Non‐thermal vasodilatation by radio frequency burst‐type electromagnetic field radiation in the frog.
Non‐thermal vasodilatation by radio frequency burst‐type electromagnetic field radiation in the frog.
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通过射频突发型电磁场辐射对青蛙进行非热血管舒张。
DOI：
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发表时间：
1991
期刊：
影响因子：
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通讯作者：
J. Okada
中科院分区：
文献类型：
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作者：
Mitsuhiko Miura;J. Okada
1.用维持在20℃的Ringer液灌流麻醉非洲爪哇时，射频(RF)爆发式电磁场辐射不仅使去甲肾上腺素预收缩的爪哇小动脉扩张，而且在非刺激条件下扩张。电磁场诱导的血管扩张缓慢增加，在照射后60min达到高峰。停止照射后，血管扩张持续10~20min，然后缓慢消退。2.在10 MHz，1V(峰峰值)产生的7.3毫高斯，2.19V cm-1电磁场作用下，以10 kHz的爆发频率施加总时间的50%时，血管扩张效果最佳。3.由于电磁场太弱而不能产生足够的热来扩张微动脉，因此血管的扩张作用不是次要的，因为电磁场太弱了，而且热一直被灌注液带走。4.温升至30℃的林格液灌流时，血管未见扩张，而温升至35℃的林格液灌流时，仅有11%的血管扩张。用Ringer液灌流至37℃可引起不可逆的血管收缩。温林格溶液的血管扩张作用模式不同于弱电磁场辐射的血管扩张作用。5.血管扩张作用程度受灌注液中钙离子浓度的影响。在正常钙离子条件下，小动脉扩张到对照直径的126%，而在无钙条件下，小动脉扩张到对照的131%，而在高钙条件下(是正常水平的两倍)，小动脉扩张到对照的111%。提示血管扩张作用可能是通过促进钙离子外流引起的，其程度可能稳定在钙离子内流与外流之间的逆流流量的平衡水平。6.无Na(+)Ringer液灌流对血管的扩张作用无抑制作用，提示Na(+)-Ca~(2+)交换系统可能不参与扩张血管的作用。血管扩张作用可被Ca(2+)-ATPase抑制剂钒酸盐所抑制，并可被鸟苷酸环化酶抑制剂亚甲蓝所阻断。有证据表明，血管扩张作用的机制可能依赖于通过平滑肌质膜的钙流出增加和/或钙离子流入肌浆网的增加。
1. When the web of the anaesthetized Xenopus laevis was perfused with Ringer solution maintained at 20 degrees C, radio frequency (RF) burst‐type electromagnetic (EM) field radiation not only dilated arterioles of the web which had been preconstricted with noradrenaline, but also dilated arterioles under non‐stimulated conditions. The EM field‐induced vasodilatation increased slowly and reached a plateau 60 min after the onset of radiation. After the cessation of radiation, vasodilatation remained for 10‐20 min, then slowly subsided. 2. When a 10 MHz, 1 V (peak to peak) generator voltage induced a 7.3 milliGauss, 2.19 V cm‐1 EM field, the vasodilatory effect was optimum when bursts were applied 50% of the total time at 10 kHz burst rate. 3. The vasodilatory effect was not secondary to dielectric heat in the web, because the EM field was too weak to have produced enough heat to dilate the arterioles and heat would have been constantly conducted away by the perfusion solution. 4. During perfusion with Ringer solution warmed to 30 degrees C, no vasodilatation was found, but perfusion with Ringer solution warmed to 35 degrees C induced only 11% vasodilatation. Perfusion with Ringer solution warmed to 37 degrees C induced irreversible vasoconstriction. The pattern of vasodilatation induced by warm Ringer solution was different from the vasodilatory effect of weak EM field radiation. 5. The extent of the vasodilatory effect was influenced by Ca2+ concentration of the perfusion medium. Under normal Ca2+ conditions arterioles dilated to 126% of the control diameter, while under Ca(2+)‐free conditions arterioles dilated to 131% of the control value and under high‐Ca2+ conditions (twice the normal level) arterioles dilated to 111% of the control value. This suggests that the vasodilatory effect may be caused by facilitation of Ca2+ outflow, and the extent of this flow may settle down to the equilibrium level of countercurrent flux between Ca2+ influx and outflow. 6. The vasodilatory effect was not inhibited under perfusion with Na(+)‐free Ringer solution, suggesting that Na(+)‐Ca2+ exchange system may not be involved in the vasodilatory effect. The vasodilatory effect was inhibited by vanadate, an inhibitor of Ca(2+)‐ATPase, and was abolished by Methylene Blue, an inhibitor of guanylate cyclase. The evidence suggests that the mechanism of the vasodilatory effect may depend on an increase in Ca2+ outflow through the plasma membrane of the smooth muscle and/or an increase in Ca2+ influx into the sarcoplasmic reticulum.(ABSTRACT TRUNCATED AT 400 WORDS)