PROSTAGLANDIN ACTION, RELEASE AND INACTIVATION BY RAT ISOLATED PERFUSED MESENTERIC BLOOD VESSELS
PROSTAGLANDIN ACTION, RELEASE AND INACTIVATION BY RAT ISOLATED PERFUSED MESENTERIC BLOOD VESSELS
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大鼠离体肠系膜灌注血管的前列腺素作用、释放和失活
DOI：
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发表时间：
1980
影响因子：
7.3
通讯作者：
I. M. Coupar
中科院分区：
文献类型：
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作者：
I. M. Coupar
1以下实验证实前列腺素是去甲肾上腺素在大鼠肠系膜血管中充分发挥血管收缩作用所必需的。前列腺素的释放和失活也进行了研究。2环加氧酶抑制剂5,8,11,14 -二十碳四烯酸对去甲肾上腺素的浓度-效应曲线有显著的抑制作用。与吲哚美辛一样，前列腺素E2 （PGE2）能将反应恢复到控制水平，但PGE2不能恢复罂粟碱抑制的去甲肾上腺素的反应。静息时组织释放PGE2样活性，相当于50±20 pg PGE2/min。该物质可能是一种稳定的前列腺素，因为其活性在酸化和提取为氯仿后仍保持不变。去甲肾上腺素刺激的释放量增加被吲哚美辛降低到静息值以下。灌注40和4 ng/min PGE2的组织净损失分别为7±1和1±0.2 ng/min。在较低的PGE2灌注率下未发生摄取。当使用吲哚美辛抑制去甲肾上腺素的反应时，15(S)‐15‐甲基PGE2甲酯在将反应恢复到控制值方面的效力是PGE2的12倍。环内过氧化物类似物U - 46619仅部分恢复吲哚美辛对去甲肾上腺素的抑制反应，但在2 ng/ml及以上时增加灌注压。结果证实内源性前列腺素的释放，可能是PGE2，对去甲肾上腺素的血管收缩作用是必需的。去甲肾上腺素增加前列腺素的释放量，然后前列腺素可能被15 -羟基前列腺素脱氢酶或β -氧化酶吸收并灭活。U‐46619可以模拟PGE2和血栓素A2。
1 The following experiments were undertaken to confirm that prostaglandin is necessary for noradrenaline to exert its full vasoconstrictor effect in rat mesenteric blood vessels. Prostaglandin release and inactivation were also studied. 2 The cyclo‐oxygenase inhibitor, 5, 8, 11, 14‐eicosatetraynoic acid caused a significant depression of the concentration‐effect curve to noradrenaline. As with indomethacin, responses were restored to control levels by prostaglandin E2 (PGE2) but PGE2 did not restore responses to noradrenaline depressed by papaverine. 3 PGE2‐like activity was released from tissues at rest, equivalent to 50 ± 20 pg PGE2/min. The substance was probably a stable prostaglandin since activity remained on acidifying and extracting into chloroform. The increase in release stimulated by noradrenaline was reduced below resting values by indomethacin. 4 There was a net loss of 7 ± 1 and 1 ± 0.2 ng PGE2/min from tissues perfused with 40 and 4 ng/min PGE2 respectively. No uptake occurred at lower PGE2 perfusion rates. 5 When indomethacin was used to depress responses to noradrenaline 15(S)‐15‐methyl PGE2 methyl ester was 12 times more potent than PGE2 in restoring responses to control values. The cyclic endoperoxide analogue U‐46619 caused only partial restoration of indomethacin‐depressed responses to noradrenaline but increased perfusion pressure at 2 ng/ml and above. 6 The results confirm that endogenous prostaglandin release, possibly of PGE2, is obligatory to the full vasoconstrictor effect of noradrenaline. Noradrenaline increases the amount of prostaglandin released which may then be taken up and inactivated by 15‐hydroxy prostaglandin dehydrogenase or β‐oxidase. U‐46619 may mimic both PGE2 and thromboxane A2.