Lin Hui, Chen Bao-yuan, Jiang Qiu-fang, Kong Cheng-ying, Zhang Jing, Zheng Li-wen
Department of Respiratory Medicine, General Hospital, Tianjin Medical University, Tianjin 300052, China.
Zhonghua Jie He He Hu Xi Za Zhi. 2012 May;35(5):345-8.
To study the role of sympathetic nerve activity during the development of hypertension resulting from chronic intermittent hypoxia, and whether or not elevated sympathetic nerve activity is related to oxidative stress, and to investigate the preventive effect and possible mechanism of Tempol.
Forty-eight male Wistar rats were randomly divided into 6 groups of 8 each, including normoxic control group (NC), intermittent hypoxia group (IH) and 4 treatment groups (IHT1, IHT2, IHN1, IHN2). Among the treatment groups, IHT1, IHT2 groups were treated with 10% Tempol 100 mg × kg(-1)× d(-1) by intraperitoneal injection before exposed to IH and on day 28 after exposed to IH respectively, while IHN1 and IHN2 groups were treated with NS as controls.
There was no statistic difference in artery systolic blood pressure (SBP) between IH group, IHN1 group [(114 ± 6) mm Hg, 1 mm Hg = 0.133 kPa], and IHN2 group [(128 ± 6) mm Hg, P < 0.05] at the end of 6(th) week. SBP in the all IH groups was significantly elevated compared with NC group (P < 0.05) and the baseline SBP (P < 0.05) except of the group IHT1. SBP in the 2 tempol treatment groups was lower than the NS groups [(138 ± 10) mm Hg, both P < 0.05], while SBP of IHT2 group was higher than the IHT1 group (P < 0.01). No significant changes were found in the NC group. There were no statistic difference of NE and E in plasma and MDA in adrenal gland tissues between IH groups, IHN1 group and IHN2 group. The levels in NE and E and MDA in the 2 tempol treatment groups were lower than the NS groups (P < 0.05 or P < 0.01), but those in the IHT2 group were higher than the NC group (P < 0.05 or P < 0.01) and IHT1 groups (P < 0.05 or P < 0.01). No significant difference were found between IHT1 group and NC group.
CIH could generate ROS by causing oxidative stress, which results in elevated sympathetic nerve activity. This may be one of the important mechanisms for CIH-induced hypertension. Tempol may be useful for prevention and treatment of OSAS-induced hypertension.
研究慢性间歇性缺氧导致高血压过程中交感神经活动的作用,以及交感神经活动增强是否与氧化应激有关,并探讨Tempol的预防作用及可能机制。
48只雄性Wistar大鼠随机分为6组,每组8只,包括常氧对照组(NC)、间歇性缺氧组(IH)和4个治疗组(IHT1、IHT2、IHN1、IHN2)。在治疗组中,IHT1、IHT2组分别在暴露于IH前及暴露于IH后第28天腹腔注射10% Tempol 100 mg×kg(-1)×d(-1),而IHN1和IHN2组用生理盐水作为对照。
第6周结束时,IH组、IHN1组[(114±6)mmHg,1 mmHg = 0.133 kPa]和IHN2组[(128±6)mmHg,P<0.05]的动脉收缩压(SBP)无统计学差异。除IHT1组外,所有IH组的SBP均显著高于NC组(P<0.05)和基线SBP(P<0.05)。2个Tempol治疗组的SBP低于生理盐水组[(138±10)mmHg,P均<0.05],而IHT2组的SBP高于IHT1组(P<0.01)。NC组无明显变化。IH组、IHN1组和IHN2组之间血浆中的去甲肾上腺素(NE)和肾上腺素(E)以及肾上腺组织中的丙二醛(MDA)无统计学差异。2个Tempol治疗组的NE、E和MDA水平低于生理盐水组(P<0.05或P<0.01),但IHT2组高于NC组(P<0.05或P<0.01)和IHT1组(P<0.05或P<0.01)。IHT1组和NC组之间无显著差异。
慢性间歇性缺氧可通过引起氧化应激产生活性氧,导致交感神经活动增强。这可能是慢性间歇性缺氧诱导高血压的重要机制之一。Tempol可能对阻塞性睡眠呼吸暂停综合征诱导的高血压有防治作用。