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一氧化氮是否介导35吉赫兹微波加热引起的循环衰竭?

Does nitric oxide mediate circulatory failure induced by 35-GHz microwave heating?

作者信息

Ryan K L, Frei M R, Berger R E, Jauchem J R

机构信息

Department of Biology, Trinity University, San Antonio, Texas 78212, USA.

出版信息

Shock. 1996 Jul;6(1):71-6. doi: 10.1097/00024382-199607000-00015.

DOI:10.1097/00024382-199607000-00015
PMID:8828089
Abstract

The purpose of this study was to determine whether nitric oxide (NO) contributes to the hypotensive state induced by exposure to radiofrequency radiation of millimeter-wavelength (MMW). This was accomplished using a synthetic analogue of L-arginine, N omega-nitro-L-arginine methyl ester (L-NAME), to competitively inhibit NO synthesis. Ketamine-anesthetized rats were instrumented for the measurement of arterial blood pressure, ECG, and temperature at five sites. Animals were exposed to 35-GHz radiofrequency radiation until mean arterial pressure (MAP) decreased to 75 mmHg. MMW exposure was then halted and either saline or L-NAME (1, 2.5, 5, or 10 mg/kg) was administered; each rat received only one dose. Following irradiation, L-NAME at each dose produced a peak increase in MAP that was smaller than that produced by the same dose of L-NAME in nonirradiated rats. There was no difference in post-MMW survival times between L-NAME-and saline-treated rats. These results indicate that bolus administration of L-NAME does not reverse hypotension induced by 35-GHz microwave heating, suggesting that excess levels of NO do not mediate this form of circulatory failure.

摘要

本研究的目的是确定一氧化氮(NO)是否参与了暴露于毫米波波长(MMW)射频辐射所诱发的低血压状态。通过使用L-精氨酸的合成类似物Nω-硝基-L-精氨酸甲酯(L-NAME)竞争性抑制NO合成来实现这一目的。用氯胺酮麻醉大鼠,并在五个部位监测动脉血压、心电图和体温。将动物暴露于35GHz射频辐射,直至平均动脉压(MAP)降至75mmHg。然后停止MMW暴露,并给予生理盐水或L-NAME(1、2.5、5或10mg/kg);每只大鼠仅接受一剂。照射后,各剂量的L-NAME使MAP达到的峰值升高幅度小于未照射大鼠接受相同剂量L-NAME时的升高幅度。L-NAME处理组和生理盐水处理组大鼠在MMW照射后的存活时间没有差异。这些结果表明,推注L-NAME不能逆转35GHz微波加热所诱发的低血压,提示过量的NO并非这种循环衰竭形式的介导因素。

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