Papaverine is a commonly used vasodilator of the internal mammary artery in cardiac surgery. The effects of papaverine with and without N(omega)-L-arginine methyl ester (L -NAME) (a nitric oxide production inhibitor) and/or zaprinast (a cyclic GMP inhibitor) or verapamil (calcium channel antagonist) on systemic vascular resistance in vivo have not been well documented. This study examines the hemodynamic responses to papaverine and attempts to identify the role of nitric oxide, cyclic guanosine monophosphate (GMP), and calcium in the vasodilation. The effects of varying doses of papaverine were evaluated with and without L-NAME and/or zaprinast or verapamil on the hindlimb vascular resistance in the male rat. With institutional approval, 40 male Sprague--Dawley rats (400--450 g) were anesthetized with intraperitoneal pentobarbital (50 mg kg(minus sign1)). The carotid artery, jugular vein, and abdominal aorta were cannulated by cutdown; mean arterial pressure (MAP) and hindlimb perfusion pressure (HPP) were recorded. Rats were heparinized (1000 U kg(minus sign1)). Papaverine (1, 3, 10, 30, and 100 &mgr;g) was injected into the hindlimb, whereas MAP was maintained constant, and the HPP was recorded. Both L-NAME (25 mg kg(minus sign1)) and/or verapamil and then papaverine (1, 3, and 10 &mgr;g) were injected into the hindlimb, and changes in HPP were recorded. A Student's t-test was used for statistical analysis, with a p < 0.05 considered significant. Papaverine, in increasing doses, decreased HPP incrementally. L-NAME partially blocked the effects of papaverine (p < 0.05), as did verapamil (p < 0.05). The combination of L-NAME and verapamil further decreased papaverine's vasodilation to almost eliminate it (p < 0.05). We demonstrated the effect of papaverine on the hindlimb vasculature is similar to its effects noted in the internal mammary artery. Nitric oxide is known to be an agent causing vasodilation. It was demonstrated that papaverine vasodilation in the hindlimb vascular bed is modified by L-NAME, which suggests that nitric oxide production inhibition is partially responsible for this effect. It was demonstrated that there is an effect of calcium channel blockade on the vasodilation caused by papaverine. Both L-NAME and verapamil together appear to modify further the vasodilation caused by papaverine, suggesting both calcium channel and nitric oxide mechanisms for vasodilation. Zaprinast, a specific cyclic GMP phosphodiesterase inhibitor, did not effect the vasodilation caused by papaverine, acetylcholine, nitroglycerin, or verapamil.
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Respir Med
January 2025
Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel; Clalit Health Services, Dan Petah Tikva District, Petah Tikva, Israel. Electronic address:
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Free Radic Biol Med
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Division of Neonatology, University & Polytechnic Hospital La Fe, Avda Fernando Abril Martorell 106, 46026 Valencia, Spain; Neonatal Research Group, Health Research Institute Hospital La Fe (IISLAFE), Avda Fernando Abril Martorell 106, 46026 Valencia, Spain; Spanish Network in Maternal, Neonatal, Child and Developmental Health Research (RICORS SAMID) (RD24/0013/0014), Instituto de Salud Carlos III, Madrid, Spain. Electronic address:
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Department of Immunology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran. Electronic address:
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MOE Key Laboratory of Bio-Intelligent Manufacturing, School of Bioengineering, Dalian University of Technology, Dalian 116024, PR China.
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Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.
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