Abstract
The possible involvement of opiate receptors in the cardiovascular depression associated with hypovolemic shock was investigated. Opiate receptor blockade with naltrexone increased mean arterial pressure, cardiac output, stroke volume and left ventricular contractility in dogs bled to a mean arterial pressure of 45 mm Hg. Naltrexone also increased survival rate. At high doses, naltrexone adversely affected cardiac performance which may outweigh its advantages of greater potency and putatively longer action than naloxone, at least in the dog. Similar actions with another opiate antagonist gives further proof for endogenous opiate involvement in the cardiovascular pathophysiology of hypovolemic shock.
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