Henley W N, Tucker A
Am J Physiol. 1987 Mar;252(3 Pt 2):R554-61. doi: 10.1152/ajpregu.1987.252.3.R554.
The mechanism by which chronic, moderate, hypobaric hypoxia attenuates systemic systolic blood pressure (SBP) in the spontaneously hypertensive rat (SHR) was investigated in a three-part study. In experiment 1, 10 wk of hypoxia (3,658 m altitude) commencing in 7-wk-old rats was partially effective in preventing the rise in SBP [hypoxic SHR (SHR-H) 154 mmHg vs. normoxic SHR (SHR-N) 180 mmHg; P less than 0.01]. When hypoxia was initiated in 5-wk-old SHR (experiments 2 and 3), protection against hypertension was nearly complete (experiment 2: SHR-H 122 mmHg vs. SHR-N 175 mmHg; P less than 0.001; experiment 3: 135 vs. 152 mmHg, respectively; P less than 0.05). Elevations in O2 consumption (VO2) and rectal temperature (Tre) in SHR vs. normotensive [Wistar-Kyoto (WKY)] rats provided evidence that the SHR is a hypermetabolic animal. Thyroid hormonal indices suggested that SHR changed from a low to high thyroid status at a time that rapid blood pressure elevation occurred; however, hypoxia did not influence thyroid status. Acute, significant decrements in VO2 and Tre in SHR-H (experiments 2 and 3) accompanied the attenuation of SBP by hypoxia, whereas large decrements in VO2 and SBP did not occur in hypoxic WKY. Timely administration of moderate hypoxia protects against the development of hypertension in the SHR. This protection may relate to a metabolic adaptation made by the hypoxic SHR.
在一项分为三个部分的研究中，对慢性中度低压缺氧降低自发性高血压大鼠（SHR）全身收缩压（SBP）的机制进行了研究。在实验1中，7周龄大鼠开始进行10周的缺氧（海拔3658米）处理，对预防SBP升高有部分效果[缺氧SHR（SHR - H）为154 mmHg，而常氧SHR（SHR - N）为180 mmHg；P小于0.01]。当在5周龄的SHR中开始缺氧处理时（实验2和3），对高血压的预防几乎是完全的（实验2：SHR - H为122 mmHg，SHR - N为175 mmHg；P小于0.001；实验3：分别为135 mmHg和152 mmHg；P小于0.05）。与正常血压的[Wistar - Kyoto（WKY）]大鼠相比，SHR的耗氧量（VO2）和直肠温度（Tre）升高，这证明SHR是一种高代谢动物。甲状腺激素指标表明，在血压快速升高时，SHR从低甲状腺状态转变为高甲状腺状态；然而，缺氧并未影响甲状腺状态。SHR - H（实验2和3）中VO2和Tre的急性显著下降伴随着缺氧导致的SBP降低，而缺氧的WKY中VO2和SBP并未大幅下降。适时给予中度缺氧可预防SHR高血压的发展。这种保护作用可能与缺氧的SHR所产生的代谢适应有关。
