Myers P R, Banitt P F, Guerra R, Harrison D G
Department of Medicine, Dalton Research Center, University of Missouri, Columbia 65211.
Cardiovasc Res. 1991 Feb;25(2):129-37. doi: 10.1093/cvr/25.2.129.
The aim was to investigate the role of the endothelium in modulating the acetylcholine response in porcine coronary microvessels and compare the results with simultaneously studied large coronary arteries.
Coronary microvessels [104 (SEM 3.3) microns; range 38-150] were removed from fresh porcine hearts and studied in vitro during no flow constant pressure conditions. Endothelium derived relaxing factor (EDRF) activity and the role of the endothelium in modulating the acetylcholine response in microvessels was assessed by measuring changes in intraluminal diameter using a video tracking device. Large coronary arteries were simultaneously studied using conventional isometric ring techniques.
Fresh porcine hearts were obtained from a local slaughterhouse.
Acetylcholine was a potent vasoconstrictor (EC50 = 0.17 microM) of passively distended microvessels. The effects of EDRF were studied by either inactivation with haemoglobin or inhibition of EDRF synthesis with N-omega-nitro-L-arginine. Preconstricted microvessels exposed to either N-omega-nitro-L-arginine or haemoglobin constricted further, consistent with basal release of EDRF. Neither drug affected passively distended microvessels. The acetylcholine vasoconstrictor response was potentiated after exposure of microvessels to either drug. Atropine, but not indomethacin, blocked the acetylcholine response in microvessels. As with microvessels, acetylcholine was a vasoconstrictor (EC50 = 0.3 microM) of large coronary arteries. In contrast to microvessels, indomethacin antagonised acetylcholine vasoconstriction in vessels with intact endothelium. Bioassay experiments using indomethacin-treated large epicardial donor artery segments showed basal release of EDRF but no EDRF release in response to acetylcholine.
The results show the microvessels and large coronary arteries are similar in their vasoconstrictor response to acetylcholine, that both release EDRF basally, and that vasoconstriction to acetylcholine is importantly modulated by the endothelium. In large arteries, acetylcholine does not stimulate EDRF release and, in contrast to microvessels, a cyclo-oxygenase product influences the vasoconstrictor action of acetylcholine.
旨在研究内皮在调节猪冠状动脉微血管乙酰胆碱反应中的作用，并将结果与同时研究的大冠状动脉进行比较。
从新鲜猪心脏中取出冠状动脉微血管[104（标准误3.3）微米；范围38 - 150]，在无血流恒压条件下进行体外研究。通过使用视频跟踪装置测量管腔内直径的变化，评估内皮衍生舒张因子（EDRF）活性以及内皮在调节微血管乙酰胆碱反应中的作用。同时使用传统的等长环技术研究大冠状动脉。
从当地屠宰场获取新鲜猪心脏。
乙酰胆碱是被动扩张微血管的强效血管收缩剂（半数有效浓度[EC50]=0.17微摩尔）。通过用血红蛋白使其失活或用N - ω - 硝基 - L - 精氨酸抑制EDRF合成来研究EDRF的作用。预先收缩的微血管暴露于N - ω - 硝基 - L - 精氨酸或血红蛋白后进一步收缩，这与EDRF的基础释放一致。两种药物均未影响被动扩张的微血管。微血管暴露于任何一种药物后，乙酰胆碱的血管收缩反应增强。阿托品而非吲哚美辛可阻断微血管中的乙酰胆碱反应。与微血管一样，乙酰胆碱是大冠状动脉的血管收缩剂（EC50 = 0.3微摩尔）。与微血管不同的是，吲哚美辛可拮抗内皮完整的血管中的乙酰胆碱血管收缩作用。使用经吲哚美辛处理的大的心外膜供体动脉段进行的生物测定实验显示有EDRF基础释放，但对乙酰胆碱无EDRF释放。
结果表明，微血管和大冠状动脉对乙酰胆碱的血管收缩反应相似，两者均基础释放EDRF，且乙酰胆碱的血管收缩作用受内皮的重要调节。在大动脉中，乙酰胆碱不刺激EDRF释放，与微血管相反，一种环氧化酶产物影响乙酰胆碱的血管收缩作用。
