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老年原发性高血压合并2型糖尿病患者动态血压及血压变异性临床研究
目的 探讨老年原发性高血压合并2型糖尿病患者动态血压及血压变异性的变化.方法 选择老年患者180例,按有无糖尿病分为两组:A组为原发性高血压病组共87例;B组为糖尿病合并原发性高血压组(93例).24小时动态血压(ABP)检测,对该两组患者进行动态血压(ABP)以及血压变异性(BPV)的对比分析.结果 老年糖尿病合并原发性高血压患者夜间收缩压明显增高(P<0.01);24 小时及日间收缩压血压变异性显著增大(p<0.05).结论 老年2 型糖尿病合并原发性高血压患者动态血压及血压变异性增大,可能与糖尿病自主神经病变相关,使正常的血压节律消失.
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慢性肾脏病与血压变异性的关系
人体的血压随时间的变化而变化,在一定时间内血压的波动称为血压变异性.目前,血压变异性的机制仍未完全明确.自主神经系统对心血管系统的反应调节被认为是血压变异性的主要机制.此外,血管斑块及硬化、年龄、饮酒、高脂饮食、体育锻炼等均可对血压产生影响.近期有学者[1]提出,基因可能是决定血压变异性的主要因素.研究[2]表明,高血压患者血压变异性大于普通人群,而慢性肾脏病(chronic kidney diseases,CKD)患者高血压的发生率显著高于普通人群,现对CKD与血压变异性的关系作一综述.
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1. Biventricular hypertrophy has been described in a high blood pressure variability (BPV) model of sinoaortic-denervated (SAD) rats without systemic hypertension. To explore the possible involvement of the lung in SAD-induced right ventricular hypertrophy (RVH), we examined lung morphology, in addition to systemic haemodynamics and ventricle morphology, in Wistar-Kyoto rats 32 weeks after SAD. 2. In Wistar-Kyoto rats 32 weeks after SAD, there existed a substantial elevation in BPV, with no change in the average level of arterial pressure. Biventricular hypertrophy following SAD was characterized by a greater hypertrophy in right than left ventricles; both absolute and normalized right ventricular weights were significantly increased by 22 and 27%, respectively, and only normalized left ventricular weight was significantly increased by 12%. No infarcts were found in any ventricles examined. 3. In the lung, the most prominent change following SAD was pulmonary vasculopathy, including wall thickening, perivascular fibrosis and cell infiltration. In pulmonary arteries with an internal diameter of 70-130 microm, the external diameter, wall thickness and wall thickness to internal diameter ratio were increased in SAD compared with control rats. 4. There was no correlation between right and left ventricular weights. In contrast with BPV-correlated left ventricular weight, right ventricular weight was correlated with the wall thickness of the pulmonary artery, but not with BPV. 5. These findings suggest that greater RVH following SAD is associated with pulmonary vasculopathy, but is not secondary to the left ventricular problems or high BPV.
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Objective:It has been proposed that blood pressure variability(BPV) is positively related to end-organ damage(EOD) in hypertension.The present work was designed to observe the effects of long-term treatment with nitrendipine and hydralazine on BPV and EOD in spontaneously hypertensive rats(SHR),to examine the hypothesis that lowering BPV with an antihypertensive drug is an important factor in organ protection.Design and methods:Drugs were mixed in rat chow.After 4 months of drug administration,blood pressure was recorded continuously in conscious freely moving rats for 24 h.The heart,kidneys,and brain were then isolated and examined.Results:It was found that nitrendipine significantly decreased blood pressure and BPV,and significantly decreased EOD score in SHR.Hydralazine decreased blood pressure,but did not lower BPV.No effect on EOD was found in hydralazine-treated rats.In control rat(n=38),EOD score was weakly related to systolic blood pressure(r=0.331,P<0.05) and closely related to long-term systolic BPV(r=0.551,P<0.01).In nitrendipine-treated rats,EOD score was closely related to long-term systolic BPV(r=0.602,P<0.01),but not to blood pressure level(r=0.174,P>0.05).Conclusion:BPV plays an important role in the organ-protecting effects of nitrendipine.
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气道正压通气治疗对老年高血压合并睡眠呼吸暂停低通气综合征血压变异性的影响