PubMed · 5015286
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1972-03-11. Studies on orgasm.. https://pubmed.ncbi.nlm.nih.gov/5015286/
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OBJECTIVES: This study sought to assess endothelium-dependent vasorelaxation in long-term users of cocaine. BACKGROUND: Cocaine use has been associated with myocardial infarction, stroke and intestinal infarction. Previously demonstrated effects of the drug, including increased heart rate and blood pressure and increased vascular tone, do not explain the sporadic nature of these vascular events or the occurrence of ischemia remote from acute administration. Abnormal endothelial function could contribute to focal vasospasm and thrombosis and predispose to premature atherosclerosis, all of which have been demonstrated in cocaine users with myocardial infarction. METHODS: Using plethysmography, we studied the change in forearm blood flow in response to intraarterial acetylcholine and nitroprusside in 10 long-term cocaine users and 13 control subjects of similar age who had not used cocaine; sample size was based on a 70% power to detect a 20% reduction in flow with acetylcholine between subjects and control subjects. Using graded doses of intracoronary acetylcholine (from 10(-9) to 10(-6) mol/liter), we studied a second group of 10 cocaine users with angiographically normal or near-normal arteries. RESULTS: Mean forearm blood flow during acetylcholine infusion was significantly lower in cocaine users than in control subjects (p = 0.02). During nitroprusside infusion, there was no difference (p = 0.2) between cocaine users and control subjects. Cigarette smoking did not explain the differences between cocaine users and control subjects. Acetylcholine elicited coronary vasoconstriction in 8 of 10 subjects. CONCLUSIONS: We conclude that endothelium-dependent vasorelaxation is impaired in long-term users of cocaine.
OBJECTIVES: This study sought to examine nitric oxide-mediated regulation of epicardial coronary arterial tone in cigarette smokers. BACKGROUND: Cigarette smoking is a major risk factor for coronary artery disease and is highly prevalent in patients with coronary spastic angina. Long-term exposure to cigarette smoking has been recently reported to suppress endothelium-dependent arterial relaxation in vivo humans. METHODS: Responses of epicardial coronary artery diameter to single or combined infusion of acetylcholine and NG-monomethyl-L-arginine (L-NMMA) into the left main coronary artery were examined in 11 current smokers and 17 nonsmokers using quantitative coronary angiography. RESULTS: Acetylcholine dilated one-third of the proximal segments and most of the distal segments of coronary arteries in nonsmokers, whereas it constricted most of the proximal and distal segments in smokers. L-NMMA decreased the basal diameter of coronary arteries in nonsmokers but had minimal effect on the basal diameter in smokers. L-NMMA abolished the dilator response to acetylcholine in the coronary arteries of nonsmokers but had minimal effect on the constrictor response to acetylcholine in the arteries of smokers. The dilator response to nitroglycerin was significantly increased in the coronary arteries of smokers compared with in those of nonsmokers. The constrictor response to L-NMMA at rest was significantly correlated with the dilator response to nitroglycerin and with the diameter changes to acetylcholine in both smokers and nonsmokers. CONCLUSIONS: Nitric oxide bioactivity at rest and at acetylcholine-stimulated conditions in smokers was decreased, leading to the supersensitivity of the artery to the dilator effect of nitroglycerin as well as the constrictor effect of acetylcholine in smokers. Cigarette smoking affects nitric oxide-mediated regulation of coronary artery tone.
We investigated the effects of IL-12 on a murine model of allergic lung inflammation. Administration of IL-12 was timed to interfere with either allergic sensitization (early dosage) or the hypersensitivity inflammatory response in the lung (late dosage), or both (early and late dosages). Comparisons of IL-12- and PBS-treated animals within each treatment group revealed several noticeable effects of IL-12. Early dosage, and the combination of early and late dosages, strikingly decreased ragweed-specific serum IgE, tracheal ring reactivity to acetylcholine, and BAL eosinophilia following allergen challenge. In contrast, late dosage had no effect on IgE levels and only a minimal effect on tracheal ring reactivity, but had a modest effect on recruitment of eosinophils. Early dosage down-regulated IL-5 and IL-10, but did not alter IL-4 or IFN-gamma expression. Late dosage down-regulated IL-5, up-regulated IL-10 and IFN-gamma, but did not change IL-4 expression. The combination of early and late dosage down-regulated IL-4, IL-5, and IL-10 expression, but increased IFN-gamma expression and production in the BAL cells and fluids. Taken together, these results indicate that IL-12 has potent immunomodulatory effects on allergic lung inflammation that depend on the timing of IL-12 administration relative to allergic sensitization and allergen challenge.