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氯沙坦减轻自发性高血压大鼠急性脑梗死损伤的ABR机制
目的:探讨氯沙坦(losartan)对自发性高血压大鼠(spontaneously hypertensive rat,SHR)急性脑梗死保护作用的动脉压力感受性反射(arterial baroreflex,ABR)机制.方法:灌胃给予氯沙坦2周,测定大鼠血流动力学指标及BRS (ABR功能用动脉压力感受性反射敏感性,baroreflex sensitivity)值.采用大脑中动脉 (middle cerebral arterial,MCA) 栓塞的方法诱发急性脑梗死,24 h后取脑组织,切片、染色,观察急性脑梗死面积;孤束核(nucleus of solitary tract,NTS)分别微量注射血管紧张素Ⅱ(angiotensionⅡ,AngⅡ)及小剂量氯沙坦,测定大鼠血流动力学指标及BRS值,采用MCA栓塞的方法诱发急性脑梗死,观察药物对急性脑梗死的影响.结果:与对照组相比,灌胃给予氯沙坦后大鼠ABR功能改善,脑梗死面积显著降低(P<0.05).孤束核微量注射AngⅡ可明显升高动物血压,降低BRS值;孤束核微量注射氯沙坦后在不改变血压的情况下可以使ABR功能明显改善(P<0.05),减轻脑梗死损伤(P<0.05).结论:氯沙坦改善了ABR的敏感性,从而对急性脑梗死起防治作用,孤束核可能是其作用部位.
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长期服用一种自由基清除剂ONO-3144对易卒中自发高血压大鼠的影响
AIM: To clarify the preventive effects of ONO-3144, a free radical scavenger, on stroke-prone spontaneously hypertensive rats (SHRSP) and free radicals related to the hypertensive disorders. METHODS: Drugs with powdered chow were administered orally to the rats from 2- to 14-month-old. Body weight, blood pressure,rectal temperature, oxygen consumption rate, thyroid hormones, lipids, platelet number, ocular fundus,autopsy, and life span were investigated. RESULTS:ONO-3144 did not affect the growth, blood pressure,concentrations of thyroid hormones and lipids in the blood, but decreased the rectal temperature and oxygen consumption rate. ONO-3144 also prevented the platelet number decrease, sclerotic change of retinal artery,edematous and hypertrophic changes in parenchymal andcirculatory organs. Both the average life-span and the longest life time of SHRSP given 40 mg/kg ONO-3144were longer than those of normotensive rats and noadministration hypertensive rats. CONCLUSION: Theoxidative free radicals closely relate to hypertensioninduced pathophysiological changes in SHRSP, and ONO-3144 prevents the changes of those disorders, and then brings longevity.
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清醒大鼠动脉压力感受性反射-血压控制的测定
目的:研究清醒大鼠动脉压力感受性反射(ABR)-血压控制(ABR-BP)的测定.方法:用计算机化清醒自由活动大鼠血压连续监测技术,记录动物的血压.ABR-BP测定的原理是比较阻断ABR前后机体对血管活性物质反应的差异.结果:(1)用血管紧张素-Ⅱ测得的ABR-BP值与用新福林测得的ABR-BP值密切相关,在一定范围内药物的剂量不影响结果.(2)ABR-BP与ABR-心动间期控制(ABR-HP)显著相关.(3)麻醉抑制ABR-BP,ABR-BP本身存在昼夜节律性变化.(4)血压波动性与ABR-BP相关,而与ABR-HP不相关.(5)高血压时ABR-BP受损.结论:本项工作使ABR-BP的测定成为可能.ABR-BP在维持血压的稳定性中起重要作用,在高血压时其功能受损.
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依降钙素在SHR股动脉介导的收缩和舒张反应
AIM: To study the effect of repeated systemic injections of elcatonin (a synthetic analog of eel calcitonin) on the responses of rat femoral artery preparation to vasoactive drugs and to determine subtypes of muscarinic cholinoceptors involved in acetylcholine ( ACh )-induced vasorelaxation in elcatonin-treated rats. METHODS:Spontaneously hypertensive rats (SHR) were treated sc with elcatonin, 0.5 and 5 U/kg, 3 times a week for 2weeks. Responses to vasoactive drugs were determined in helically cut strips of femoral arteries of these rats.Schild plot data for muscarinic cholinoceptor antagonists were obtained on these vascular strips, using ACh as an agonist. RESULTS: Elcatonin did not alter systemic blood pressure and contractile responses of the femoral artery to KCl, norepinephrine, 5-hydroxytryptamine, and prostaglandin F2α. Elcatonin attenuated isoproterenolinduced relaxation, increased ACh- and ATP-induced relaxations, and did not change relaxant responses to sodium nitroprusside and cromakalim in the femoral artery. Nitro L-arginine in the combination with tetraethylammonium ( or charybdotoxin) completely abolished the relaxant response to ACh in the control but not in the elcatonin-treated arteries. The muscarinic cholinoceptor subtype involved in the ACh-induced relaxation was Ma in the elcatonin-treated as well as control SHR. CONCLUSION: Elcatonin decreases β-adrenoeeptor-mediated relaxation and increases M3 cholinoceptor-mediated relaxation in the SHR femoral artery. Although the AChinduced relaxation is explained by stimulated releases of nitric oxide (NO) and endothelium-derived hyperpolarizing factor (EDHF) in the SHR artery, a NO- and EDHFindependent mechanism in addition to NO and EDHF is responsible for the response to ACh in the femoral artery from the elcatonin-treated SHR.
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组织蛋白酶B对自发性高血压大鼠胸腺细胞凋亡的影响
目的：本实验研究自发性高血压大鼠胸腺机能异常的机制.方法：用原位杂交确定蛋白酶B的表达位置，Northern杂交分析组织蛋白酶B的表达水平，用TUNEL和流式细胞仪分别检测胸腺细胞的凋亡情况.结果：在离体和在体水平，胸腺组织蛋白酶B的表达与胸腺细胞凋亡伴行，在胸腺细胞的胞浆中检测到组织蛋白酶B的转录产物在6周和8周的自发性高血压大鼠胸腺中的表达高于WKY大鼠.结论：自发性高血压大鼠的胸腺细胞凋亡增加，与组织蛋白酶B的表达相关.
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Valsartan与benazepril联合应用对自发性高血压大鼠血压和左心室肥厚的影响
目的：评价血管紧张素转换酶抑制剂苯那普利钠和AT1受体拮抗剂缬沙坦联合应用对自发性高血压大鼠(SHR)的降压疗效及其逆转心肌肥厚作用和对肾素-血管紧张素-醛固酮系统(RAAS)、内洋地黄素水平的影响.方法：24只14周龄雄性SHR随机分成空白对照组、Benazepril组、Valsartan组和Benazepril+Valsartan组，另设WKY正常对照组.分别于药物干预前、药物干预后2、4、6、8周末测定大鼠SBP；于药物干预后8周末检测心肌组织和血浆肾素活性、血管紧张素Ⅱ浓度、心肌组织Na+-K+ -ATP酶活性和内洋地黄素水平，并行心肌组织形态学检查.结果：药物干预各组SHR动脉收缩压(SBP)水平明显下降，尤以联合用药组SBP下降显著；药物干预各组血浆和心肌组织肾素活性均明显升高；Benazepril组和Benazepril+Valsartan组血浆和心肌组织AngⅡ水平降低，而Valsartan组血浆和心肌组织AngⅡ水平则明显升高；随SBP水平的降低，心肌组织Na+-K+-ATP酶活性明显升高，而内洋地黄素水平则明显下降；药物干预各组LVM/BW、TDM均明显减低，尤以联合用药组改变为显著.结论：ACEI Benazepril和AT1拮抗剂Valsartan均有明显的降低SHR的SBP作用，能明显逆转左室肥厚；联合用药效果为显著，并能有效防止单一AT1拮抗剂所致血浆和心肌组织AngⅡ水平的升高的副作用.
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卡托普利对高血压与血管结构及功能的分离效应
研究卡托普利(Cap)对血管的结构与功能的作用是否与其降压作用分离.方法:SHR从胎仔期起分别接受Cap 20与100 mg·kg-1·d-1,A组和B组)至生后16周停药,40周实验.血压用尾动脉法测定.肠系膜动脉第三级分支的壁/腔比测定用形态计量法,阻力血管性质测定用后肢灌注压对递增量phenylephrine,灌注液内加L-NAME或L-arginine.结果:两种剂量的Cap都能完全防止血管壁肥厚(肠系膜动脉第三级分支的壁/腔比Cap A:0.38±0.08,Cap B:0.29±0.05 vs WKY:0.34±0.11,P＞0.05)结果与WKY者类似.Cap组后肢灌注压曲线的参数与WKY组几乎完全相同,与未治疗SHR有明显差别(EC50,Cap B:4.05±2.58 vs SHR:1.15±0.96 mL·L-1,P＜0.01,vs WKY:5.13±1.97 mL·L-1,P＞0.05).在灌注液内加入L-NAME或L-argi-nine可加强或减弱Cap治疗组的血管收缩反应.结论:Cap从胎仔期治疗可以使SHR的阻力血管结构与收缩反应正常化,而血压仍维持在不同程度的较高水平.
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卡托普利和依那普利对血管平滑肌细胞内钙的影响
检测ACE抑制剂对主动脉平滑肌细胞内Ca2+的影响.方法:用荧光标计和图象处理技术结果:SHR细胞内Ca2+以及KCl,NE和Ang在SHR细胞引起的Ca2+增加多于WKY细胞.Cap和Ena不影响KCl和Ang在WKY细胞的作用,但Cap,Ena和Nif抑制KCl,NE和Ang在SHR细胞的作用.结论:Cap和Ena阻断功能和特异性已改变的电压依赖性钙通道.
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u和δ阿片样受体在自发高血压大鼠和正常血压WKY大鼠中枢神经系统中的分布
目的:比较自发高血压大鼠(SHR)和对照组WKY大鼠中枢神经系统中阿片受体亚型的分布.方法:用放射自显影法,选用3H-OMF,3H-U69593分别标记μ和κ受体,用遮盖法以3H-etorphine标记δ受体.结果:δ受体密度在SHR下丘脑、中央灰质高于WKY,μ受体密度在SHR杏仁基底外侧核、僵核、孤束核低于WKY,κ受体密度没能检测出.结论:阿片受体亚型不同分布与SHR的血压有关,并且δ受体对高血压的维持作用大于μ受体.
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清醒大鼠动脉压力感受性反射的功能研究
本文综述本室近10年来对清醒自由活动大鼠动脉压力感受性反射(ABR)的功能性研究.首先,建立了ABR对血压的控制(ABR-BP)的测量方法.ABR-BP是与用经典方法测量的ABR功能(ABR-HP)不同的成份.其次,我们的研究表明ABR功能与高血压的器官损伤有关.损毁ABR功能可导致严重的器官损伤.该损伤的机制与血压波动性增高、肾素血管紧张素系统激活有关.酮色林能改善ABR功能.基于对酮色林研究的结果,我们提出改善ABR功能可作为改善某些心血管疾病预后的新策略.后,提到了我们正在进行中的自发性ABR功能缺陷大鼠的培育.
