力竭性运动对大鼠脑组织中一氧化氮合成酶活性的影响

目的研究力竭性运动对机体脑组织中一氧化氮合成酶(NOS)活性的影响.方法大鼠进行力竭游泳,测定脑组织中构建型NOS(cNOS)和诱导型NOS(iNOS)活性.结果力竭性运动后,脑组织中iNOS活性显著升高,而cNOS活性无显著变化.结论力竭运动可使脑组织中iNOS活性升高,,从而诱导合成大量的NO,这可能是导致中枢性运动疲劳产生的原因.     

运动训练对大鼠损伤远端脊髓及骨骼肌血管内皮生长因子表达的影响

目的:明确运动训练对大鼠损伤远端脊髓及骨骼肌血管内皮生长因子(VEGF)表达的影响,探讨运动促脊髓损伤功能恢复的机制。方法:成年雌性SD大鼠24只,采用改良Allen撞击法制作T9不完全性脊髓损伤模型。术后随机分为损伤后1d组、1周组、训练组(术后1周开始训练,共4周)、对照组(未行训练)。分别在损伤前、损伤后第1、2、3、4及5周时采用Basso-Beattie-Bresnahan(BBB)评分评定运动功能。取损伤后1d、1周,对照组及训练组大鼠L5—S1节段脊髓及腓肠肌新鲜组织,采用RT-PCR及Westernblot法测定VEGFmRNA及蛋白表达。结果:①对照组与训练组BBB评分均较损伤后1周、2周明显提高,但训练组较对照组增加更为显著(P<0.05);②训练组脊髓及腓肠肌VEGFmRNA及蛋白表达较对照组、损伤后1d、1周组显著增加(P<0.05);对照组与损伤1周组、1d组比较脊髓及腓肠肌内VEGF表达差异无显著性(P>0.05);但1周组脊髓内VEGF较1d组表达增加(P<0.05),而腓肠肌内VEGF表达较1d组降低(P<0.05)。结论:运动训练能有效诱导脊髓损伤大鼠远端脊髓及骨骼肌VEGF表达,促进运动功能恢复。     

参芎葡萄糖注射液对脊髓损伤后一氧化氮合成酶和血管内皮生长因子表达及运动功能恢复的影响

摘要 目的：研究参芎葡萄糖注射液对大鼠脊髓损伤(SCI)后诱导型一氧化氮合成酶(iNOS)和血管内皮生长因子(VEGF)蛋白表达变化,探讨参芎葡萄糖注射液对急性脊髓损伤后运动功能恢复的影响和可能机制。 方法：用改良Allen法制作大鼠T12脊髓损伤模型60只,随机分为对照组（30只）和药物组（30只）。术后第1、3、7、14、21天采用BBB评分和斜板试验对大鼠急性脊髓损伤后的运动功能进行评估,病理学检查观察脊髓损伤后病理改变,免疫组织化学方法和免疫印迹方法观察损伤脊髓iNOS、VEGF的表达变化,并进行比较分析。 结果：术后各时相点BBB评分和斜板试验,除第1天外,第3、7、14、21天药物组明显高于对照组;药物组各时相点的病理改变明显较轻,药物组各时相点iNOS阳性表达均明显低于对照组,而VEGF的阳性表达均明显高于对照组,两组差异有显著性意义(P<0.05)。 结论：脊髓损伤后应用参芎葡萄糖注射液可以抑制iNOS的表达,增强VEGF的表达,抑制脊髓损伤区iNOS的表达和上调脊髓损伤区VEGF的表达可能是参芎葡萄糖注射液减轻继发脊髓损伤,促进损伤脊髓功能恢复的机制之一。     

运动训练对高血压患者血压、内源性一氧化氮及内皮素的影响

目的：明确原发性高血压病患者的运动康复与血压、血一氧化氮、内皮素水平变化的关系。方法：62例原发性高血压病患者，分为训练组(n=51)和对照组(n=11)。训练组进行为期7周，每周6次，每次1小时的轻、中度运动训练。结果：训练组患者运动后血压、血一氧化氮、内皮素水平均显著下降。对照组无明显变化。结论：在原发性高血压患者的运动康复中血一氧化氮、内皮素水平有明显改变。     

力竭性运动对大鼠脑组织中一氧化氮合成酶活性的影响

目的：研究力竭性运动对机体脑组织中一氧化氮合成酶（ＮＯＳ）活性的影响。方法：大鼠进行力竭游泳,测定脑组织中构建型ＮＯＳ（ｃＮＯＳ）和诱导型ＮＯＳ（ｉＮＯＳ）活性。结果：力竭性运动后,脑组织中ｉＮＯＳ活性显升高,而ｃＮＯＳ活性无显变化。结论：力竭运动可使脑组织中ｉＮＯＳ活性升高,从而诱导合成大量的ＮＯ,这可能是导致中枢性运动疲劳产生的原因。     

高糖对内皮型一氧化氮合成酶的表达及功能的影响

目的：研究高糖对内皮型一氧化氮合成酶的基因和蛋白表达及其功能的影响。方法：将分离的小牛主动脉内皮细胞在含有不同浓度右旋葡萄糖的DMEM中培养24小时。内皮型一氧化氮合成酶的基因和蛋白表达分别以RT—PCR和Western Blotting方法进行分析,其产物一氧化氮以高效液相层析法(HPLC)测定。结果：与低糖(5．6mM)相比高糖(12．5mM,25mM)可以刺激内皮型一氧化氮合成酶的基因和蛋白表达,并伴有一氧化氮的浓度降低。结论：高糖可致内皮型一氧化氨合成酶的基因和蛋白表达增加,并可能导致其功能障碍。     

有氧运动对高血压患者血管内皮功能的影响

研究表明，有规律地进行中等强度的有氧运动。可使轻度原发性高血压患者的收缩压下降6-10mmHg，舒张压下降4-8mmHg。WHO，特别是美国预防、检测、评估和治疗高血压全国联合委员会第七次报告（JNC-Ⅶ）建议那些轻中度原发性高血压患者，每天要进行50％VO2max强度的有氧运动30min，每周5—7次。按照上述指南．要坚持每次30min以上，每周3次以上的运动，10周后运动的降压效应方能显现出来。研究表明，运动训练有利于改变冠心病的危险因素，包括高血压患者的安静状态血压。     

运动训练对原发性高血压患者血压、内皮素、一氧化氮及心钠素的影响

目的 探讨原发性高血压患者的运动训练与血心钠素（ANP）、一氧化氮（NO）及内皮素（ET）水平变化的关系。方法 将62例原发性高血压病患者分为运动组（n=51）和对照组（n=11）。训练组进行为期7周，每周6次，每次1h的轻、中度运动训练。结果 训练组患者运动后血压、ANP、NO及ET水平均显著下降，对照组无明显变化。结论运动训练可使原发性高血压患者的血压降低，ET、NO及ANP水平下降。     

卡维地洛对高血压患者血管内皮功能的影响

卡维地洛是一种新型的口受体阻滞剂，有降血压、改善心肌重构、抗氧化等多方面的作用。作者通过轻、中度高血压患者服用卡维地洛降血压治疗后血浆一氧化氮（NO）、内皮素（ET-1）和24h尿白蛋白变化，探讨卡维地洛对高血压患者血管内皮功能的保护作用。     

应用高频超声对高血压及高血压伴吸烟患者血管内皮舒张功能的研究

目的　应用高分辨超声技术对原发性高血压及高血压伴吸烟患者的内皮依赖性血管舒张功能进行研究和分析。方法　采用高频超声技术 ,对 6 3例患者其中 2 2例原发性高血压 (EH) ,2 2例高血压伴吸烟患者(EH+SM) ,和 19例正常血压无吸烟史者 (NT)的血管内皮依赖性舒张功能进行测定评价 ,并测定其血浆一氧化氮 (NO) ,内皮素 (ET) ,血栓素 B2 (TXB2 )和前列腺环素 (PGI2 )等血管活性物质的浓度变化。结果　发现 EH+SM和 EH组肱动脉血流介导的血管舒张百分率 FMD%均较 NT组明显减弱 (P均 <0 .0 0 1) ,EH+SM组又较EH组明显减弱 (P=0 .0 2 3) ,而三组对硝酸甘油的反应无显著性差异 (P均 >0 .0 5 )。 EH+SM及 EH组血浆 NO,PGI2 水平均较 NT组减低 (P均 <0 .0 1) ,EH+SM组又较 EH组明显降低 (P=0 .0 2 9)。结论　高血压患者存在血管内皮依赖性舒张功能受损 ,高血压伴吸烟患者 ,内皮功能损伤进一步加重 ,高频超声是评价血管内皮依赖性舒张功能的简单、无创、可靠的方法。     

Effects of diuretics on stroke development in Kyoto-Wistar stroke-prone spontaneously hypertensive rats.

1. Previous studies have indicated that increases in dietary K+ promote diuresis and retard stroke development in stroke-prone spontaneously hypertensive rats (spSHR) fed a Japanese-style diet containing 4% NaCl. 2. It is possible that elevations in dietary K+ retard stroke development by inducing natriuresis and facilitating the clearance of Na+, and that diuretics associated with natriuresis might also be capable of retarding stroke development in spSHR. To test if this was the case, the onset of stroke development in spSHR fed a low (0.75%) K+ diet containing 4% NaCl (controls) was monitored and compared with that in spSHR treated with (a) frusemide, (b) chlorothiazide, (c) amiloride or (d) acetazolamide, and with (e) untreated spSHR fed a high (2.11%) K+ diet. 3. The onset of stroke, as well as death resulting from stroke, occurred at a significantly later age in spSHR fed a high K+ diet than in spSHR fed a low-K+ diet, despite the fact that both groups of spSHR rats had comparable blood pressures. 4. Treatment of spSHR with the above-named diuretics before stroke development did not alter the blood pressure of the rats. The onset of stroke development and death in spSHR treated with chlorothiazide, amiloride or acetazolamide was comparable with that observed in untreated control spSHR. In spSHR treated with frusemide, the onset of stroke was comparable with that of untreated control spSHR, whereas the onset of death after stroke development was accelerated. 5. Post mortems performed on spSHR that developed stroke indicated the presence of haemorrhagic stroke of comparable severity in the six groups of spSHR studied.(ABSTRACT TRUNCATED AT 250 WORDS)     

Pharmacological studies of alcohol susceptibility and brain monoamine function in stroke-prone spontaneously hypertensive rats (SHRSP) and stroke-resistant spontaneously hypertensive rats (SHRSR)

Differences of alcohol drinking behavior, brain dopamine (DA) and serotonin (5-HT) levels and releases in the striatum were investigated in stroke-prone spontaneously hypertensive rats (SHRSP) and age-matched stroke-resistant spontaneously hypertensive rats (SHRSR). Voluntary alcohol (EtOH) consumption in SHRSP rats increased at 1 and 2 hours in the 4 hour time access. In the DA level, SHRSP showed decreases in the caudate-putamen (C/P) and dorsal raphe nucleus (DRN) compared with in SHRSR. 5-HT levels in the C/P, ventral tegmental area-subtantia nigra (V/S) and DRN of the SHRSP were decreased compared with that in SHRSR. The basal extracellular levels of 5-HT release in the C/P were increased in SHRSP as compared with those in SHRSR. K(+)- or EtOH-induced DA and 5-HT releases in the C/P of the SHRSP were a lower magnitude than those in SHRSR. Increased basal extracellular 5-HT releases showing low levels of 5-HT in the C/P of SHRSP mean an abnormality of serotonergic neuronal functions in a normal physiological condition. Higher voluntary alcohol drinking behavior, so called lower susceptibility to EtOH, in the SHRSP may be associated with the degenerated rewarding system including the DRN. These results suggest that the hypertensive state causes the dysfunction in the striatum of the brain rewarding system and induces the risk for increasing alcohol consumption to compensate for the alteration of serotonergic neurons.     

Angiotensin II-induced cardiomyocyte hypertrophy and cardiac fibrosis in stroke-prone spontaneously hypertensive rats

Angiotensin-converting enzyme inhibitors (ACEIs) cause regression of hypertensive left ventricular hypertrophy (LVH) by reducing angiotensin II, increasing bradykinin, or both. The mechanisms of these cardioprotective effects remain controversial. The aims of this study were to determine whether the cardioprotective effects of ACEIs are mediated by reducing angiotensin II and whether ACEIs ameliorate the morphologic, physiologic, and biochemical changes in the hearts of stroke-prone spontaneously hypertensive rats (SHRSPs). Male SHRSPs were treated with hydralazine, captopril, or candesartan, an angiotensin II type 1 receptor (AT1R) antagonist, from age 12 to 24 weeks. We measured systolic blood pressure (SBP), left ventricular weight (LVW), left ventricular (LV) myocyte cross-sectional area (myocyte size), LV Interstitial collagen volume fraction (ICVF), perivascular collagen area/luminal area ratio (PVCA/LA), the medial area to luminal area ratio (MA/LA), the relative amount of V3 myosin heavy chain (MHCV3), and coronary reserve maximum (coronary flow max/ventricular weight (CFmax/VW)). These parameters were compared with those of untreated SHRSPs and Wistar-Kyoto rats (WKYs). SHRSPs exhibited decreased coronary reserve and LVH with an increase in myocyte size, PVCA/LA, MA/LA, and MHCV3 at 12 weeks of age. In addition to these changes, 24-week-old SHRSPs showed an increase in ICVF. The LVW, coronary reserve, myocyte size, PVCA/LA, ICVF, and MHCV3 of SHRSPs treated with captopril or candesartan all approached control values. In contrast, hydralazine decreased only ICVF. These results suggest that ACEIs regress LVH and normalize coronary reserve by modulating the effects of angiotensin II via AT1R on the induction of cardiomyocyte hypertrophy, perivascular fibrosis, and medial thickening of intramyocardial coronary arteries in SHRSPs. We concluded that these effects, in addition to the reduction of SBP, are important in causing the regression of LVH.     

运动训练及依那普利对自发性高血压慢性肾功能衰竭大鼠模型肾功能的影响

目的:应用高血压肾功能衰竭大鼠模型,探讨运动训练与肾素血管紧张素转换酶抑制剂依那普利联合应用对肾功能的影响。方法:8周龄雄性自发性高血压大鼠24只,行右肾2/3切除,左肾全摘除,建立5/6肾切除自发性高血压慢性肾功能衰竭模型。于10周龄时,随机分为非运动组、中等强度运动训练组和运动训练加依那普利组。其中运动训练组所有动物进行跑台训练,速度20m/min,60min/d,5d/w。依那普利2mg/(kg·d)腹腔内持续给药。结果:4周运动训练明显抑制尿蛋白分泌,减小肾小球硬化指数。而运动训练加依那普利使血压明显下降和进一步减小肾小球硬化指数。结论:中等强度运动训练对慢性高血压肾功能衰竭模型有延缓肾衰进展、保护肾功能的作用。运动训练与依那普利联合应用能进一步增强这种肾脏保护作用。     

运动对高血压大鼠血压和内皮素的影响

目的押观察原发性高血压大鼠运动后血压、体质量以及血清内皮素的变化。方法押实验于2003-07/09在扬州大学实验动物中心完成。采用18只高血压大鼠作为实验动物,按实验需要将动物分为运动组穴10只雪和安静组穴8只雪。运动组经过10周的60min/d的训练熏5d/周,与安静组一起测量其血压、体质量;取静脉血,用放射免疫法测定内皮素。结果押实验进行至第5周运动组死亡1只大鼠。①血压:运动前两组大鼠血压无显著差异熏经过4,10周运动后运动组大鼠与安静组相比血压明显降低眼(174.1±1.4),(185.0±1.4)mmHg;(166.6±1.1),(193.9±1.8)mmHg,P<0.01演。②体质量:两组动物在生长过程中体质量均逐渐增高,但运动组增长的趋势低于安静组,经10周运动后运动组的体质量明显低于安静组眼(344.60±2.57),(362.00±5.26)g,P<0.05演。③内皮素:经过10周的游泳训练后,运动组内皮素明显低于安静组眼穴44.75±4.45雪,穴68.36±5.93雪ng/L,P<0.01演。结论押运动对高血压大鼠的体质量增长有抑制作用,且高血压大鼠经过游泳训练后其血内皮素水平下降,而血压也随之下降,提示运动对高血压大鼠的降压部分是通过影响内皮素的产生和释放来实现的。     

低强度游泳运动对自发性高血压大鼠C反应蛋白的影响

目的研究低强度游泳运动对自发性高血压大鼠(SHR)C反应蛋白(CRP)的影响。方法24只8周龄SHR大鼠随机分为对照组及运动组,运动组进行游泳运动1 h/d,5 d/w,共10 w。每周测量大鼠尾动脉压,实验结束时检测CRP水平。结果10 w低强度游泳运动明显降低SHR大鼠血压及CRP水平。结论低强度游泳运动有助于降低高血压患者的血压并减少心血管系统并发症。     

运动联合培哚普利对自发性高血压大鼠大动脉顺应性的影响

目的:探讨运动训练联合血管紧张素转换酶抑制剂(培哚普利)对自发性高血压大鼠(SHR)高血压和大动脉硬化的影响,确定运动对于被降压药物调整为正常血压水平的高血压症的大动脉顺应性的影响.方法:7周龄SHR分为对照组,运动组,培哚普利投药组,培哚普利与运动并用组,观察8周,每周1次用tail-cuff方法测定大鼠的血压.15周龄时,用主动脉脉搏波传播速度来评估大动脉顺应性.结果:培哚普利完全抑制了血压的上升,运动也起到了一定的降压效果.同时培哚普利可以抑制大动脉顺应性的低下.单独运动对于大动脉顺应性的低下并没有起到抑制效果,而且在培哚普利投药的基础上加上运动也没有达到抑制的效果.结论:对于高血压进展期SHR,运动有一定的降压效果,但对于被培哚普利调整为正常血压水平的SHR的大动脉顺应性没有效果.     

Dosing time-dependent effect of temocapril on the mortality of stroke-prone spontaneously hypertensive rats

This study was undertaken to evaluate a dosing time-dependent effect of temocapril, an angiotensin-converting enzyme (ACE) inhibitor, on the mortality of stroke-prone spontaneously hypertensive rats (SHRSP). Temocapril (1 mg/kg/day) prolonged the survival rate of these animals, with a maximum effect after dosing at the early resting period and a minimum effect after dosing at the early active period. The pharmacokinetics of temocaprilat, an active metabolite of temocapril, did not differ significantly between the two dosing times. However, the inhibition of ACE activity in serum and organs (brain and aorta) and the reduction of blood pressure were significantly greater after dosing at the early resting period than at the early active period. These data suggest that the effect of temocapril on the mortality of SHRSP depends on the time of dosing, with a maximum effect seen after dosing at the early resting period. Dosing time-dependent differences in the pharmacodynamics of temocapril might be involved in explaining this phenomenon.     

Effect of sodium chloride and sodium bicarbonate on blood pressure in stroke-prone spontaneously hypertensive rats

1. To test the hypothesis that NaCl increases blood pressure, while NaHCO3 does not, we measured the effect of an NaHCO3-containing mineral water on blood pressure in stroke-prone spontaneously hypertensive (SHR-SP) and Wistar-Kyoto (WKY) rats. We compared mineral water with equimolar amounts of NaCl and demineralized drinking water in six groups of 20 rats each over 24 weeks. 2. NaCl consistently increased blood pressure in both SHR-SP and WKY compared with demineralized water, while mineral water did not. 3. We studied the possible role of sodium-regulating hormones. Sodium, potassium-dependent adenosine triphosphatase activity was decreased by NaCl and by age, but not by mineral water. The concentration of atrial natriuretic peptide was greater in SHR-SP, but was not influenced by the two regimens. Components of the renin-angiotensin-aldosterone system and 18-hydroxydeoxycorticosterone tended to decrease with NaCl, but not with mineral water. 4. Plasma pH values in the six groups of rats were not different; however, SHR-SP had consistently lower PCO2 and HCO3- values and higher anion gap values than WKY rats. These values were not influence by the two regimens. 5. NaCl elevates blood pressure in SHR-SP while NaHCO3 does not. The changes in hormones regulating sodium homoeostasis suggest that NaCl induces volume expansion while NaHCO3 does not. The effect may be related to influences on renal sodium reabsorption by chloride and bicarbonate. The possible role of increased proton excretory activity in SHR-SP remains to be determined.     

Voluntary physical exercise-induced vascular effects in spontaneously hypertensive rats

Forced training has been shown to have beneficial vascular effects in various animal exercise models. In the present study, we explored possible physiological and molecular effects of voluntary physical exercise on various vascular beds. SHR (spontaneously hypertensive rats) performed voluntary exercise for 5 weeks in a computerized wheel cage facility. Ex vivo myograph studies revealed an increased sensitivity of the ACh (acetylcholine)-mediated vasodilation in resistance arteries of the exercised animals (ED50=15.0+/-3.5 nmol/l) compared with the controls (ED50=37.0+/-8.8 nmol/l; P=0.05). The exercise/control difference was abolished after scavenging reactive oxygen radicals. In conduit arteries, ACh induced a similar vasodilatory response in both groups. The in vivo aortic wall stiffness, assessed by means of Doppler tissue echography, was significantly lower in the exercising animals than in controls. This was demonstrated by significantly increased peak systolic aortic wall velocity (P=0.03) and the velocity time integral (P=0.01) in exercising animals compared with controls. The relative gene expression of eNOS (endothelial nitric oxide synthase) was similar in both groups of animals, whereas Cu/ZnSOD (copper/zinc superoxide dismutase) gene expression was significantly increased (+111%; P=0.0007) in the exercising animal compared with controls. In conclusion, voluntary physical exercise differentially improves vascular function in various vascular beds. Increased vascular compliance and antioxidative capacity may contribute to the atheroprotective effects associated with physical exercise in conduit vessels.