LONG-TERM EXPOSURE OF HUMAN BLOOD-VESSELS TO HIV GP120, MORPHINE, ANDANANDAMIDE INCREASES ENDOTHELIAL ADHESION OF MONOCYTES - UNCOUPLING OF NITRIC-OXIDE RELEASE

Acute exposure of human saphenous vein or internal thoracic artery end othelium to either morphine [27.4 +/- 3.7 and 35.4 +/- 4.1 nM nitric o xide (NO), respectively] or anandamide (18.3 +/- 2.2 and 24.3 +/- 3.0 nM,, respectively) results in NO release, whereas exposure to the huma n immunodeficiency virus envelope protein gp120 does not. After the sh ort-term exposure of the vessel endothelium, monocyte adherence is dim inished with morphine and anandamide treatment (jointly by -80%), wher eas it is enhanced with that of gp120 (similar to 40%), indicating tha t gp120 enhances the ability of the endothelium to adhere monocytes. L ong-term or continuous exposure of the endothelia to all agents result s in a significant enhancement of monocyte adherence (p < 0.05), which is further increased when exposed to either morphine and anandamide p lus gp120. This is caused by a desensitization of the endothelium to f urther NO release after the initial exposure to either anandamide or m orphine. The results serve to indicate that in individuals abusing opi ates and or cannabinoids, a tissue [i.e., central nervous system (CNS) ] viral load may he higher, and acquired immunodeficiency syndrome (AI DS) may progress more rapidly because monocyte adherence and mobility is significantly increased, indicating a higher level of transmembrane migration.