Opiate action in the pulmonary circulation.
To gain insight into the mechanisms underlying the association between acute pulmonary edema and narcotic abuse, the direct action of morphine was examined in isolated, perfused left lower lobe (LLL) preparations in dogs and cats. Morphine sulphate injected (0.6 mg/kg) into the pulmonary artery of the LLL increased the pulmonary vascular resistance (PVR) by about 100% in both species. The increase in PVR was primarily due to constriction of the veins, as determined with the arterial and venous occlusion technique. The increase in PVR with morphine injection was unaffected by alpha-adrenergic antagonists, but was reversed by chlorpheniramine, a histamine H1-receptor antagonist. Pretreatment, but not post-treatment with the opiate antagonist, naloxone, blocked the effect of morphine on PVR. Thus, the rapid administration of morphine produces pulmonary venoconstriction via histamine release from the lung, and the latter may account for the well-documented association between acute pulmonary edema and narcotic abuse.[1]References
- Opiate action in the pulmonary circulation. Hakim, T.S., Grunstein, M.M., Michel, R.P. Pulmonary pharmacology. (1992) [Pubmed]
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