Non-steroidal anti-inflammatory drugs potentiate the vasoconstrictor effects of ouabain in the dog.
Non-steroidal anti-inflammatory drugs potentiate the vasoconstrictor effects of ouabain in the dog.
复制标题
非甾体类抗炎药可增强哇巴因对狗的血管收缩作用。
DOI：
10.1161/01.res.48.6.844
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发表时间：
1981
影响因子：
20.1
通讯作者：
Gerber,JG
中科院分区：
文献类型：
--
作者：
Nies,AS;Gerber,JG
本研究的目的是确定前列腺素合成抑制剂是否改变强心苷哇巴因的外周血管效应。将哇巴因（35 μ g/kg）给予12只杂种犬，其中6只犬在1小时前已用非甾体类抗炎药（NSAID）、吲哚美辛或甲氨蝶呤（6 mg/kg，iv，推注，随后1 mg/min输注）进行预处理。在哇巴因给药前30分钟和给药后3小时监测血流动力学变量。哇巴因给药后45分钟，所有犬的平均动脉压均显著升高，心输出量无变化。在没有接受非甾体抗炎药的动物中，哇巴因短暂（15分钟）减少肾血流量并增加肾血管阻力。直到90分钟，哇巴因才改变肠系膜血流量，此后血流量显著增加。在用NSAID预处理的狗中，哇巴因给药后肾血流量减少60分钟。此外，哇巴因给药后30分钟，肠系膜血流量从基线值192 ± 42 ml/min减少了43 ± 17 ml/min（P< 0.05），并且这种减少持续整个3小时观察期。没有接受哇巴因的对照动物在实验期间既没有显示出动脉压的增加，也没有显示出肾或肠系膜血流的减少。因此，NSAID预处理增强了哇巴因对犬肾血管收缩作用的持续时间，并将晚期肠系膜血管舒张转化为早期和持续的血管收缩。这些数据意味着一个潜在的重要作用，血管扩张的mesenteric以及肾循环哇巴因的反应，在调制中的作用。
The purpose of this study was to determine whether inhibitors of prostaglandin synthesis alter the peripheral vascular effects of the cardiac glycoside, ouabain. Ouabain (35/ŧg/kg) was given to 12 mongrel dogs, six of which had been pretreated 1 hour previously with the non-steroidal antiinflammatory drugs (NSAID), indomethacin or meclofenamate (6 mg/kg, iv, bolus followed by 1 mg/min infusion). Hemodynamic variables were monitored for 30 minutes before and for 3 hours after ouabain administration. Mean arterial pressure was significantly increased in all dogs for 45 minutes after ouabain, and cardiac output was unchanged. In the animals that did not receive non-steroidal anti-inflammatory drugs, ouabain transiently (15 min) decreased renal blood flow and increased renal vascular resistance. Mesenteric blood flow was not altered by ouabain until 90 minutes, after which time it was significantly increased. In the dogs pretreated with NSAID, renal blood flow was reduced for 60 minutes after administration of ouabain. In addition, 30 minutes after ouabain, the mesenteric blood flow was reduced by 43 ą 17 ml/min from a baseline value of 192 ą 42 ml/min (P< 0.05), and this reduction persisted for the entire 3-hour observation period. Control animals that did not receive ouabain showed neither an increase in arterial pressure nor a decrease in renal or mesenteric blood flow over the period of the experiment. Thus, pretreatment with NSAID enhanced the duration of the renal vasoconstrictor effects of ouabain in the dog and converted late mesenteric vasodilation to early and persistent vasoconstriction. These data imply a potentially important role for vasodilating prostaglandins in modulating the mesenteric as well as the renal circulatory responses to ouabain.