{"title":"前列腺素有助于豚鼠内皮依赖性冠状动脉血管舒张。","authors":"L Lee, C A Bruner, R C Webb","doi":"10.1159/000158828","DOIUrl":null,"url":null,"abstract":"<p><p>This study characterizes the contribution of prostanoids to endothelium-dependent responses in two vascular regions of the guinea pig. We compared the mechanisms of relaxation responses to acetylcholine and adenosine triphosphate (ATP) in the coronary vasculature and in the abdominal aorta of the guinea pig. Endothelium-dependent responses were examined in an isolated, potassium-arrested guinea pig heart utilizing a modified Langendorff preparation. Coronary vessels were constricted with prostaglandin F2 alpha and dilated with acetylcholine (10(-9)-10(-6) mol) or ATP (10(-10)-10(-7) mol) before and after exposure to indomethacin (14 microM, n = 6) or ibuprofen (150 microM, n = 5). Helically cut strips of abdominal aorta (n = 6) were suspended in isolated tissue baths for measurement of isometric force. Relaxation to acetylcholine (5.5 x 10(-7) M) and ATP (10(-5) M) was quantified in strips contracted with norepinephrine before and after exposure to indomethacin (14 microM). In addition, the endothelium was damaged by exposing vessels to free radicals generated by electrolysis of the buffer (4 Hz, 9 V, 1 ms, 5 min). Following electrolysis of the buffer, relaxation responses to acetylcholine and ATP were significantly attenuated in both preparations. In the perfused heart, endothelium-dependent dilatation to acetylcholine, but not ATP were significantly inhibited in the presence of indomethacin or ibuprofen. In contrast, acetylcholine- and ATP-induced relaxation responses in the aorta were not altered by indomethacin. We conclude that prostaglandins contribute to acetylcholine-induced dilatation in the coronary bed but not in the abdominal aorta of the guinea pig. Furthermore, in the coronary bed, different endothelial factors mediate relaxation to acetylcholine and ATP.</p>","PeriodicalId":9009,"journal":{"name":"Blood vessels","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"1990-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000158828","citationCount":"11","resultStr":"{\"title\":\"Prostanoids contribute to endothelium-dependent coronary vasodilation in guinea pigs.\",\"authors\":\"L Lee, C A Bruner, R C Webb\",\"doi\":\"10.1159/000158828\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>This study characterizes the contribution of prostanoids to endothelium-dependent responses in two vascular regions of the guinea pig. We compared the mechanisms of relaxation responses to acetylcholine and adenosine triphosphate (ATP) in the coronary vasculature and in the abdominal aorta of the guinea pig. Endothelium-dependent responses were examined in an isolated, potassium-arrested guinea pig heart utilizing a modified Langendorff preparation. Coronary vessels were constricted with prostaglandin F2 alpha and dilated with acetylcholine (10(-9)-10(-6) mol) or ATP (10(-10)-10(-7) mol) before and after exposure to indomethacin (14 microM, n = 6) or ibuprofen (150 microM, n = 5). Helically cut strips of abdominal aorta (n = 6) were suspended in isolated tissue baths for measurement of isometric force. Relaxation to acetylcholine (5.5 x 10(-7) M) and ATP (10(-5) M) was quantified in strips contracted with norepinephrine before and after exposure to indomethacin (14 microM). In addition, the endothelium was damaged by exposing vessels to free radicals generated by electrolysis of the buffer (4 Hz, 9 V, 1 ms, 5 min). Following electrolysis of the buffer, relaxation responses to acetylcholine and ATP were significantly attenuated in both preparations. In the perfused heart, endothelium-dependent dilatation to acetylcholine, but not ATP were significantly inhibited in the presence of indomethacin or ibuprofen. In contrast, acetylcholine- and ATP-induced relaxation responses in the aorta were not altered by indomethacin. We conclude that prostaglandins contribute to acetylcholine-induced dilatation in the coronary bed but not in the abdominal aorta of the guinea pig. 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引用次数: 11
摘要
本研究表征了前列腺素对豚鼠两个血管区域内皮依赖性反应的贡献。我们比较了豚鼠冠状血管和腹主动脉对乙酰胆碱和三磷酸腺苷(ATP)的松弛反应机制。内皮依赖性反应被检查在一个孤立的,钾停止豚鼠心脏利用改良朗根多夫制剂。在暴露于吲哚美辛(14 μ m, n = 6)或布洛芬(150 μ m, n = 5)前后,用前列腺素F2 α收缩冠状血管,用乙酰胆碱(10(-9)-10(-6)mol)或ATP (10(-10)-10(-7) mol)扩张冠状血管。将螺旋切割的腹主动脉条(n = 6)悬浮于离体组织浴中,测量等长力。在吲哚美辛(14微米)暴露前后,用去甲肾上腺素收缩的条带定量测定乙酰胆碱(5.5 × 10(-7) M)和ATP (10(-5) M)松弛。此外,将血管暴露于缓冲液电解(4 Hz, 9 V, 1 ms, 5 min)产生的自由基中,内皮细胞受到损伤。电解缓冲液后,两种制剂对乙酰胆碱和ATP的弛豫反应均显著减弱。在灌注的心脏中,吲哚美辛或布洛芬显著抑制乙酰胆碱而非ATP的内皮依赖性扩张。相反,乙酰胆碱和atp诱导的主动脉松弛反应不受吲哚美辛的影响。我们得出结论,前列腺素有助于乙酰胆碱诱导的豚鼠冠状动脉床扩张,而不是腹主动脉扩张。此外,在冠状动脉床上,不同的内皮因子介导对乙酰胆碱和ATP的松弛。
Prostanoids contribute to endothelium-dependent coronary vasodilation in guinea pigs.
This study characterizes the contribution of prostanoids to endothelium-dependent responses in two vascular regions of the guinea pig. We compared the mechanisms of relaxation responses to acetylcholine and adenosine triphosphate (ATP) in the coronary vasculature and in the abdominal aorta of the guinea pig. Endothelium-dependent responses were examined in an isolated, potassium-arrested guinea pig heart utilizing a modified Langendorff preparation. Coronary vessels were constricted with prostaglandin F2 alpha and dilated with acetylcholine (10(-9)-10(-6) mol) or ATP (10(-10)-10(-7) mol) before and after exposure to indomethacin (14 microM, n = 6) or ibuprofen (150 microM, n = 5). Helically cut strips of abdominal aorta (n = 6) were suspended in isolated tissue baths for measurement of isometric force. Relaxation to acetylcholine (5.5 x 10(-7) M) and ATP (10(-5) M) was quantified in strips contracted with norepinephrine before and after exposure to indomethacin (14 microM). In addition, the endothelium was damaged by exposing vessels to free radicals generated by electrolysis of the buffer (4 Hz, 9 V, 1 ms, 5 min). Following electrolysis of the buffer, relaxation responses to acetylcholine and ATP were significantly attenuated in both preparations. In the perfused heart, endothelium-dependent dilatation to acetylcholine, but not ATP were significantly inhibited in the presence of indomethacin or ibuprofen. In contrast, acetylcholine- and ATP-induced relaxation responses in the aorta were not altered by indomethacin. We conclude that prostaglandins contribute to acetylcholine-induced dilatation in the coronary bed but not in the abdominal aorta of the guinea pig. Furthermore, in the coronary bed, different endothelial factors mediate relaxation to acetylcholine and ATP.