Gerritsen M E, Printz M P
Circ Res. 1981 Nov;49(5):1152-63. doi: 10.1161/01.res.49.5.1152.
Metabolically active coronary microvessels (generally less than 100 micrometers in diameter) were isolated from bovine hearts. These preparations were virtually free of contaminating myocytes and consisted of a mixture of arterioles, venules, capillaries, and collagen fibers. The prostaglandin biosynthetic capacity of isolated coronary microvessels was assessed by quantitating conversion of 14C-arachidonic acid and 14C-prostaglandin endoperoxide (PGH2) to prostaglandins. Coronary microvessels were found to exhibit low cyclooxygenase activity, i.e., minimal conversion (less than 1%) of arachidonic acid (AA) to prostaglandins when compared with either the coronary artery (3.6% conversion of AA) or coronary vein (3.3%). Isolated myofibril fractions demonstrated virtually no cyclooxygenase activity (less than 0.1%). Two enzymatic endoperoxide metabolizing activities were evident in the microvessels, prostacyclin synthetase and PGE isomerase. When compared on a microsomal protein basis, the coronary artery exhibited higher prostacyclin synthetase activity than the microvessels but was devoid of PGE isomerase activity. In contrast, whereas PGE isomerase activity was detectable in the coronary vein, the activity was lower than that of the microvessels; further, it could not be demonstrated in the other myocardial fractions. A glutathione-enhanced PGD-forming activity was present in high speed supernatants derived from the coronary artery and vein preparations, but was not present in the coronary microvessel or isolated myofibril fractions. From these studies we conclude that (1) the major source of prostaglandins released into the coronary circulation is the coronary vasculature, and (2) the resistance elements of the coronary circulation differ from the larger elements (i.e., arteries and veins) in the enzymes of the prostaglandin biosynthetic pathway present and thus in the nature and perhaps quantity of prostaglandins biosynthesized.
从牛心脏中分离出代谢活跃的冠状动脉微血管（直径一般小于100微米）。这些制剂几乎没有污染的心肌细胞，由小动脉、小静脉、毛细血管和胶原纤维混合组成。通过定量14C-花生四烯酸和14C-前列腺素内过氧化物（PGH2）向前列腺素的转化来评估分离的冠状动脉微血管的前列腺素生物合成能力。发现冠状动脉微血管表现出低环氧化酶活性，即与冠状动脉（花生四烯酸转化率为3.6%）或冠状静脉（3.3%）相比，花生四烯酸（AA）向前列腺素的转化率极低（小于1%）。分离的肌原纤维部分几乎没有环氧化酶活性（小于0.1%）。微血管中有两种明显的内过氧化物酶代谢活性，即前列环素合成酶和PGE异构酶。以微粒体蛋白为基础进行比较时，冠状动脉的前列环素合成酶活性高于微血管，但缺乏PGE异构酶活性。相反，虽然在冠状静脉中可检测到PGE异构酶活性，但其活性低于微血管；此外，在其他心肌部分未检测到该活性。冠状动脉和静脉制剂的高速上清液中存在谷胱甘肽增强的PGD形成活性，但冠状动脉微血管或分离的肌原纤维部分中不存在该活性。从这些研究中我们得出结论：（1）释放到冠状动脉循环中的前列腺素的主要来源是冠状动脉血管系统；（2）冠状动脉循环的阻力成分在前列腺素生物合成途径的酶方面与较大成分（即动脉和静脉）不同，因此在生物合成的前列腺素的性质和可能的数量方面也不同。
