高血压急症

高血压急症是指原发性或继发性 (症状性 )高血压在疾病发展过程中 ,或在某些诱因作用下 ,使血压突然升高 ,病情急剧恶化 ,并常伴有心、脑、肾功能障碍。此症必须及时处理 ,否则可危及生命。1　高血压脑病是指在高血压病程中脑循环发生急剧障碍 ,导致脑水肿和颅内压增高而产生的一系列临床表现。本症多见于急进型高血压病或严重缓进型高血压伴明显脑动脉硬化者。高血压脑病的发病机理极为复杂 ,有两种学说 :①过度调节或小动脉痉挛学说。②自身调节破裂或脑血流过度灌注学说。本病的主要病理变化为急性脑水肿、脑部毛细血管坏死、点状出血和…     

高血压危象

<正> 概念临床上所称高血压危象是指血压急剧升高引起的严重临床表现,主要为高血压脑病和恶性高血压。少数高血压病患者,血压可一时性急剧增高,达到(26.7～36.0/16.0～21.3)kPa。亦可由肾性高血压、醛固酮增多症、妊娠高血压、嗜铬细胞瘤以及其它一些病因引起的一时性血压急剧升高。此时因脑血管严重痉挛、脑循环急剧障碍而引起脑水     

高血压复方制剂控制高血压更有效

目前全球有近6亿的高血压患者,即使在发达国家也只有不到1/4的患者血压得到控制,与此相关的脑卒中,冠心病等的发病率和死亡率均明显增加,给社会带来了沉重的负担.近年来随着生活水平的提高,我国高血压患病率正迅速增加,2000～2001年亚洲国际心血管病合作研究的结果显示,中国35～74岁的人口中,高血压的患病率已达27.2%,估计全国患者人数约为1.3亿,在城市的血压控制率也仅为4.2%,远远低于全球的该比例.根据1991年的普查显示,血压控制率(经治疗:收缩压＜140mmHg,舒张压＜90mmHg)仅2.9%(城市4.2%;农村0.9%).     

高血压急症

<正> 高血压急症包括两种情况,一种是需要立即降压(不必降至正常水平)的情况,另一种是指需在数小时之内使血压降至安全水平的情况。前者指具有脑病或主动脉破裂等靶器官损害者,这种情况需在严密监视下静脉用药以立即降压,后者则指那些血     

儿童高血压及高血压危象的治疗

青少年高血压治疗的目的是用最简单有效的方法控制血压在正常范围内,一般控制在同性别、年龄和身高儿童血压的第95百分位以下,减少不良反应,防止高血压远期并发症的发生.小儿高血压多是继发性高血压,因此首先强调病因治疗,比如：通过经皮球囊血管腔内成形术治疗肾动脉狭窄和主动脉缩窄,通过手术切除嗜铬细胞瘤、肾上腺皮质腺瘤等.对于原因未明的高血压应采用减轻体重和改变生活方式等非药物治疗方法控制血压.而对于非药物治疗无效、症状性高血压、严重高血压和伴随靶器官损害的高血压,则应考虑药物治疗。     

高血压与非高血压脑梗死患者的临床观察

目的比较高血压与非高血压脑梗死的危险因素、发病类型和预后的差异。方法根据高血压病史将我院2006年10月~2007年12月收治的525例脑梗死患者分为高血压组（n=301例）,非高血压组（n=224例）,对其危险因素,脑梗死的类型和预后进行单变量和多变量分析。结果高血压脑梗死多于非高血压脑梗死,男性的比例较高。高血压组腔隙性脑梗死和后循环脑梗死发生率明显高于非高血压组,而非高血压组的高龄,心血管疾病和糖尿病明显高于高血压组,差异有统计学意义。结论高血压是引起脑梗死最重要的危险因素,特别是男性的风险较高;而高龄、糖尿病、心血管疾病是非高血压脑梗死的主要危险因素。不论高血压组还是非高血压组引起脑梗死最常见的类型为腔隙性脑梗死和后循环梗死。     

原发性高血压患者应用抗高血压药物状况分析

目的 探讨原发性高血压群体应用抗高血压药物情况。方法 应用统一调查表，回顾性调查原发性高血压患者用药史，分析抗高血压药物应用、疗效及其不良反应。不同用药情况人群分别统计药物疗效，并排除药物自身影响。结果 40．1％正确用药的患者，疗效达93．07％，不良反应发生率为5．19％；32．5％基本正确用药的患者，疗效达85．56％，不良反应发生率为9．09％；27．4％不正确用药的患者，疗效为77．85％，不良反应发生率为17．72％。三组间上述两指标相互比较差异显著。结论 应提供科学合理应用抗原发性高血压药物。     

抗高血压因子对正常及高血压动物动脉平滑肌Ca~(2+)内流的影响

通过实验观察到从自发性高血压大鼠(SHR)红细胞提取的抗高血压因子(AHF)可以明显抑制SHR血管平滑肌(VSM)Ca~(2+)内流,呈剂量依赖关系。而对正常血压大鼠(WKY)无影响。这种抑制作用及与剂量的关系在肠系膜动脉比主动脉更明显。结果表明,AHF的降压作用可能与抑制VSM Ca~(2+)内流有关。     

大鼠红细胞抗高血压因子的降压作用

本实验表明,从自发性高血压大鼠(SHR)红细胞提取的抗高血压因子(antihyper-tensive factor,AHF)可明显而持久地降低SHR和肾性高血压大鼠(RHR)的血压,而对正常大鼠血压无影响,表明AHF的降压作用与动物原来的血压水平密切相关,即具有血压依赖性;AHF耐热,在沸水中处理15min仍保持其强烈的降压效果,提示其不可能是体内已知的一些舒血管物质。目前,作者正在对AHF的理化特性和降压机理进行更深入的研究。     

Effects of antihypertensive factor from erythrocyte of spontaneously hypertensive rats on the blood pressure and Ca2+ influx of arterial smooth muscle in rats.

The effects of a partially purified antihypertensive factor (AHF) from erythrocytes of spontaneously hypertensive rats (SHR) on the blood pressure (BP) and Ca2+ influx of vascular smooth muscle (VSM) in rats were studied. The results indicated that AHF could produce a marked prolonged depressor effect and significantly inhibit the Ca2+ influx dose-dependently on both SHR and renal hypertensive rat (RHR) either in acute or in chronic experiments, but not on normotensive rats. It suggested that the inhibition of Ca2+ influx might be one of the important mechanisms for AHF as an endogenous depressor substance.

     

抗高血压因子对自发性高血压大鼠心脏功能的影响

本实验观察正常人红细胞抗高血压因子(antihypertensive factor,AHF)对卒中易感型自发性高血压大鼠(SHRsp)在体和离体心脏功能的影响。结果表明:AHF显著降低SHRsp在体心脏的心率(HR)、左心室收缩压(LVESP)和左心室内收缩及舒张压最大变化速率(±LVdP/dtmax)。而对正常血压的WKY大鼠上述指标无明显影响,表明AHF对高血压动物在体心脏具有负性变时和变力作用。AHF能明显降低SHRsp离体心脏的收缩幅度和静息张力,而对HR和冠状动脉流量无明显影响,表明AHF对离体心脏具有负性变力效应。以上结果提示AHF的降压作用与其降低心脏功能有关。     

硝普钠对SHRsp阻力血管平滑肌钙激活钾通道的影响

目的 观察硝基类扩血管药硝普钠（ｓｏｄｉｎｍ ｎｉｔｒｏｐｒｕｓｓｉｄｅｍ,ＳＮＰ）对卒中易感型自发高血压大鼠（ＳＨＲｓｐ）及其正常血压对照ＷＫＹ大鼠肠系膜动脉Ａ４－Ａ５分支阻力血管平滑肌钙激活钾通道（ＫＣａ）的作用。方法 用细胞贴附式膜片箝（ｏａｔｃｈ ｃｌａｍｐ）技术。结果 发现ＳＮＰ可激活ＳＨＲｓｐ与ＷＫＹ阻力血管平滑肌ＫＣａ。在同等剂量（１ ｎｍｏｌ／Ｌ）ＳＮＰ作用下,被激活的ＳＨＲｓｐ     

心钠素对高血压大鼠动脉平滑肌细胞离子泵活性和基因表达的影响

目的 探讨心钠素(ANP)对自发性高血压大鼠(SHR)动脉平滑肌细胞膜(ASMC)Na+,K+-ATP酶、Ca2+-ATP酶活性及Na+,K+-ATP酶α,亚单位、Ca+-ATP)酶亚型1(PMCA1)mRNA表达的影响.方法 对SHR大鼠,予不同浓度ANP和血管紧张素Ⅱ(Ang Ⅱ)干预,通过放射免疫、生化酶学和逆转录-聚合酶链反应等方法,检测ASMC的ANP、AngⅡ含量,ATP酶活性及其mRNA表达变化并设WKY大鼠为对照.结果 SHR大鼠ANP含量比WKY大鼠下降[(7.3±2.4)pg·10-6比(19.3±3.3) Pg·10-6,P＜0.01],Ang Ⅱ含量增加[(57±4)pg·10-6比(44±4) pg·10-6,P＜0.01],Na+,K+-ATP酶、Ca2+-A11)酶活性及Na+,K+-ATP酶α1亚单位、PMCA1 mRNA表达均显著降低[Na+,K+-ATP:(4.3±0.8) μmol·h-1·mg-1比(5.3±1.0) μmol·h-1·mg-1,Ca2+-ATP酶:(3.2±0.7)μmol·h-1·mg-1比(4.5±0.7) μmol·h-1·mg-1,α1亚单位:0.524±0.025比0.704±0.116,PMCA1:0.193±0.030比0.547±0.045](P＜0.05～P＜0.01).ANP可增加SHR大鼠Na+,K+-ATP酶、Ca2+-ATP酶活性及Na+,K+-ATP酶α1,亚单位及PMCA1 mRNA表达(均P＜0.01),Ang Ⅱ则抑制Ca2+-ATP酶活性和PMCA1 mRNA表达(P＜0.05～P＜0.01),仅1×10-7 mol/L AngⅡ抑制Na+,K+-ATP酶活性及α1亚单位mRNA表达,ANP能拮抗AngⅡ对两种ATP酶活性及其mRNA表达的效应.ANP也能拮抗AngⅡ对WKY大鼠Ca2+-ATP酶活性及PMCA1mRNA表达的效应,对Na+,K+-ATP酶活性及α1亚单位mRNA表达无影响(P＞0.05).结论 高血压大鼠ASMC两种ATP酶活性和基因表达下降与局部ANP和AngⅡ分泌异常有关,ANP能拮抗AngⅡ对两种ATP酶活性和基因表达的效应.     

An antihypertensive factor in the erythrocytes of essential hypertensive subjects--effects on blood pressure and calcium uptake by vascular tissue in rats.

An extract prepared from the erythrocytes of essential hypertensive subjects was found to significantly lower systolic blood pressure (SBP) in spontaneously (SHR) and renal hypertensive rats (RHR) following a single intravenous or intraperitoneal injection: The maximum SBP reduction was 42.8 mmHg in SHR and 38.3 mmHg in RHR. In contrast, this hypertensive factor (AHF) had little effect on normotensive Wistar Kyoto and Wistar rats. AHF was also found to significantly suppress Ca2+ uptake by vascular smooth muscle in the mesenteric artery and aorta of hypertensive and normotensive rats (P less than 0.05, respectively). Furthermore, AHF prepared from the erythrocytes of normotensive subjects was shown to have a similar effect.     

Atrial natriuretic factor and renin synthesized in cultured aortic smooth muscle cells of rats.

This study was designed to determine whether or not atrial natriuretic factor (ANF) is present in the vascular walls and to observe the differences in ANF between control (WKY) and stroke-prone spontaneously hypertensive rats (SHRsp). It was found that ANF is indeed present in the vascular wall of the distal aorta. HPLC analysis of the extracts from cultured aortic smooth muscle cells (ASMC) and medium revealed that intracellular ANF was mainly in the form of ANF(1-126), at levels of 0.82 +/- 0.03 (SHRsp) and 1.04 +/- 0.10 ng/10(6) cells (WKY), while the major form in the medium was ANF(99-126), at levels of 0.40 +/- 0.06 and 0.60 +/- 0.06 ng/10(6) cells, respectively. Both forms were present in smaller amounts in SHRsp than in WKY rats. On the contrary, both renin activity and angiotensin I concentrations in SHRsp cells were significantly higher than those in the WKY controls. In addition, immunocytochemistry showed positive ANF staining in cultured ASMC of both strains. The results suggest that ANF can be synthesized and secreted by cultured ASMC from rats.     

抗高血压因子对心肌氧自由基损伤及花生四烯酸代谢的影响

目的 探讨抗高血压因子（ＡＨＦ）对心肌缺血损伤保护的机理。方法 以导丙肾上腺素性心肌损伤大鼠为模型,观察ＡＨＦ对其心肌丙二醛、钙含量、血栓素Ｂ２和６－酮－前列腺素Ｆ１ａ（６－ｋｅｔｏ－ＰＧＦ１ａ）的影响,结果 ＡＨＦ保护组较心肌损伤组上述指标分别减少４６．０％,６２．２％和５８．６％,而６－ｋｅｔｏ－ＰＧＦ１ａ增加１２３．４％（均Ｐ〈０．０５）。心肌病理损伤程度也显著减轻（Ｐ〈０．０５）。结论 Ａ     

The influence of chloroethylclonidine-induced contraction in isolated arteries of Wistar Kyoto rats: alpha1D- and alpha1A-adrenoceptors, protein kinase C, and calcium influx.

BACKGROUND: It has recently been reported that chloroethylclonidine (CEC) elicited contraction in tail arteries (alpha(1A)-adrenoceptors) and aorta (alpha(1D)-adrenoceptors) from normotensive and spontaneously hypertensive rats (SHR). This study investigated the relationship between CEC-induced contraction and the role of protein kinase C (PKC) and extracellular Ca(++) influx in tail arteries and aorta from Wistar Kyoto rats (WKY). METHODS: Time-course of CEC-induced contraction in endothelium-denuded arteries from Wistar, WKY, and SHR rats was evaluated. In WKY arteries, calphostin C (1 x 10(-6) M) and nitrendipine (1 x 10(-6) M) were used to determine the role of PKC and extracellular Ca(+1) in the contractile response to CEC, respectively. RESULTS: Chloroethylclonidine (1 x 10(-4) M) elicited contraction in tail arteries and aorta from normotensive and hypertensive rats. Maximal response to CEC was similar in tail arteries among strains (approximately 30% of norepinephrine effect), while in aorta CEC elicited a higher contraction in WKY and SHR than in Wistar (59, 86, and 18% of norepinephrine effect, respectively). CEC-elicited maximal contractile responses were reached in 5 min in tail arteries and in 30-45 min in aorta irrespective of the rat strain, suggesting that different intracellular signaling pathways are involved in the contractile response to CEC in these arteries. In WKY tail arteries, calphostin C and nitrendipine blocked CEC-induced contraction while in aorta nitrendipine, but not calphostin C, inhibited CEC action. CONCLUSIONS: This study confirms marked strain-dependent differences in rat aorta responsiveness to CEC and suggests a central role for PKC in response to CEC in tail arteries and for extracellular Ca(+1) influx in aorta.