Objective To study the effect of HTK solution and perfadex solution on the function of pulmonary artery endothelium. Methods Fifty-four porcine pulmonary rings (2 mm long) were randomly divided into three groups, including control group (n =18) incubated in Krebs-Henseleit (KH) at 4 ℃ for 4 hours, group A (n =18) incubated in HTK solution and group B (n =18) incubated in perfadex solution at 4 ℃ for 4 hours. The vasoconstriction responses induced by indomethacin (7 μmol/L), N-nitro-L-arginine(300 μmol/L), oxyhemoglobin (20 μmol/L) and prostaglandin F2α (1×10 -7.5 mol/L) were detected. The vasodilator responses induced by bradykinin and non-receptor-mediated calcium ionophore were also detected in three groups. Results The maximum contraction of the vascular ring was caused by prostaglandin F2α. The maximum relaxtion responses of the vascular ring were caused by bradykinin and non-receptor-mediated calcium ionophore. There were no significant differences between three groups (P > 0.05). Conclusion There was no significant difference in endothelium-derived hyperpolarizing factor (EDHF)-mediated relaxation of porcine pulmonary artery between HTK,perfadex and KH solutions.

Objective To study the effect of hypoxic preconditioning on the function of coronary artery endothelium after hypoxia-reoxygenation.Methods Thirty-six porcine coronary rings in 2 mm long were randomly divided into four groups.Control group(n=9):incubation in Krebs-Henseleit(KH) at 37 ℃ for 90 minutes with a constant suply of oxygen;Group A(n=9):60-minute hypoxia(PO2<15 mm Hg) followed by 30 minute reoxygenation in KH at 4 ℃;Group B(n=9):hypoxia for 5 minutes followed by reoxygenation for 10 minutes before hypoxia-reoxygenation.Group C(n=9):5-hydroxydecanoate(10 μmol/L) was given 20 miuntes prior to hypoxia preconditioning.The endothelium-derived hyperpolarizing factor(EDHF)-mediated relaxation(percentage of 30 nmol/L U46619 precontraction) induced by bradykinin in the present of indomethacin(7 μmol/L),LNNA(300 μmol/L) and oxyhemoglobin(20 μmol/L) were measured in the organ chambers.Results Compared with control group,the relaxation induced by bradykinin was significantly decreased in group A,C,while there was no significant difference in group B.Conclusion Hypoxia-reoxygenation impairs EDHF mediated relaxation in coronary artery.This function can be restored by hypoxia preconditioning it′s effect might be related to mitochondrial ATP-sensitive K+ channels.

Objective To study the effect of Perfadex and Wisconsin Unviersity solution on the function of pulmonary artery endothelium.Methods Small lobe pulmonary arteries were dissected from nine porcine lungs.The artery from each lung was cut into six rings in 2mm.Two of them were randomly incubated in Krebs,Perfadex or Wisconsin Unviersity solution (UW solution) at 4℃ for 4 hours.Endothelium-derived hyperpolarizing factor (EDHF)-mediated relaxation (percentage of-7.5 logM U46619 precontraction) induced by bradykinin or calcium ionophone A23187 in the present of indomethacin,L-NNA and oxyhemoglobin were measured at 37 ℃ in the organ chambers.Results Vasoconstriction induced by U46619 is no significant difference among three groups (P＞ 0.05).Compared with Krebs group,the relaxation induced by bradykinin or A23187 was significantly decreased in Perfadex group (P＜0.01),while there is no significant difference in UW group (P＞0.05).Conclusion Endothelium-derived hyperpolarizing factor (EDHF) plays an important role in endothelium-mediated relaxation of porcine pulmonary artery.EDHF-mediated relaxation is impaired when the lung preserved with Wisconsin Unviersity solution,wheras its function is not affected by Perfadex solution.

Objective To study the effect of nicorandil on the function of coronary artery endothelium during hypoxiareoxygenation.Methods Forty-five fresh porcine left anterior descending coronary artery rings in 2mm long were randomly divided into five groups.Control group ( n =9):incubation in Krebs-Henseleit (KH) at 37℃ for 90 minutes with a constant supply of oxygen ; Group A ( n =9):30-minute hypoxia ( PO2 ＜ 15 mm Hg) followed by 30 minutes reoxygenation in KH at 37℃ ; Group B ( n =9):60-minute hypoxia followed by 30 minutes reoxygenation in KH at 37 ℃ ; Group C ( n =9):60-minute hypoxia followed by 30 minutes reoxygenation in KH added nicorandil ( 0.2 μmol/L) at 37 ℃ ; Group D ( n =9 ):60-minute hypoxia followed by 30 minutes reoxygenation in KH added nicorandil (0.2 μmol/L) and 5-hydroxydecanoate ( 10μmol/L) at 37 ℃.The endothelium-derived hyperpolarizing factor (EDHF) -mediated relaxation ( U46619 precontraction) induced by bradykinin in the present of indomethacin (7 μmol/L),LNNA (300 μmol/L) and oxyhemoglobin (20 μmol/L)were measured in the organ chambers.Results Compared with control group,the relaxation was significantly decreased in group A,B and D ( P ＜ 0.001 ),while there is no significant difference in group C ( P ＞ 0.05 ).Compared with group A,the relaxation was significantly reduced in group B and D (P ＜0.001 ).Conclusion Hypoxia-reoxygenation impairs EDHF mediated relaxation in coronary artery with more injury during prolonged hypoxia.This function can be restored by preconditioning with nicorandil The mechanism is mainly related to the mitochondrial ATP-sensitive K + channels.

Objective To observe the effect of tetrahydrobiopterin ( BH4 ) on endothelium function of the great saphenous vein from smokers. Methods The rings of great saphenous vein were selected from 22 patients with coronary artery bypass grafting, which including smoking (experimental group,n = 12) and non-smoking (control group,n = 10) patients. After incubation in Krebs-Henseleit (KH), KH plus BH4 (20 μ mol/L) or N-nitro-L-arginine ( L-NNA, 0. 1 mol/L), the vasoconstriction and vasodilatation were induced by phenylephrine (1 × 10-5 mol/L) and non-receptor-mediated calcium ionophore (A23187,1 × 10-9-1 × 10 -5 mol/L) separately in an organ chamber. Results The maximum constriction in all groups had no significant difference ( P ＞ 0. 05 ). The maximum relaxation was significantly decreased in experimental group as compared with control group [(29.50 ± 6. 22 ) % vs (48.20 ± 7. 74 ) %, P ＜ 0. 01]after incubation in KH, while there was no significant difference (P ＞ 0. 05 ) after incubation in KH plus L-NNA [(24.50±5.72)% vs (28.8 ±5.64)%] or BH4[(46.40 ±6.32)% vs (50.80±6.91)%].Conclusion Smoking impairs the relaxation function mediated by endothelium-derived nitric oxide in great saphenous, which may be restored by BH4.

Objective To study the impact of type 2 diabetes mellitus on endothelium of great saphenous vein in patients with coronary heart disease.Methods Patients undergoing coronary artery bypass grafting were selected, 20 with type 2 diabetes mellitus (experimental group) and another 20 patients without (control group).The rings of great saphenous vein in I cm length were taken from those patients and then divided into 3 segments.The structure of endothelium was evaluated by the microscope and the changes of venous tone were measured in organ chamber at 37C with a constant supply of oxygen.Venous vasoconstriction was induced by phenylephrine (10-5 mol/L) and vasodilatation induced by nitroglycerin or acetylcholine (10-9 ～ 10-5 mol/L).Results More damages of ultrastructure of the endothelium of saphenous vein were found in experimental group than in control group.There were no significant differences regarding the venous tone between the two groups (P ＞0.05) when vasoconstriction induced by phenylephrine and vasodilatation by nitroglycerin.However, the vasodilatation induced by acetylcholine was significantly decreased in experimental group than in control group (P ＜ 0.05).Conclusion Type 2 diabetes mellitus can aggravate the damage of endothelium of saphenous vein in patients with coronary artery disease.

Objective To compare the condition of the structure and oxidative stress of great saphenous vein grafts between the patients with and without type 2 diabetes mellitus,and to study the mechanisms for providing the theory evidence of the protective way for great saphenous vein graft in patients with type 2 diabetes mellitus.Methods The segments of human great saphenous vein graft were collected from 36 patients undergoing coronary artery bypass graft surgery,who were divided into 2 groups,experimental group(17 patients with type 2 diabetes mellitus) and control group(19 patients without type 2 diabetes mellitus).There was no significant difference in age,gender,hypertension,serum creatinine,hyperlipidemia,smoking,and the number of pathological coronary arteries between 2 groups(P 0.05).Two cm distal great saphenous vein from each patient was obtained.The structure of great saphenous vein was observed by the microscope,and nicotinamide adenine dinucleotide phosphate(NADPH) oxidase enzymatic activity and superoxide anion level were quantified by lucigenin-enhanced chemilumi nescence.Results The NADPH oxidase activity and superoxide anion levels were significantly higher in experimental group [(308.8 ± 33.7) counts/μg and(1 951.71 ± 355.2) counts/(min.mg)] than in control group [(202.7 ± 29.5) counts/μg and(1 230.73 ± 340.5) counts/(min.mg)](P 0.05).HE staining showed the damage of ultrastructure of great saphenous vein endothelium in experimental group,including necrosis and exfoliation of endoepithelial cells,splitting of the basement membrane,thickened lower layer of the endothelium with vacuoles and deformed vascular smooth muscle cells;however,integrated vessel intima was observed in control group.Conclusion Type 2 diabetes mellitus can aggravate the damage extent and oxidative stress in the great saphenous vein grafts.