久强脑立清对自发性高血压大鼠重要器官的保护作用

目的探讨久强脑立清 (JNQ )对自发性高血压大鼠 (SHR)重要器官心、脑、肾组织形态学的影响。方法动物分为 4组 ,Wistar大鼠对照组、SHR组、SHR服用JNQ高剂量组 (0 5 3 0g/kg)和低剂量组 (0 2 65 g/kg) ,给药 5周。采用尾脉搏测压法测定动物血压 ;动物经组织灌流后 ,低温下快速取出心、脑、肾 ,固定于 10 %福尔马林中 ,4℃保存 ,常规组织切片 ,HE染色。结果给药前各组SHR的血压明显高于对照组 (P <0 0 1) ,给药 3周和 5周后血压未见明显下降。组织病理结果显示 ,未治疗组SHR心肌细胞肥大 ,肌束间小动脉壁增厚 ,官腔变窄 ;大脑皮层血管管腔狭窄 ,管壁增厚 ,血管周围间隙增大 ;肾小球萎缩 ,有玻璃样变。上述病理性改变在经JNQ治疗 5周后得到不同程度的改善 ,以高剂量组明显。结论SHR经JNQ治疗 5周后血压未见明显降低 ,但对重要器官心、脑、肾的病变有较明显改善作用     

培多普利逆转肾血管性高血压大鼠心肌肥厚及对心功能的影响

目的探讨血管紧张素转换酶抑制剂—培多普利在逆转两肾一夹高血压大鼠心肌肥厚过程中对心功能的影响。方法两肾一夹法制作肾性高血压大鼠模型,通过心脏超声和心室内插管,以射血分数(EF)和左室短轴缩短率(FS)、零负荷下等容收缩期心肌纤维收缩成分的最大缩短速度(Vmax)作为心脏收缩功能指标,以左心室舒张末压(LVEDP),等容舒张期压力下降的时间常数(T)作为心脏舒张功能指标。结果培多普利在逆转心肌肥厚同时,可使心肌肥厚时升高的LVEDP、T值下降,同时对心脏EF、FS和Vmax值无明显影响。结论培多普利在逆转两肾一夹高血压大鼠心肌肥厚同时,可改善大鼠心脏舒张功能。     

重症患者的心功能障碍:病理生理与治疗

重症患者常常发生心功能障碍,其病理生理的改变涉及多种机制,包括血流动力学的变化,神经、内分泌因素的作用,炎症反应,心肌损伤和重构。除了心脏本身病变引起心功能异常外,心外器官如肺、肾、脑、胃肠道等发生功能障碍时亦可引起心功能障碍。对于心功能障碍的重症患者,在改善心功能的同时,需维持血流动力学稳定、加强心外器官的功能支持。     

高血压和左心室肥厚

高血压对心、脑、肾三大重要脏器的危害可概括为大心、小肾及脑卒中。大心代表左心肥厚、心脏扩大和心力衰竭,小肾意指肾萎缩,脑卒中包括脑出血和脑血栓。高血压所引起的上述靶器官损害(ＴＯＤ)中,左心室肥厚(ＬＶＨ)的出现率最高,而且发生较早。引起ＬＶＨ的可能原因:①高血压使心脏排血时所遇到的阻力负荷即后负荷增加,心脏作功增加,代偿性心肌收缩力加强,导致左心室心肌肥厚;②随高血压病程延长,肥厚的左心室逐渐扩大(离心性肥厚),左心室容量负荷即前负荷增加,早期可代偿性增加心排血量;晚期失代偿后,便会导致心功能不全;③神经体液因素…     

18例脑-肾综合征的原因分析及护理

脑血管疾病（CVD）并发肾功能障碍即脑一肾综合征，约占CVD患者的2％。其疾病基础以高血压和动脉硬化最为多见，常常影响心、脑、肾等重要器官功能。一旦发生急性肾功能障碍，往往提示预后较差。因此，明确脑-肾综合征的发生原因，严密监测肌酐、尿素氮、尿比重等反映肾功能的重要指标，采取有效的护理措施是关键。我科2005至2006年共收治重症脑卒中并发急性肾功能损害18例，现将护理体会介绍如下．     

原发性高血压的健康教育指导

原发性高血压是一种以动脉血压升高为特征并伴有动脉、心、脑和肾等器官病理改变的全身性疾病.     

高机械指数联合高剂量造影剂行心肌声学造影的安全性研究

目的探讨高机械指数（MI）超声辐照联合高剂量国产超声造影剂心肌声学造影,对大鼠血流动力学及组织器官损伤情况的影响。方法20只正常SD大鼠,经颈静脉注射全氟丙烷人血白蛋白微球注射剂（1ml／kg）,在造影模式下调节MI至最大（MI=1．9）,采用R波触发,每6个心动周期一次。造影前后分别监测心率、心电图、血压、肌钙蛋白T,结束后取大鼠心、肝、肾进行病理检查。结果大鼠心率、血压、肌钙蛋白T测值在造影前后无明显变化（P〉0．05）;造影后心脏病理检查见轻微损伤（心肌纤维稍变粗,胞浆呈细颗粒状;间质血管扩张充血）,肝、肾未见异常结构改变;一只大鼠在注射造影剂的过程中出现室性期前收缩,注射结束5min后恢复正常。结论在常规超声条件下高MI及高剂量造影剂心肌声学造影对正常实验大鼠血流动力学无明显影响,肌钙蛋白T升高不明显,病理示心肌轻微损伤,偶致短暂室性早搏,但短时间内可恢复正常。本实验证实,高MI联合高剂量国产声学造影剂行心肌声学造影对于正常大鼠是安全的。     

茶色素对SHRSP血脂和高血压靶器官结构的影响

目的　探讨茶色素对卒中易感型自发性高血压大鼠血脂和高血压靶器官结构的影响。方法　治疗组大鼠用大剂量茶色素 [6 0 0mg/(kg·d) ]或小剂量茶色素 [3 0 0mg/(kg·d) ]灌胃 ,对照组用同体积 1%盐水灌胃。每 2周进行一次尾动脉血压测量。实验 8周后 ,进行血脂测定 ,然后断头处死动物 ,观察心、脑、肾结构的变化。结果　茶色素对SHRSP血压和体重无显著影响 ,但它能够显著降低血浆胆固醇和甘油三酯水平 ,升高高密度脂蛋白水平 ;显著降低大鼠心脏和大脑的脏器系数和卒中率 ,显著改善大鼠主动脉、心肌和脑基底动脉的结构。结论　茶色素能够减缓SHRSP高血压的发展过程。     

高血压病并靶器官损害动态血压变化观察

高血压病并靶器官损害动态血压变化观察山东省滨州医学院附属医院（２５６６０３）李翠香阮萍尚炳英薛艳为探讨高血压病并心、脑、肾靶器官损害患者动态血压的变化规律及特点，正确地评估高血压患者的病情及预后，指导临床用药和护理，减少心、脑急性事件的发生。本文对１...     

单次维持性血液透析对慢性肾衰患者心功能影响的研究

目的 探讨慢性肾衰（CRF）患单次血透前后的心功能及血肌酐、血压的变化。方法 用血液循环动力学脉图检测技术仪测定22例CRF患因透前后的各项心功能系数，用酶电极法与血压计分别测定血肌酐和血压。结果 发现血透后肌酐、收缩压与舒张压明显下降。心功能系数包括左室舒张末期容量（LDV），心输出量（CO），心脏指数（CI），每搏心输出量（SV），中心静脉压（CVP），有效循环血量（ECV），心肌耗氧量（MVO）均显降低，而射血分数（EF）显升高。结论 CRF患血透后可因全身血容量减少，左室舒张末期容量降低，心脏前负荷减少，心肌收缩力增加，心肌耗氧量减少而使心功能明显好转。另外，血透对尿毒症毒素的消除亦可直接减少对心肌的损害而改善心功能。     

Vasopressin impairs brain, heart and kidney perfusion: an experimental study in pigs after transient myocardial ischemia

Introduction

Arginine vasopressin (AVP) is increasingly used to restore mean arterial pressure (MAP) in low-pressure shock states unresponsive to conventional inotropes. This is potentially deleterious since AVP is also known to reduce cardiac output by increasing vascular resistance. The effects of AVP on blood flow to vital organs and cardiac performance in a circulation altered by cardiac ischemia are still not sufficiently clarified. We hypothesised that restoring MAP by low dose, therapeutic level AVP would reduce vital organ blood flow in a setting of experimental acute left ventricular dysfunction.

Methods

Cardiac output (CO) and arterial blood flow to the brain, heart, kidney and liver were measured in nine pigs using transit-time flow probes. Left ventricular pressure-volume catheter and central arterial and venous catheters were used for haemodynamic recordings and blood sampling. Transient left ventricular ischemia was induced by intermittent left coronary occlusions resulting in a 17% reduction in cardiac output and a drop in MAP from 87 ± 3 to 67 ± 4 mmHg (p < 0.001). A low-dose therapeutic level of AVP (0.005 U/kg/min) was used to restore MAP to pre-ischemic values (93 ± 4 mmHg).

Results

AVP further impaired systemic perfusion (CO and brain, heart and kidney blood flow reduced by 29, 18, 23 and 34%, respectively) due to a 2.0-, 2.2-, 1.9- and 2.1-fold increase in systemic, brain, heart and kidney specific vascular resistances. The hypoperfusion induced by AVP was associated with an increased systemic oxygen extraction. Oxygen saturation in blood drawn from the great cardiac vein fell from 29 ± 1 to 21 ± 3% (p = 0.01). Finally, these effects were reversed 40 min after AVP was withdrawn.

Conclusion

Low dose AVP induced a pronounced reduction in vital organ blood flow in pigs after transient cardiac ischemia. This indicates a potentially deleterious effect of AVP in patients with heart failure or cardiogenic shock due to impaired coronary perfusion.     

环孢霉素A对肾性高血压大鼠重要脏器钙调神经磷酸酶活性的调控

背景近来大量研究表明,钙调神经磷酸酶依赖的信号转导通路在免疫系统、神经系统、心血管系统具有广泛的生物学效应,钙调神经磷酸酶活性改变与多种疾病发生发展密切相关.目的通过建立一肾一夹肾性高血压大鼠模型,观察高血压大鼠心脏、脾、肾脏、肺、脑、肝、主动脉等重要组织脏器钙调神经磷酸酶活性变化及环孢霉素A的调控作用.设计完全随机分组设计,对照实验.单位解放军总医院南四科.方法实验于2002-11/2003-06在解放军总医院老年外科实验室完成.选用雄性Wistar大鼠(清洁级)20只.动物随机分为3组肾性高血压组[n=7,行一肾一夹手术,术后第4天开始给予生理盐水1 mL/(kg·d)腹腔注射,9 g/L盐水代饮水至4周],环孢霉素A干预组(n=7,行一肾一夹手术后第4天给予环孢霉素A 5 mg/(kg·d)腹腔注射,9 g/L盐水代饮水至4周),假手术组(n=6,除不切除右肾及狭窄左肾动脉外,其余操作同手术组,假手术后第4天开始给予生理盐水1 mL/(kg·d)腹腔注射,正常饮水至4周).一肾一夹模型制作方法将大鼠腹腔注射麻醉后,行右肾切除,左肾用直径0.2 mm银夹狭窄左肾动脉.采用tail-cuff测压法测鼠尾收缩压.以对硝基磷酸酚为底物测定术后4周大鼠各组织器官钙调神经磷酸酶活性.两组差异性比较采用成组资料t检验.主要观察指标①各组大鼠各重要组织及器官钙调神经磷酸酶活性比较.②各组大鼠术前及术后4周收缩压比较.结果大鼠20只均进入结果分析.①收缩压术前三组大鼠相近(P＞0.05).术后4周环孢霉素A干预组低于肾性高血压组,但差异不明显;肾性高血压组和环孢霉素A干预组大鼠均明显高于假手术组(t=2.54,3.01,P＜0.05).②肾、肺、心、脾、脑组织钙调神经磷酸酶活性肾性高血压组大鼠明显高于假手术组(t=3.17～7.08,P＜0.05),环孢霉素A干预组明显低于肾性高血压组(t=2.91～7.25,P＜0.05).③肝细胞钙调神经磷酸酶活性肾性高血压组和环孢霉素A干预组均明显低于假手术组(t=2.63,2.83,P＜0.05).④主动脉钙调神经磷酸酶活性各组大鼠相近.结论①肾性高血压大鼠心、脑、肾脏、脾脏、肺脏组织钙调神经磷酸酶活性均有显著升高,环孢霉素A对肾性高血压大鼠上诉各组织脏器钙凋神经磷酸酶活性具有广泛的抑制作用.②环孢霉素A无明显降肾性高血压大鼠收缩压作用.     

Modification of the cardiovascular effects of l-dopa by decarboxylase inhibitors

Intravenously infused L-dopa (0.3 mg/kg per min) produced hypertension and cardiac arrhythmias in halothane anesthetized dogs. Biochemical studies showed that the heart, kidney, and brain of these animals accumulated significant amounts of catecholamines formed from the administered precursor.Pretreatment of dogs with an extracerebral inhibitor of dopa decarboxylase [D,L-alpha-hydrazino-alpha-methyl-beta-(3.4-dihydroxyphenyl) propionic acid] prevented the development of hypertension and arrhythmias with infusion of L-dopa. Instead, these animals developed significant hypotension. The heart and kidney of these animals accumulated markedly reduced amounts of catecholamines formed from L-dopa compared with dogs receiving L-dopa alone: the amount of catecholamines accumulated in brain was unchanged. L-dopa, after extracerebral decarboxylase inhibition, appeared to produce hypotension by reducing peripheral vascular resistance without altering sympathetic nerve function. During hypotension, cardiac output was not altered and arterial pressure in perfused hindlimbs fell, even though flow was maintained. The pressor response to intravenous injections of norepinephrine and dopamine was unchanged. Hindlimb arterial pressure response to direct electrical stimulation of the lumbar sympathetic trunk was also unchanged.Pretreatment with a drug which inhibits brain as well as extracerebral dopa decarboxylase [D,L-seryl-2,3,4-trihydroxybenzylhydrazine hydrochloride] abolished all effects of L-dopa on blood pressure. In these animals, there was a marked reduction of catecholamine formation from L-dopa in the brain as well as the heart and kidney.It appears that L-dopa produces opposite effects on blood pressure depending on the site of accumulation of its metabolic products, dopamine and norepinephrine. If L-dopa is rapidly decarboxylated to catecholamines in peripheral organs, hypertension and cardiac arrhythmias occur. If peripheral dopa decarboxylase is selectively inhibited, a centrally mediated hypotensive effect, probably secondary to the accumulation of catecholamines in the brain, becomes apparent. If dopa decarboxylase is inhibited in the brain in addition to extracerebral organs, L-dopa has no effect on blood pressure.     

梭曼中毒进行性循环衰竭时重要生命体征的变化

目的 研究梭曼中毒导致进行性循环衰竭条件下,犬心率、血压、心脏功能、呼吸功能、血液酸碱平衡、血电解质等生命体征的变化以及重要器官的损伤情况.方法 杂种犬7只,雄性,体质量(12～15)kg.梭曼累积染毒,方法为每次肌肉注射1/3致死剂量(LD)梭曼(1 LD=10 μg/kg),每10 min追加1次;以平均动脉压降至(40～45)mmHg为循环哀竭标准.八导生理记录仪检测梭曼染毒前后的心率、血压、血流动力学参数,股动脉取血检测血气和pH值,股静脉取血检测电解质浓度和反映各重要器官损伤的指标.以梭曼染毒前各指标为对照组,染毒后实验结果用SAS 6.12软件进行自身对照t检验分析.结果 梭曼染毒导致麻醉犬循环哀竭发生后,心率、血压和血流动力学参数都被显著抑制(P<0.05).动脉血氧分压低于60 mmHg,血氧饱和度低于90%;即使在正压人工呼吸状态下,血二氧化碳分压依然高于50 mmHg,仍发生呼吸衰竭.犬血液pH值由染毒前的(7.345±0.064)降低到染毒后的(6.956±0.022),发生了明显的代谢性酸中毒(P<0.01).血电解质钠离子浓度和氯离子浓度仅有轻度变化.血液中GTP、COT、Cr、BUN、CK-MB和LDH在染毒后都有显著增加(P<0.05).结论 胆碱酯酶抑制剂类毒物梭曼中毒可引起机体出现严重的进行性循环衰竭,同时导致各种重要生命体征和重要器官发牛显著损伤.     

高血压病与血液流变关系探讨

高血压（hypertension）是以动脉压升高为特征,可伴有心脏、血管、脑和肾等器官功能性或器质性改变的全身性疾病.流行病学研究已征明,人群中动脉血压水平随年龄的增长而升高.据世界卫生组织报道,澳大利亚、美国、新西兰及日本等倒曾进行了大规模的人群调查,确诊成人高血压患病率为8%～18%.血压升高不仅给人类健康带来损害,而且它也是冠心病、脑卒中的主要危险因素之一.近年来,血液流变性改变与高血压病的相关研究引起了人们的重视,为进一步明确病因、发病机制,预防心脑血管病的发生,该文就高血压与血液流变（尤其是红细胞流变）的关系进行探讨.     

原发性高血压与靶器官损害相关因素的研究

为探讨血压升高与靶器官心、脑、肾损害的关系,应用无创性血压监测仪对164例原发性高血压病病人进行24h动态血压监测。结果：单纯收缩压升高占28.0%,单纯舒张压升高占14.0%,混合型血压升高占57.7%;白昼血压升高占25.6%,夜间血压升高占17.1%,持续性血压升高占57.3%;原发性高血压靶器官损害以脑损害为主,其次为心脏、肾脏损害,提示：原发性高血压病程、血压负荷值与心、脑、肾损害密切相关;血压升高类型、血压升高时间与心脑损害相关。     

下调miR-126对大鼠降血压作用的实验研究

目的探讨原发性高血压中miR-126是否可作为一种新的治疗靶点。方法 24只自发性高血压大鼠(SHR)随机分为4组,每周测量收缩压、舒张压、平均动脉压及心率。经过8周的病毒载体转染的处理,心、肾、脑、肝、肺组织被制成冰冻切片,通过荧光显微镜观察慢病毒载体在各个组织中的分布。应用ELISA试剂盒来测定血清NO含量。结果大鼠中下调miR-126无明显降血压的作用。结论通过下调miR-126来治疗原发性高血压并没有显著降血压的作用。高血压患者中miR-126表达的增加可能是由于一种代偿机制,具体机制有待进一步的研究。     

高血压合并糖尿病患者的降压药物治疗

糖尿病与高血压均为常见疾病,二者关系密切。根据调查,临床很多高血压患者尤其是肥胖型高血压患者常合并糖尿病,使得心、脑、肾、视网膜等靶器官的危害性具有乘积效应,甚至大大增加了死亡率,给患者及家属造成极大的痛苦。因此要控制好此类患者的血糖和血压就需要制定更合理的降压治疗方案,充分发挥相应心血管药物的最佳作用,从而有效提高患者的生活质量,降低并发症的发生率。     

Alterations in tissue oxygen consumption and extraction after trauma and hemorrhagic shock

OBJECTIVES: Although trauma and hemorrhage are associated with tissue hypoperfusion and hypoxemia, changes in oxygen delivery (DO2), oxygen consumption VO2), and oxygen extraction at the organ level in a small animal (such as the rat) model of trauma and hemorrhage have not been examined. Therefore, the objectives of this study were to determine whether blood flow, DO2, VO2, and oxygen extraction ratio in various organs are differentially altered after trauma-hemorrhagic shock and acute resuscitation in the rat. DESIGN: Prospective, randomized animal study. SETTING: A university research laboratory. SUBJECTS: Male Sprague-Dawley rats (n = 6-7 animals/group) weighing 275-325 g. INTERVENTIONS: Male rats underwent laparotomy (i.e., soft tissue trauma) and were bled to and maintained at a blood pressure of 40 mm Hg until 40% of shed blood volume was returned in the form of lactated Ringer's solution. They were then resuscitated with four times the volume of shed blood with lactated Ringer's solution for 60 mins. At 1.5 hrs postresuscitation, cardiac output and blood flow were determined by using strontium-85 microspheres. Blood samples (0.15 mL each) were collected from the femoral artery and vein and the hepatic, portal, and renal veins to determine total hemoglobin and oxygen content. Systemic and regional DO2, VO2, and oxygen extraction ratio were then calculated. MEASUREMENTS AND MAIN RESULTS: Both the systemic hemoglobin and systemic arterial oxygen content in hemorrhaged animals at 1.5 hrs postresuscitation were >50% lower as compared with sham-operated controls. Cardiac output and blood flow in the liver, small intestine, and kidneys decreased significantly, but blood flow in the brain and heart remained unaltered after hemorrhage and resuscitation. Systemic DO2 and VO2 were 73% and 54% lower, respectively, than controls at 1.5 hrs after resuscitation. Similarly, regional DO2 and VO2 in the liver, small intestine, and kidneys decreased significantly under such conditions. In addition, the liver had the most severe reduction in VO2 (76%) among the tested organs. However, the oxygen extraction ratio in the liver of sham animals was the highest (72%) and remained unchanged after hemorrhage and resuscitation. CONCLUSION: Because the liver experienced the most severe reduction in VO2 associated with an unchanged oxygen extraction capacity, this organ appears to be more vulnerable to hypoxic insult after hemorrhagic shock.     

Abnormality of calmodulin activity in hypertension. Evidence of the presence of an activator.

An apparent increase of calmodulin (CaM) activity was previously observed in the heart and kidney but not in the liver of spontaneously-hypertensive rats (SHR) and mice compared with their corresponding normotensive controls. As this change was due to an elevated recovery of CaM in the organs of the hypertensive animals, the present study was designed to evaluate its activity in hypertension. A CaM activator, detected in heart and kidney supernatants from hypertensive animals, was found to be responsible for this enhanced recovery. Similar results were obtained with passaged, cultured aortic smooth muscle cells from SHR, indicating that the anomaly was not a mere consequence of elevated blood pressure but rather a genetic expression of cells of hypertensive origin. The activator was heat stable, nondialyzable, and recovered in the fraction precipitated with 30-50% ammonium sulfate. Preliminary extraction studies suggest that the activator is contained in a glycolipid fraction. The stimulation of phosphodiesterase by this activator was calcium and CaM dependent. The activator appears to affect the affinity of the phosphodiesterase for CaM rather than the maximal stimulation. The activator was also present at a low concentration in the heart and kidney of normotensive animals. These findings indicate that at least some of the calcium abnormalities implicated in the pathogenesis of hypertension could be the result of interactions between CaM, calcium, and this activator.