The effects of iloprost (ZK 36 374), a stable analogue of prostacyclin, and prostaglandin E2 (PGE2) were studied on isolated spirally cut strips of rabbit aorta, celiac, mesentenc and renal arteries continuously superfused in cascade. Iloprost and PGE2 elicited a concentration-dependent relaxation of phenylephnne-contracted celiac and mesenteric strips having equal affinities as verified by identical pD2 values. Iloprost also produced a concentration-dependent relaxation in precontracted renal artery strips at relatively higher concentrations but had little relaxing action on precontracted aortic strips. Contrary, PGE2 induced a concentration-dependent relaxing effect on precontracted aortic strips without producing an appreciable action on renal artery strips. Acetylsalicylic acid (ASA) when added to the superfusion medium elicited an increase in basal tonicity of celiac and mesenteric strips without altering the basal tonicity of renal artery and aortic strips. Iloprost at very low concentrations (10–10–10–9 mol/l) produced a complete recovery in increased tonicity of both strips while at the same concentrations PGE2 had little effect. These results indicate that endogenous PGI2 may have an important role in the regulation of vascular tonicity in celiac and mesenteric arteries.
Histamine has a dual action on the isolated perfused ear preparation of the rabbit. The amine induced a dose-dependent rise in perfusion pressure when the preparation was perfused with Krebs' solution. This pressor response was reversed to a depressor effect when meypramine was added to the perfusion fluid. This depressor effect of the amine was also dose-related. Metiamide competitively inhibited the depressor effect of histamine. Prior treatment of the ear vessels with metiamide alone caused an increase in histamine-induced perfusion pressure. From these results it was concluded that the predominant pressor effect of histamine on the vascular bed of the rabbit ear is mediated through the H1-receptors and the depressor effect of the amine through histamine H2-receptors.
α-Naphthylthiourea (ANTU) when injected intraperitoneally to rats at a dose of 10 mg/kg elicited lung oedema indicated by an increase in lung weight/body weight (LW/BW) ratio and pleural effusion. The injection of acetylsalicylic acid, which is a cyclo-oxygenase inhibitor, and BW 755C, a cyclo-oxygenase and lipoxygenase inhibitor, prior to ANTU produced a significant inhibition in pleural fluid accumulation without changing the LW/BW ratio. BW A4C, a selective 5-lipoxygenase inhibitor, however, caused a highly significant inhibition in pleural effusion and a slight but significant decrease in LW/BW ratio. Thromboxane A2 synthetase inhibitor, UK 38485, caused a slight but significant inhibition in pleural fluid accumulation without altering the LW/BW ratio. Iloprost, however, produced a slight but significant inhibition in the LW/BW ratio without reducing the pleural effusion rate. A significant decrease in angiotensin-converting enzyme (ACE) activity in the isolated perfused lungs of ANTU-treated rats was noted. This observation was thought to be an evidence of a functional alteration of the lung vascular endothelium. The possible role of eicosanoids in lung oedema induced by ANTU and the related mechanisms of decreased ACE activity are discussed.
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