氢水对高血压后血管病变有治疗作用

本文转摘自：2015-09-18 孙学军  氢思语

来自东华大学和第二军医大学药学院的关于氢气对自发性高血压大鼠效应的研究，在Biochemical Pharmacology（4.9）发表。研究结果发现，动物自发性高血压用氢水治疗后血压影响不明显，但是对血管病变有改善。

从表面上看，本研究只观察到氢水对高血压后血管病变有治疗作用。但是对降低血压没有作用。其实对原发性高血压来说，血管病变是非常关键的病变因素。甚至血管病变和继发性血管硬化会成为血压升高的病因，那么如果对血管病变有治疗作用，只要足够的时间，血压降低也是非常有可能的。要注意本研究观察的时间仍然不够长，如果继续进行更长期的观察，或许会看到血压的改善。许多高血压患者，结合改善生活方式和大量饮用氢水，有的竟然摆脱长期依赖的降血压药物。高血压非常容易自我检测，停止或减少用药完全是能自我控制的。考虑到长期服用药物本身可以带来肝脏和肾脏，甚至血管等副作用。如果能减少或停止服用药物，对高血压患者来说，实在是求之不得的好事。虽然不能说100%能达到这种效果，哪怕只有一定比例的患者实现停药，那么也值得尝试。

高血压患者氧化应激是导致血管功能异常的重要因素。最近研究表明，氢气作为一种抗氧化物质可以选择性中和强毒性自由基（羟基自由基和亚硝酸阴离子）。本研究观察用氢气生理盐水慢性给药对高血压后血管功能异常的治疗作用及其机制。8周年龄自发高血压大鼠和对照Wistar-Kyoto 鼠随机分为氢气盐水治疗组（6 mg/kg/d3月腹腔注射）对照组。氢气盐水治疗组可显著改善异常的血管功能，包括血管增生和内皮细胞异常。氢气治疗对血压无明显影响，但可以显著提高压力感受反射功能。特别对高血压后氧化应激具有显著的改善作用，包括抗氧化酶（SOD\CAT\Gpx\NADP氧化酶等），对炎症反应如炎症因子和相关信号分子也有显著影响。对线粒体功能也有正面作用，虽然对一氧化氮的产物没有影响，但可以抑制eNOS的表达，促进二甲基精氨酸二甲胺水解酶(DDAH)表达，说明对内皮细胞功能有改善作用。

Chronichydrogen-rich saline treatment attenuates vascular dysfunction in spontaneoushypertensive rats

HaoZhenga, 1, Yong-Sheng Yub, 1, ,

aDepartment of Pharmaceutical Science and Technology, College of Chemistry andBiology, Donghua University, Shanghai, China

The 8-week-old spontaneously hypertensive rats (SHR) and age-matched Wist ar-Kyotorats (WKY) were randomized into HRS-treated (6 ml/k). In hypertensive patients,increased oxidative stress is thought to be one important cause of vasculardysfunction. Recently, it has been suggested that hydrogen exerts a therapeuticantioxidant activity by selectively reducing hydroxyl radical andperoxynitrite, the most cytotoxic chemicals of reactive oxygen species (ROS).Herein, we investigated the protective effect of chronic treatment withhydrogen-rich saline (HRS) against vascular dysfunction in SHR and theunderlying mechanism.

Treatmentwith HRS ameliorated vascular dysfunction including aortic hypertrophy andendothelial function in SHR.

Treatmentwith HRS had no significant effect on blood pressure, but it signi ntlyimproved baroreflex function in SHR. Treatment with HRS abated oxidativestress, restored antioxidant enzymes including superoxide dismutase,glutathione peroxidase, and catalase, and suppressed NADPH oxidase.Furthermore, treatment with HRS depressed pro-inflammatory cytokines expressionincluding IL-6 and IL-1β and suppressed NF-κB activation, restoredmitochondrial function including ATP formation and membrane integrity. Inaddition, although treatment with HRS had no significant effect on nitric oxideamount in circulating or aorta, it suppressed endothelial nitric oxide synthaseexpression and upregulated dimethylarginine dimethylaminohydrolase 2 expressionin SHR. In conclusion, treatment with HRS alleviates vascular dysfunctionthrough abating oxidative stress, restoring baroreflex function, suppressinginflammation, preserving mitochondrial function, and enhancing nitric oxidebioavailability.