肥胖相关高血压的研究进展

近年来越来越多的研究证实肥胖与血压升高密切相关。鉴于世界范围内肥胖与肥胖相关疾病的患病率上升,明确两者之间发生发展的病理生理机制对于肥胖人群高血压的诊断、预防及治疗意义重大。然而不同地域肥胖的诊断标准不同,肥胖相关高血压的病理生理机制与交感神经系统激活、肾素-血管紧张素-醛固酮系统(renin-angiotensin-aldosterone system,RAAS)激活、瘦素抵抗、食欲素过表达等神经体液因素复杂影响相关。肥胖相关高血压患者群体心血管系统损害不容忽视。互联网健康干预,外科手术治疗及合理降压药选择也为肥胖相关高血压防治提供了新思路。     

肥胖与高血压

众所周知，高血压是心脑血管病最主要的独立的危险因素，同时，高血压也是最常见的心脑血管疾病。肥胖也随着经济的迅猛发展和人民生活水平的提高，其患病率成倍上升。并且越来越多的资料表明，肥胖与健康密切相关。肥胖者发生多种疾病的机会增多，尤其是高血压、冠心病、脑卒中、血脂异常、糖尿病、乳腺癌、前列腺癌、腰腿关节痛等。本     

中医药治疗肥胖相关性高血压的进展

正现如今肥胖相关性高血压的患病率逐年递增。在西方国家,有65%~75%的原发性高血压患者体重超重[1],肥胖人群高血压患病率是非肥胖人群的2倍[2]。本文拟从现代医学、中医学两方面简要阐述肥胖相关性高血压的发病机制,并从药物、针灸、饮食导引等方面来阐明中医药在治疗及预防肥胖相关性高血压上的独到之处和显著疗效,进而展望未来中医     

瘦素与肥胖 高血压的初步探讨

瘦素(leptin)是Zhang等[1]在1994年发现由肥胖基因编码,脂肪细胞合成分泌的肽类激素。它是一种脂肪组织分泌的脂源性内分泌多肽激素,进入血液循环后作用于瘦素受体,参与糖、脂肪及能量代谢的调节,促使机体减少摄食、增加能量释     

瘦素与肥胖、高血压的关系

瘦素是1994年由美国学者首先克隆出的肥胖基因产物，因与代谢综合征的多个方面具有相关性，它包括高血压肥胖胰岛素抵抗脂质代谢异常。近年来越来越受到医学界的关注。本文主要将瘦素与肥胖高血压的关系作一简单综述。     

肥胖与高血压、高脂血症患病相关性研究

肥胖与多种成人代谢性疾病如高血压、高脂血症、糖尿病等疾病的发生密切相关。体脂增多及脂肪分布异常各自是上述疾病的独立风险因素。体质指数 (ｂｏｄｙｍａｓｓｉｎｄｅｘＢＭＩ)和腰臀比 (ｗａｉｓｔ -ｈｉｐ-ｃｉｒｃｕｍｆｅｒｅｎｃｅｒａｔｉｏＷＨＲ)是判断肥胖和肥胖     

胰岛素抵抗对老年男性肥胖高血压的影响

目的分析胰岛素抵抗与老年肥胖高血压的关系。方法用放射免疫法测定40例高血压和22例正常血压的老年男性患者血清胰岛素的含量。结果在高血压和肥胖分组中空腹血糖变化无显著性差异。非肥胖组高血压与正常血压者血清胰岛素的水平变化无显著性。肥胖组高血压者较正常血压者血清胰岛素含量平均升高2.7mIU/L(P<0.01)。高血压组中肥胖者较非肥胖者血清胰岛素水平平均升高4.7mIU/L(P<0.001)。胰岛素敏感指数在肥胖高血压组、肥胖非高血压组、非肥胖高血压组、非肥胖非高血压组中依次递减。结论老年肥胖高血压存在胰岛素抵抗,胰岛素与肥胖高血压有密切关系。     

成人高血压、糖尿病与肥胖的关系

目的：了解成人高血压、糖尿病与肥胖的关系，为心脑血管疾病的防治提供依据。方法：参照1995年全国糖尿病流行病学调查操作指南，随机抽取3个生活小区的成人居民作为调查对象。结果：此次调查实际人数为2932人，其中有效资料份数为2891份，有效率98．60％。标化后的高血压患病率为10．95％（男12．02％，女9．86％）。标化后的肥胖现患率为3.23％（男3．05％，女3．42％），超重现患率为19．55％（男24．42％，女16．50％）。不同BMI高血压患病率差异有显著性（X^2=113．36，P〈0.01）。随着BMI的增大，高血压患病率有避渐上升的趋势。有651人做空腹血糖、餐后血糖或口服葡萄糖耐量试验。结果显示，BMI≥24葡萄糖耐量异常患病率为11．43％（32／280），高于BMI〈24葡萄糖耐量异常的患病率[6．74％（25／371）]（X^2=4．39，P〈0.05）；有高血压者葡萄糖耐量异常患病率为16．38％（19／116），高于无高血压者葡萄糖耐量异常的患病率[7．10％（38／535）]（X^2=10,27，P〈0．005）。结论：超重、肥胖组的葡萄糖耐量异常患病率及高血压患病率均高于非肥胖组。肥胖与高血压、糖尿病往往共存，是心脑血管疾病的危险因素。控制胰岛素抵抗，去除可能导致胰岛素抵抗的因素，改善高胰岛素血症，对高血压、糖尿病、心脑血管病的防治有着极其重要的意义。     

胰岛素抵抗对老年男性肥胖高血压的影响

目的：分析胰岛素抵抗与老年肥胖高血压的关系。方法：用放射免疫法测定40例高血压和22例正常血压的老年男性患者无显著性差异。非肥胖组高血压与正常血压者血清胰岛素的水平变化一。肥胖组高血压者较正常血压者血清胰岛素含量平均升高2．7mIU/L(P&;lt;0.01)。高血压组中肥胖者较非肥胖者血清胰岛素水平平均升高4．7mIU/L(P&;lt;0.001)。胰岛素敏感指数在肥胖高血压组、肥胖非高血压组、非肥胖高血压组、非肥胖非高血压组中依次递减。结论：老年肥胖高血压存在胰岛素抵抗，胰岛素与肥胖高血压有密切关系。     

健步走对老年高血压患者肥胖和中心性肥胖的干预研究

目的探索由护士引导的“健步走老年高血压社区干预”对其肥胖和中心性肥胖的作用,为老年高血压的社区运动干预实践提供一定的指导。方法选取宁夏银川市两个经济水平、地理位置无明显差异的社区,进行系统的高血压知识健康教育后,各随机抽取45位高血压患者,然后将两个社区随机分为干预社区和对照社区。干预社区采取由护士引导的：运用社会认知理论及个体化运动处方的“健步走干预”;对照社区采用现有的高血压社区干预模式,6个月后比较其效果。两组均保持原有的饮食习惯及高血压用药。结果（1）干预组的收缩压和舒张压均数分别降低11．25mmHg和9．09mmHg,与对照组比较差异有统计学意义（P〈0．05）;（2）干预6个月后,干预组的体重、腰围、体重指数分别下降3．36kg、6．39cm和1．41,与对照组相比,腰围的差异具有统计学意义（P〈0．05）;（3）干预组超重和肥胖各减少4例（9．09％）,中心性肥胖减少20例（45．45％）,与对照组相比,干预后中心性肥胖的差异具有统计学意义（P〈0．05）。结论健步走对Ⅰ级、Ⅱ级高血压的控制能起到良好的辅助作用;对减重有一定效果,尤其是中心性肥胖者。     

Management of obesity

Advanced dressings have developed considerably over the last 40 to 50 years since research by George Winter realized the benefit of moist wound management. Coupled with the prevention of wound infection and removal of wound debris, the choices available under the heading of ‘Advanced’ wound management are over 2000 in number!     

Management of obesity

We live in an overweight society. Although food consumption has not increased dramatically over the last two decades, physical activity has markedly diminished. However, recent studies suggest that weights up to 20% above ideal body weight do not carry a significant risk of increased mortality in the absence of other chronic diseases. A team approach helps maintain patient motivation, the key to an effective weight-loss program. An efficient weight-loss and weight-maintenance program in the moderately obese patient includes modification of eating patterns, an individualized balanced fuel-source diet, and an exercise program to allow caloric deficit of approximately 500 calories a day. We must realize that for morbidly obese patients in whom the amount of caloric restriction necessary to reach and maintain a desirable body weight may be incompatible with a reasonable quality of life, surgery is warranted. The aggressiveness of our therapeutic regimen should always depend on the risk of morbidity and mortality associated with the patient's degree of obesity.     

Overweight and obesity in hypertension

Many studies have shown body weight to correlate with blood pressure and the prevalence of hypertension, but few have examined whether the correlation between overweight and hypertension holds at higher levels of blood pressure. This study evaluated the degree of overweight and hypertension among 1795 adult men and women with hypertension (diastolic pressure greater than or equal to 90 mmHg) who were referred to a community-based hypertension clinic in Milwaukee during a five-year period. Using a nomogram for body mass index (BMI), we found that more than one-third of the subjects were overweight and over one-third were obese, with black and white females showing slightly higher indices than males. There was a trend for BMI to decline with age in both ethnic groups. Among the group not on antihypertensive medication (1344 patients), there was no correlation between BMI and blood pressure. Blood pressure correlated positively with age but BMI showed an opposite trend. After BMI was corrected for age, the correlation was the same and tended to be in the negative direction. A striking trend observed is that the higher the BMI, the greater the percentage of subjects with diastolic pressures between 90-104 mmHg. These results do not necessarily contradict a possible role of obesity in hypertension. Rather, they confirm the high prevalence of overweight among hypertensives and suggest that a large proportion of obese hypertensives tend to have a relatively mild pressure elevation. In view of the known hypotensive effect of weight reduction, the likelihood of reducing blood pressure to normotensive levels in this group by diet is stressed.     

Management of obesity cardiomyopathy

Obesity causes a variety of hemodynamic alterations that may lead to changes in cardiac structure and function. Although such abnormalities may occur in patients with mild-to-moderate obesity, they are most pronounced in those with morbid obesity. When these alterations produce congestive heart failure, obesity cardiomyopathy is said to be present. In this review, the authors will first discuss the pathogenesis and clinical manifestations of obesity cardiomyopathy and then describe the management of this clinical syndrome with emphasis on the effects of weight reduction.     

Renal functional reserve in obesity hypertension

The capacity to increase glomerular filtration rate in response to an acute oral protein load is known as the renal functional reserve; the loss of such capacity is used as a marker of hyperfiltration. This physiological response in obese hypertensives is not yet fully understood. We aimed to study the interdependent effects of obesity and hypertension on renal reserve, taking into account renal kallikrein and nitric oxide in the modulation of that parameter. Fourteen obese hypertensives (mean age, 50.5 +/- 0.9 years) and nine lean hypertensives (mean age, 50.6 +/- 2.7 years) were evaluated. Renal haemodynamics and the levels of serum nitric oxide and urinary kallikrein were assessed at baseline and after a protein load (1 g/kg of body weight). An increase in the following parameters was observed when comparing obese and lean hypertensives: basal glomerular filtration rate; renal plasma flow; and urinary kallikrein and nitric oxide levels (129.2 +/- 2.9 vs. 101.4 +/- 3.4 ml/min/1.73 m2; 587.5 +/- 18.2 vs. 502.8 +/- 16.7 ml/min/1.73 m2; 0.120 +/- 0.02 vs. 0.113 +/- 0.02 mU/ml; 23.2 +/- 0.8 vs. 19.5 +/- 1.2 mmol/ml, respectively). The renal reserve was lower in obese hypertensives when compared with that of lean hypertensives (4.1 +/- 0.5 vs. 11.8 +/- 0.8 ml/min, p < 0.005). After a protein load, contrasting with the lean group, inability to elevate the nitric oxide serum levels and a lower increase in urinary kallikrein were observed in the obese group. These data suggest that obese hypertensives lose renal reserve earlier in the evolution to renal dysfunction. This may be due to the defective modulation of renal vasodilatation mechanisms by renal kallikrein and nitric oxide production.     

Management of obesity cardiomyopathy

Obesity causes a variety of hemodynamic alterations that may lead to changes in cardiac structure and function. Although such abnormalities may occur in patients with mild-to-moderate obesity, they are most pronounced in those with morbid obesity. When these alterations produce congestive heart failure, obesity cardiomyopathy is said to be present. In this review, the authors will first discuss the pathogenesis and clinical manifestations of obesity cardiomyopathy and then describe the management of this clinical syndrome with emphasis on the effects of weight reduction.     

肥胖相关性肾病病理机制及研究进展

近年来,肥胖相关性肾病引起越来越多的关注。本文将概述肥胖相关性肾病的临床特点,总结其病理生理机制包括肾脏血流动力学异常、蛋白尿、血脂异常、高血压、高胰岛素血症及微炎症状态的作用机制,并归纳其病理学改变以及展望肥胖相关性肾病的研究方向。