine release from cardiac sympathetic nerves (17) /or the interruption of sympathetic centrally (26). Although circulating are elevated during hypotension, chromatography
AJP - Heart and Circulatory Physiology – The American Physiological Society
Published: Dec 1, 1995
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