Effects of a high K+/low Na+ diet on blood pressure in young spontaneously hypertensive rats

Blood pressure was measured after treatment with a high K+, a low Na+ and a combined high K+/low Na+ diet in young spontaneously hypertensive rats (SHR). A high K+ diet reduced blood pressure by approximately 10 mmHg during the development of hypertension. This decrease was accompanied by a significant increase in water intake and urine volume and a significant decrease in plasma renin activity (PRA). A low Na+ diet also decreased blood pressure significantly, but, in contrast to the high K+ diet, water intake and urine volume significantly decreased and PRA increased. When both diets were given together, the antihypertensive effects of both were eliminated. Thus while an increase in dietary K+ and a decrease in dietary Na+ are both effective antihypertensive regimens in SHR, the mechanism of action of each appears to be different and may be antagonistic in these animals.     

膳食钙对高血压大鼠血压的影响

目的：观察膳食钙对一氧化氮缺乏性高血压大鼠血压、血清一氧化氮浓度及一氧化氮合酶活性的影响。方法：实验于2005-10—22／20016—01—13在解放军第四军医大学动物实验室及形态学实验室进行。取雄性SD大鼠24只，随机区组等分成4组（n=6）：①对照组：基础饲料喂养，40mg／（kg&;#183;d）去离子水灌胃，饲养期间饮去离子水。②高钙组：第3周开始给予5．0％的高钙膳食，40mg/（kg&;#183;d）去离子水灌胃，饲养期间饮去离子水。③L-NAME＋高钙组：第3周始将40mg／（kg&;#183;d）左旋硝基精氨酸甲酯（L-NAME）溶于去离子水中每天灌胃，第7周停止给予L—NAME，开始给予5．0％的高钙膳食，饲养期间饮去离子水。④L—NAME组：第3周始将40me,／（kg&;#183;d）L—NAME溶于去离子水中灌胃，基础饲料喂养，饮去离子水。每周应用RBP—1型大鼠血压仪测量血压，10周后处死所有大鼠，硝酸还原酶法检测血清中一氧化氮的浓度和一氧化氮合酶活性。结果：24只大鼠全部进入结果分析。①血压：从实验第4周开始L-NAME＋高钙组和L-NAME组明显高于对照组和高钙组（P〈0．01）。从第7周到第10周实验结束时，L-NAME组血压明显高于其他3组（P〈0．01）。②血清一氧化氮浓度：对照组低于高钙组和L-NAME＋高钙组[（8．81&;#177;6．63），（14．80&;#177;5．32），（15．26&;#177;3．55）μmol／L，P〈0．05]，但高于L-NAME组[（2．89&;#177;1．71）μmol／LP〈0．05]；高钙组和L-NAME＋高钙组比较差异无显著性（P〉0．05）；L-NAME＋高钙组则高于L-NAME组（P〈0．05）。③血清一氧化氮合酶活性：对照组低于高钙组和L-NAME＋高钙组[（334．57&;#177;74．35），（436．09&;#177;69．35），（448．76&;#177;45．68）μkat／L，P〈0．05]，但高于L-NAME组[（255．88&;#177;35．17）μkat/L,P〈0．05]；高钙组和L-NAME＋高钙组比较差异不显著（P〉0．05）；L-NAME＋高钙组则高于L-NAME组（P〈0．05）。结论：①高钙膳食可以降低一氧化氮缺乏型高血压大鼠的血压，升高其血清一氧化氮浓度和一氧化氮合酶活性。②高钙膳食可以增加正常血压大鼠体内一氧化氮水平和一氧化氮合酶活性。     

膳食钙对高血压大鼠血压的影响

目的:观察膳食钙对一氧化氮缺乏性高血压大鼠血压、血清一氧化氮浓度及一氧化氮合酶活性的影响。方法:实验于2005-10-22/2006-01-13在解放军第四军医大学动物实验室及形态学实验室进行。取雄性SD大鼠24只,随机区组等分成4组(n=6):①对照组:基础饲料喂养,40mg/(kg·d)去离子水灌胃,饲养期间饮去离子水。②高钙组:第3周开始给予5.0%的高钙膳食,40mg/(kg·d)去离子水灌胃,饲养期间饮去离子水。③L-NAME 高钙组:第3周始将40mg/(kg·d)左旋硝基精氨酸甲酯(L-NAME)溶于去离子水中每天灌胃,第7周停止给予L-NAME,开始给予5.0%的高钙膳食,饲养期间饮去离子水。④L-NAME组:第3周始将40mg/(kg·d)L-NAME溶于去离子水中灌胃,基础饲料喂养,饮去离子水。每周应用RBP-1型大鼠血压仪测量血压,10周后处死所有大鼠,硝酸还原酶法检测血清中一氧化氮的浓度和一氧化氮合酶活性。结果:24只大鼠全部进入结果分析。①血压:从实验第4周开始L-NAME 高钙组和L-NAME组明显高于对照组和高钙组(P<0.01),从第7周到第10周实验结束时,L-NAME组血压明显高于其他3组(P<0.01)。②血清一氧化氮浓度:对照组低于高钙组和L-NAME 高钙组[(8.81±6.63),(14.80±5.32),(15.26±3.55)μmol/L,P<0.05],但高于L-NAME组[(2.89±1.71)μmol/L,P<0.05];高钙组和L-NAME 高钙组比较差异无显著性(P>0.05);L-NAME 高钙组则高于L-NAME组(P<0.05)。③血清一氧化氮合酶活性:对照组低于高钙组和L-NAME 高钙组[(334.57±74.35),(436.09±69.35),(448.76±45.68)μkat/L,P<0.05],但高于L-NAME组[(255.88±35.17)μkat/L,P<0.05];高钙组和L-NAME 高钙组比较差异不显著(P>0.05);L-NAME 高钙组则高于L-NAME组(P<0.05)。结论:①高钙膳食可以降低一氧化氮缺乏型高血压大鼠的血压,升高其血清一氧化氮浓度和一氧化氮合酶活性。②高钙膳食可以增加正常血压大鼠体内一氧化氮水平和一氧化氮合酶活性。     

Central effects of quinpirole on blood pressure of spontaneously hypertensive rats.

The i.v. administration of the dopamine D-2 receptor agonist quinpirole induced a rapid increase in blood pressure in spontaneously hypertensive rats (SHR). Heart rate showed little change. The pressor response to quinpirole was similar in SHR and normotensive Wistar-Kyoto rats (WKY) at doses of 0.03 to 0.3 mg/kg but, at 1 mg/kg, quinpirole induced a greater increase in blood pressure in SHR than in WKY. In contrast, although both strains showed a decreased locomotor activity after administration of 0.01 to 0.05 mg/kg of quinpirole, only in WKY was activity enhanced by 0.25 to 1.25 mg/kg of quinpirole. The i.v. administration of the dopamine agonists apomorphine, N-propylnorapomorphine and (R)-(+)-3-(3-hydroxyphenyl)-N-propylpiperidine, but not the putative presynaptic D-2 agonist (S)-(-)-3-(3-hydroxyphenyl)-N- propylpiperidine, induced pressor responses in SHR comparable to those after quinpirole administration. The pressor effect of quinpirole was enhanced by pretreatment with the peripheral D-2 antagonist domperidone, but blocked by the centrally acting dopamine antagonists haloperidol or sulpiride. In SHR, which were pretreated centrally with pertussis toxin, quinpirole induced a significantly smaller increase in blood pressure than in control SHR. Pretreatment centrally with 6-hydroxydopamine had no effect on the pressor action of quinpirole in SHR. Thirty minutes after i.v. administration of quinpirole, an additional injection of quinpirole did not significantly change blood pressure. Increasing the interval between two subsequent injections of quinpirole showed that this desensitization slowly reversed, but only after 24 hr had the pressor response to quinpirole fully recovered.(ABSTRACT TRUNCATED AT 250 WORDS)     

The effects of NG-nitro-L-arginine methyl ester on systolic pressure, diastolic pressure and pulse pressure according to the initial level of blood pressure

The objective of this study was to re-examine whether the effect of the nitric oxide synthesis inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME), on blood pressure depends on peripheral vascular tone. The effects of L-NAME (10 mg/kg, i.v.) on diastolic blood pressure (DBP), systolic blood pressure (SBP), pulse pressure (PP) and heart rate (HR) were studied in pithed rats. Sal-pithed rats received 0.9% NaCl, 10 microl/kg/min. Vascular tone was step-wise increased with 3, 10 and 30 microg/kg/min intravenous phenylephrine infusion (LPhe-pithed, MPhe-pithed and HPhe-pithed rats respectively). L-NAME elicited vasopressor responses in all the animals studied. L-NAME increases in SBP and DBP in Sal-pithed rats were significantly smaller than the ones obtained in phenylephrine infused rats. The increases in DBP elicited by L-NAME were greater in LPhe-pithed rats compared with those of MPhe-pithed and HPhe-pithed rats (i.e. the step-wise rises in DBP obtained with phenylephrine were inversely related to the increases in DBP produced by L-NAME); however, the increases in SBP were similar between these experimental groups. The PP increased during L-NAME-induced pressor responses in phenylephrine-infused rats. l-NAME increases in PP showed the following order: Sal-pithed < LPhe-pithed < MPhe-pithed < or = HPhe-pithed rats. HR was not modified by L-NAME. In conclusion, the vasopressor responses produced by L-NAME in pithed rats are influenced by the pre-existing vasomotor tone in complex form. We did not find a simple positive correlation between the vascular tone or level of arterial pressure, and the magnitude of the diastolic and systolic pressor responses elicited by L-NAME. Interestingly, the increase in PP induced by l-NAME was greater in accordance with the increasing value of baseline arterial pressure. NO synthesis inhibition in the arterial endothelium may possibly explain the increase in PP caused by L-NAME, as resulting from the reduction in proximal conduit artery compliance.     

The effects of hyperinsulinaemia on myocardial mass, blood pressure regulation and central haemodynamics in rats

Left ventricular hypertrophy is a condition with high mortality. An association with insulin resistance and hyperinsulinaemia has recently been suggested. The aim of this study was to examine the effects of isolated hyperinsulinaemia on cardiac weight and haemodynamic regulation. Rats were exposed to hyperinsulinaemia for 7 weeks after adrenalectomy with corticosterone substitution and continuous infusion of propranolol to control counter-regulatory mechanism ( n =15) (AIP group). Hypoglycaemia was prevented by glucose in the drinking water. Hyperinsulinaemic (AIP) rats were heavier and had increased relative masses of the myocardium (left ventricle 17% and right ventricle 20%), kidneys and adipose tissues in comparison with normoinsulinaemic adrenalectomized, corticosterone- and propranolol-treated controls (AP) ( n =10). Blood pressure in the insulin-exposed animals, measured weekly by the tail-cuff method in conscious rats, was not different from (AP) controls over 5 weeks, but increased in the sixth week. At the end of the seventh experimental week, blood pressure measured intra-arterially was also found to be elevated. Heart rate was not changed but total peripheral resistance was about twice that of controls ( P <0.001). Cardiac output and stroke volume was 30–40% lower in the AIP rats ( P <0.05). It is concluded that exposure to elevated insulin levels with control of counter-regulating mechanisms from β-adrenergic mechanisms and adrenals is not immediately followed by blood pressure elevation. It is, therefore, suggested that early onset of blood pressure elevation after insulin exposure might be caused by insulin counter-regulatory events, causing both insulin resistance and blood pressure elevation. The long-term adaptations may involve a direct influence by insulin as a 'trophic factor' on myocardial and on peripheral resistance vessels, followed by increased blood pressure, decreased cardiac output and stroke volume.     

Na+, K+ and water balance in young spontaneously hypertensive rats: relationship to blood pressure after high K+ treatment

These studies were designed to investigate the effects of high dietary K+ on electrolyte and water balance in young spontaneously hypertensive rats (SHR) and to relate these effects to changes in blood pressure. The high K+ diet reduced blood pressure by approximately 10 mmHg during the development of hypertension. Blood pressure, however, plateaued at the same maximum level as control by age 13 weeks. Rats fed the high K+ diet showed a significant increase in water intake and urine volume throughout the treatment period but no change in plasma volume or extracellular fluid volume occurred. A slight natriuresis was also observed in rats on the high K+ diet, but this was not of sufficient magnitude to decrease total body Na+. These results confirm previous findings that K+ causes a diuresis and a natriuresis, but demonstrate that the diuretic action of K+ cannot explain its antihypertensive properties in young SHR.     

Chronic lead exposure in rats: effects on blood pressure

Abstract. The influence of Pb exposure on blood pressure was investigated in Wistar Kyoto, Sprague Dawley and stroke prone spontaneously hypertensive rats. In short-term experiments, a dose-dependent decrease of blood pressure was found with administration of Pb acetate in drinking fluid. This effect was more pronounced in young, male as compared to old, female animals. Pressor responses to noradrenalin and ANG II were decreased. In contrast, long-term Pb exposure of more than 1 year duration consistently caused hypertension. In SHR-sp a high proportion of animals died from cerebrovascular haemorrhage even before developing hypertension. Chronically Pb exposed hypertensive rats had increased plasma volume and total body sodium despite normal renal function. Plasma concentrations of catecholamines and PRA were normal. The results show a biphasic effect of Pb on blood pressure. An important role of renal sodium retention in chronic Pb-induced experimental hypertension is suggested.     

复方壳多糖对生长期大鼠体质量和血脂水平的影响

背景实验和临床研究证实壳多糖具有减肥和降低血脂的作用,但是因用量较大存在一定的副作用.目的观察复方壳多糖对生长期大鼠体质量和血脂水平的影响.设计完全随机化分组实验.地点和材料 80只 SPF级别的 3～ 4周龄健康雄性 SD大鼠分为 4组饲养于四川省卫生管理干部学院具有屏障系统的恒温动物房内,各实验指标检测在本院实验室进行.干预 A组为正常对照组,喂饲基础饲料、 B组为高脂对照组,喂饲高脂饲料、 C组为壳多糖组,喂饲壳多糖饲料、 D组为复方壳多糖组,喂饲复方壳多糖.主要观察指标饲养 4周后检测各组动物体质量等生长发育指标和血清脂质.结果①体长和尾长各组动物饲后均有不同程度的增加,尤其是 C组 [(17.73± 0.99)cm]明显,与 A组 [(16.50± 1.03)cm]和 B组 [(16.35± 0.74)cm]差异有显著性意义( P《 0.05).②三酰甘油 B组 [(1.5680± 0.3000)mmol/L]显著高于 A[(0.9404± 0.2864)mmol/L]、 D[(0.6665± 0.2567)mmol/L]和 C组 [(0.8629± 0.3382)mmol/L]( P《 0.05); D组最低,与 A、 C组差异也有显著性意义( P《 0.05).③ HDL-c和 HDL-c/三酰甘油 D组 [分别为( 0.6367± 0.1223) mmol/L和 0.265]明显增高,与 B组 [分别为( 0.4821± 0.1058) mmol/L和 0.200]、 C组 [分别为( 0.5213± 0.0938) mmol/L和 0.209〗比较差异有显著性意义( P《 0.05).结论一定量的壳多糖摄入对生长期动物发育无影响,同时使三酰甘油水平降低,复方壳多糖减肥降脂作用明显优于单纯使用壳多糖,并使 HDL-c升高.     

高尿酸血症对血压水平及高血压患病率的影响

目的研究高尿酸血症对血压水平及高血压患病率的影响。方法对体检检出5 058例高尿酸血症及性别相同、年龄相同或相近的5058例非高尿酸血症进行分析,探讨其对血压水平、高血压患病率的影响及与多种心血管危险因素的关系。结果高尿酸血症组收缩压、舒张压分别较对照组升高4 mm Hg和3 mm Hg,高血压患病率为41.9%(95%C I:40.5%~43.3%),显著高于对照组31.3%(95%C I:30.0%~32.6%),差异有统计学意义。高尿酸血症组肥胖、高胆固醇血症及高三酰甘油血症患病率均高于对照组,差异有统计学意义。高尿酸血症、男性、年龄增长、肥胖、糖尿病、高胆固醇血症和高三酰甘油血症是高血压的独立危险因素。结论高尿酸血症与较高的血压水平有关,可能是高血压患病率增加的独立危险因素。     

Effects of the K+ channel activators, RP 52891, cromakalim and diazoxide, on the plasma insulin level, plasma renin activity and blood pressure in rats

In normo- or hyperglycemic (i.v. infusion of 50 mg/kg/min glucose over 30 min) pithed rats, diazoxide (1 mg/kg/min i.v. over 20 min) significantly reduced plasma insulin content. By contrast, cromakalim, nicorandil or RP 52891 even at doses 40-fold higher than those producing the same hypotensive effect as diazoxide in intact anesthetized normotensive rats, failed to change insulin plasma levels. Glibenclamide (0.01-0.3 mg/kg i.v.) pretreatment antagonized dose-dependently the hypoinsulinemic activity of diazoxide with an i.v. ED50 value of 49 +/- 1 microgram/kg. In pithed rats, diazoxide increased markedly plasma renin activity. This effect was almost inhibited completely by 20 mg/kg i.v., but not at all by a 1-mg/kg i.v. dose of glibenclamide. In pentobarbital-anesthetized rats, diazoxide (0.5-2 mg/kg/min i.v. over 20 min) produced decreases in mean carotid artery blood pressure which were antagonized dose-dependently by glibenclamide (5-20 mg/kg i.v.). This sulfonylurea (20 mg/kg i.v.) also prevented the hypotensive effects of several i.v. administered K+ channel activators (cromakalim, RP 52891 and nicorandil) but not those of numerous hypotensive agents such as acetylcholine, adenosine, bradykinin, clonidine, histamine, salbutamol, dihydralazine, papaverine, platelet aggregating factor, nitroglycerin, nitroprusside, nitrendipine and diltiazem. Although glibenclamide lowered plasma glucose levels, its blocking activity vis-à-vis the hypotension evoked by cromakalim was not affected when its hypoglycemic effects were reversed with an i.v. injection of glucose.(ABSTRACT TRUNCATED AT 250 WORDS)     

The effects of captopril on blood pressure, urinary water and electrolyte excretion and drinking behaviour in Brattleboro rats

The effects of the orally active converting enzyme inhibitor, captopril (SQ 14225), on blood pressures and intakes and urine outputs of water and electrolytes were studied in rats with hereditary hypothalamic diabetes insipidus (Brattleboro strain) and in Long Evans rats (parent strain). Captopril given in the drinking water (30 mg day-1 kg-1) caused an increase in fluid intake and urine output in both strains of rat; the difference between intake and measured output did not change. Captopril caused a significant natriuresis when given to animals in the non-steady state but did not significantly affect the urinary electrolyte excretion of animals in a steady state; in the latter group, however, captopril caused a significant reduction in food intake. Hence, under both conditions, captopril caused a reduction in sodium balance. Systolic blood pressures were reduced by captopril (given in the drinking water) in Long Evans rats and in Brattleboro rats; there was no accompanying change in heart rate. Bolus administration of captopril (30 mg day-1 kg-1) either intragastrically or subcutaneously did not change the fluid intakes or outputs in either strain of rat. In a separate experiment, rats were given the choice to drink water or a captopril solution. The results showed that the increased fluid intake in response to captopril was not due to a liking for the taste of the solution. The dipsogenic response to captopril may have been due to the fall in blood pressure which occurred, leading to renin release and a peripheral build-up of angiotensin I, which was converted into angiotensin II in the central nervous system. The possibility that the same dose given as a bolus may have inhibited central, as well as peripheral, converting enzyme activity is discussed.     

新生鼠窒息后肾组织Na+、K+-ATPase、TNF-α和NO的变化

目的探讨Na+、K+-ATPase、TNF-α和NO在新生鼠窒息后肾组织的变化及意义.方法将20只7～10日龄Wistar大白鼠随机分为窒息组和对照组,每组10只.制成常压窒息模型.在窒息30 min复氧120 min时,并分别采用酶联免疫吸附法(ELISA)、单一试剂法和定磷法检测肾组织肿瘤坏死因子-α(TNF-α)、NO含量、Na+、K+-ATPase活性.结果窒息后复氧120 min时,肾组织TNF-α、NO的含量较对照组显著升高(P＜0.05),而Na+、K+-ATPase活性下降(P＜0.05),且Na+、K+-ATPase的改变与TNF-α和NO含量之间呈显著的负相关关系(r＝-0.68和-0.72,P＜0.05),TNF-α和NO含量之间呈显著的正相关关系(r＝0.64,P＜0.05).结论窒息后肾组织Na+、K+-ATPase活性下降,其机制可能与TNF-α、NO造成细胞损伤有关.     

低声压级次声对大鼠脑缺血再灌注损伤的影响

目的：研究低声压级次声对大鼠局灶性脑缺血再灌注损伤的影响。方法：用线栓法制备右侧大脑中动脉脑缺血模型。以Infrasound 8TM次声治疗仪产出的次声作为处理因素。将64只大鼠随机分为3组,分别为假手术组（n=16）、模型组（n=16）、次声组（n=32）,次声组按每天作用时间分为20min组及120min组,每组16只大鼠。动态观察（第2小时、1天、3天和7天）各组神经功能状态,7d后大鼠断头取脑,每组中的8只用于HE染色,另外8只用于TTC染色以测定脑梗死相对体积。结果：与模型组相比,次声120mi     

Mechanisms of effects of intrathecal serotonin on nociception and blood pressure in rats

The effects of intrathecal (i.t.) serotonin (5-HT) and a number of serotonergic receptor agonists on nociception and blood pressure were examined in rats. Intrathecal 5-HT produced dose-dependent inhibition of the nociceptive tail-flick reflex (ED50 = 100.0 micrograms) and dose-dependent depressor effects. The 5-HT1A agonist 8-hydroxy-N,N-dipropyl-2-aminotetralin and the 5HT1B agonist 5-methoxy-3-(1,2,3,6-tetrahydro-4-pyridinyl)-1H-indole (RU-24969) also produced depressor effects but, in contrast to 5-HT, facilitated the tail-flick reflex, whereas the 5-HT2 agonists 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane, 6-chloro-2-(1-piperazinyl)-pyrazine (MK-212) and quipazine produced dose-dependent antinociception and had little or no effect on blood pressure. These results suggest that the antinociceptive and depressor effects of i.t. 5-HT are mediated by spinal 5-HT2 and 5-HT1 receptors, respectively. In other experiments, rats chronically treated with i.t. 5-HT developed tolerance to its antinociceptive effects, whereas chronic i.t. morphine or clonidine did not produce cross-tolerance to i.t. 5-HT. These results suggest that serotonergic spinal antinociceptive mechanisms are distinct from the mechanisms by which opioid receptor and alpha-2 adrenoceptor agonists produce antinociception in the spinal cord.     

复方中药四泰片对胰岛素抵抗综合征大鼠血压、血脂、血糖、胰岛素的影响

目的探讨复方中药四泰片对胰岛素抵抗综合征(insulin resistance syndrome,IRS)大鼠、血压、血脂、血糖、胰岛素的影响.方法选用清洁级雄性SD大鼠40只,按随机区组设计分为正常对照组、模型组、四泰片组、卡托普利组4组.采用高糖高脂饲料喂养大鼠8周,造成IRS大鼠模型,观察四泰片对IRS大鼠血压、血糖、血脂、胰岛素水平及胰岛素敏感性指数(insulin sensitivityindex,ISI)的影响.结果治疗后四泰片组、卡托普利组大鼠收缩压[(128±4),(110±2)mm Hg,(1 mm Hg=0.133 kPa)]与治疗前[(158±8),(157±7)mm Hg]和模型组[(165±6)mm Hg]比较,差异具有显著性意义(t=11.86～28.99,P<0.01).四泰片组大鼠总胆固醇、三酰甘油均较模型组下降(t=44.27,9.14,P<0.01),高密度脂蛋白胆固醇(high density lipoprotein cholesterol,HDL-C)升高(t=703,P<0.01).模型组大鼠空腹胰岛素(fastinginsulin,FINS)均升高,ISI下降,与正常对照组比较,差异均有显著性意义(t=7.14,9.35,P<0.01),胰岛素抵抗明显,造模成功;四泰片组、卡托普利组大鼠空腹血糖、FINS均下降,与模型组比较,差异均有显著性意义(t=11.95,6.71,P<0.01),卡托普利组空腹血糖与四泰片组比较,差异有显著性意义(t=8.33,P<0 01);四泰片组、卡托普利组ISI均升高,与模型组比较差异均有显著性意义(t=9.82,9.35,P<0.01).结论四泰片对IRS大鼠具有明显降压、降糖、降脂,提高胰岛素敏感性,改善胰岛素抵抗的综合效应.     

体重指数对血糖、血脂及血压的影响

目的探讨不同体重指数(BMI)水平对血糖、血脂及血压的影响。方法对1568例年龄≥20岁的健康体检者的资料进行统计学分析,按BMI不同分为四组:G1组(BMI≤18.5 kg/m2)、G2组(18.5 kg/m2BMI≤23.9 kg/m2)、G3组(24 kg/m2≤BMI≤27.9 kg/m2)和G4组(BMI≥28 kg/m2)。结果随BMI逐渐升高,收缩压、舒张压、空腹血糖(FPG)、餐后2 h血糖(PG 2 h)、总胆固醇、甘油三酯(TG)、低密度脂蛋白胆固醇均呈线性上升趋势,而高密度脂蛋白胆固醇呈下降趋势,组间比较差异有统计学意义。在G3组,FPG(6.2 0.4)mmol/L,PG 2 h(8.1 1.3)mmol/L,但血压和TG尚正常,G4组FPG(6.5 0.3)mmol/L,PG 2 h(9.0 1.6)mmol/L,血压均值139.5/88.3 mm Hg(1 mm Hg=0.133 kPa),TG(1.8 1.0)mmol/L。经Logistic逐步回归分析,G3及G4组均与糖尿病、高甘油三酯血症和高血压病呈独立正相关关系。结论 BMI≥24 kg/m2后发生糖尿病、高甘油三酯血症及高血压病的危险性大大增加。