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Chylothorax is an unusual complication of various malignant neoplasms, generally lymphomas. The few reported cases of chylothorax with gastric and other abdominal malignancies have involved large abdominal masses with prominent adenopathy and chylous ascites. We describe a patient in whom chylothorax was the presenting manifestation of an adenocarcinoma with probable gastric primary, developing prior to any clinical or radiologic evidence of tumor.

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In this study the role of the endothelium was evaluated in the relaxation of rat aortic rings induced by a number of alpha adrenergic antagonists. Phentolamine, a nonselective alpha adrenergic antagonist, relaxed rat aortic rings that were previously contracted with an EC80 dose of phenylephrine, in a concentration-dependent manner. Removal of the endothelium significantly reduced the sensitivity but not the amplitude of the response. The presence of endothelium also enhanced the vascular relaxation induced by yohimbine, a specific alpha-2 adrenergic antagonist (10(-8)-10(-6) M), and by prazosin, a specific alpha-1 adrenergic antagonist (10(-11)-10(-9) M). Both methylene blue (10(-5) M), an inhibitor of soluble guanylate cyclase, and eicosatetraynoic acid (3.2 X 10(-5) M) blocked the endothelial augmentation of vascular relaxation to phentolamine. Vessels precontracted with potassium chloride were slightly relaxed by phentolamine (10(-8)-10(-6) M) only with the endothelium was intact. Both methylene blue and eicosatetraynoic acid also inhibited the response to phentolamine in the intact vessels precontracted with potassium chloride. Prazosin (10(-9)-10(-7) M) and yohimbine (10(-8)-10(-6) M), unlike phentolamine, failed to induce relaxation in potassium chloride-precontracted vessels. When the vessels were precontracted with the thromboxane analog U46619 none of the three alpha antagonists induced vascular relaxation. These results indicate that the endothelium has a significant role in promoting relaxation induced by the three alpha adrenergic antagonists tested.

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A number of beta adrenergic blocking drugs were evaluated on ring preparations of endothelium intact and denuded segments of the rat aorta. The preparations were preconstricted under isometric conditions with an EC80 dose of phenylephrine. Labetalol (10(-7)-10(-5) M), MK-761 10(-7)-10(-5) M), timolol (10(-7)-10(-4) M) and propranolol (10(-6)-10(-4) M) relaxed both endothelium intact and denuded vessels in a dose-dependent manner. Spirendalol (2.8 X 10(-8)-8.1 X 10(-6) M), a specific beta-2 receptor antagonist and L643717 (1.8 X 10(-7)-3.6 X 10(-6) M), a specific beta-1 receptor antagonist did not elicit relaxation. Labetalol, MK-761, timolol and propranolol promoted relaxation only when vascular segments were preconstricted with phenylephrine or norepinephrine and failed to do so when prostaglandin F2 alpha or U46619 were used. This indicates a possible displacement of alpha adrenergic agonists with the beta antagonists. The degree of relaxation induced by labetalol, MK-761, timolol and propranolol was significantly less (P less than .05) when the endothelium was removed. Eicosatetraynoic acid (3.2 X 10(-5) M) significantly attenuated the relaxation response to labetalol, MK-761 and timolol in the intact but not in denuded vascular preparations. These studies suggest that some of the vascular effects of beta blockers may relate to the endothelium.

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The vascular endothelium appears obligatory for the expression of the vasodilating property of most polypeptides. A number of polypeptides were studied on the rat aortic ring preparation which was pre-contracted with phenylephrine and only basic polypeptides containing one or more arginine residues elicited relaxation which was endothelium dependent. These peptides included melittin and poly-L-Arg. The basic polypeptide poly-L-Lys also elicited endothelium dependent relaxation, but to a lesser extent than arginine containing polypeptides. Two basic polypeptides, apamin and mastoparan do not promote endothelium dependent relaxation. The former contains arginine between disulfide bonds and in the latter arginine is absent. Basic amino acids and dipeptides which contain arginine, and also polyamines did not elicit relaxation even at high concentrations (10(-3) M). The relaxation elicited by melittin, poly-L-Arg and poly-L-Lys was inhibited by ETYA, NDGA, p-bromophenacyl bromide and not by indomethacin. Methylene blue, an inhibitor of soluble guanylate cyclase, also abolished the relaxation. We suggest that arginine containing peptides may relax vascular smooth muscle by acting directly on the vascular smooth muscle (eg: atriopeptins) and/or or by eliciting release of a relaxing factor(s) from the endothelium.

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Bovine serum albumin which is fatty acid free, enhances the endothelium-dependent vasodilating effect of various agonists like acetylcholine, carbachol, ATP, ADP and ionophore on rat aortic rings. The maximum effect was observed in buffers containing 5% albumin. Albumin has no effect on rings devoid of endothelium. On the other hand, both plasma and serum completely abolished the vasodilating effect of these agents.

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