自发性高血压大鼠血压和左心室肥厚发展过程中去甲肾上腺素、血管紧张素Ⅱ的变化规律（摘要）

自发性高血压大鼠血压和左心室肥厚发展过程中去甲肾上腺素、血管紧张素Ⅱ的变化规律（摘要）党爱民，郑德裕，金律高血压左心室肥厚是增加心血管病发病率和死亡率的一个独立危险因子。交感神经系统（ＳＮＳ）和心脏肾素一血管紧张素系统（ＲＡＳ）的主要活性成份去甲肾上...     

高效液相色谱法测定血浆去甲肾上腺素、肾上腺素及多巴胺

建立了用电化学检测器同时测定血浆去甲肾上腺素、肾上腺素和多巴胺的方法。本方法简便、敏感而稳定,已用于高血压病的鉴别诊断及嗜铬细胞瘤的定位。     

右颈静脉孔区嗜铬细胞瘤一例

右颈静脉孔区嗜铬细胞瘤一例张云王蕾礼金律刘国仗⒇１临床资料患者男性，２０岁。因血压升高２年伴阵发性心悸、头痛１年入院。患者２年前发现血压升高达２９．３／１７．３ｋＰａ（２２０／１３０ｍｍＨｇ），因症状不明显未做诊治。一年前患者出现阵发性心悸、头痛，心...     

心钠素对肾血管性高血压的临床作用

肾血管性高血压有复杂的病理生理特点,适于全面评价心钠素的生理、药理作用。给7例患者静脉滴注心钠素0.025μg·kg~(-1)/min×60min,引起肾素—血管紧张素—醛固酮系统及交感神经系统的抑制,血浆加压素浓度的降低,产生了利尿、利钠效应并伴有红细胞压积和肌酐清除率的增加,血压轻度平续的下降。一些因素参与了肾血管性高血压的形成和维持。本研究提示,心钠素对这些因素均有一定作用     

新喋呤与细胞介导免疫

新喋呤(Neopterin)是一种由鸟苷三磷酸(GTP)衍生的低分子化合物。GTP 经其环水解酶作用生成二氢新喋呤三磷酸,再经丙酮酰二氢喋呤综合酶和鸟喋呤还原酶作用生成四氢生物喋呤(BH_4),二氢新喋呤三磷酸是BH_4生物合成途径关键的中间产物,BH_4是苯丙氨酸、酪氨酸和色氨酸羟化酶的辅酶。当综合途径受阻时,此中间产物可不用酶的催化直接转变为新喋呤。如BH_4缺乏可发生血苯丙氨酸过高,因缺乏神经介质使精神严重迟钝。在临床上称为非典型苯丙酮尿,其血和尿中新喋呤浓度增高。     

地拉普利对32例原发性高血压患者降压疗效的分析

32例原发性高血压患者服用地拉普利治疗6周,获得较满意的疗效,降压有效率为87.5%,其中显效率50%。此药具有缓慢持续降压效果,无明显副作用,对轻至中度原发性高血压患者治疗有效。     

慢性充血性心力衰竭患者心率变异性与病情的相关性分析

目的：为探讨心力衰竭（心衰）患者心率变异性与病情的关系。方法：本文采用时域及频域２种分析方法，对９２例心衰患者和５１例对照组健康人进行了心率变异性对比分析，并对部分患者（ｎ＝１０）及对照组健康人（ｎ＝２０）进行血浆儿茶酚胺（去甲肾上腺素、肾上腺素）浓度测定及心率变异性随访。结果：心衰患者的心率变异性显著低于对照组健康人；并且与病情及心功能明显相关（Ｐ＜０．０５～０．００１）；心衰患者中近期死亡者心率变异性进一步降低（Ｐ＜０．０５～０．００１）；心衰患者血浆去甲肾上腺素及肾上腺素浓度明显高于健康组（Ｐ＜０．０２～０．０１）。结论：心衰患者心率变异性降低提示，心衰患者心率变异性的数量变化，反应患者病情变化。高的血浆儿茶酚胺浓度间接说明了心衰患者心脏自主神经功能受损是神经激素系统持续激活的结果     

CALCIUM ANTAGONISTS IN PREVENTION OF HYPERTENSION AND STROKE IN STROKE-PRONE SPONTANEOUSLY HYPERTENSIVE RATS

To investigate the effect of Calcium antagonists (Ca-An) with different tissue specificity in the devel- opment of hypertension and stroke in salt-loading SHRSP, three experiments were conducted. In exper- iment I (1), 50 8-week-old male SHRSP were divided into three groups and given nifedipine (NF, 32mg / kg /day), menidipine (MN 32mg / kg / day)and placebo (control group)respectively. In the controJ group 83.3%(15 / 18)died of stroke and 17 showded renal vascular sclerosis. Their average lifespan was 84 days. NF and MN significantly re- duced systolic blood pressure (SBP), and no stroke of renal vascular sclerosis developed.ln experiment I(2), 54 7-week-old male SHRSP were divided into three groups (18 in each group). They were treated with nimodipine (NM)20mg / kg / day, 2mg / kg / day and placebo respectively. NM (20mg / kg / day) markedly lowered SBP and postponed the onset of stroke. Only 11% died in 17 weeks. NM (2mg / kg / day did not lower SBP but postpond the onset of stroke. In exper- iment 11 (1), 29 10-week-old female SHRSP were di- vided into three groups: Group A was given NF 32mg / kg / day, group B was parathyoidectomized (PTX) and group C served as control. PTX group did not lower SBP but could postpone the onset of stroke. In experiment Ⅱ (2), 33 male SHRSP were divided into three groups and ticated as desctibed above :in experiment Ⅱ (I)(ll in each group). Seven weeks after the experiment, the brain blood flow of NF group was significantly greater (67.5%)than that of the control and PTX groups. In experiment II, 27 7-week-old male SHRSP were divided into three groups as described above in experiment I(2). Two weeks after the treatment, significant difference was found in norepinephrine (NE)contents of the anterior hypothalamic region (AHR)between NM (20mg / kg / day)group and control group (2 870 vs 2 304 pg / mg tissue). Our results show that Ca-An (nimodipine)can re- verse the NE depletion by high salt in SHRSP, thus lower SBP and prevent stroke.     

内毒素休克发生机制的实验研究(微聚物形成在内毒素休克发生中的意义)

本文从血液动力学、血粘度、血象及形态学研究了24条狗内毒素休克发生机制。动物于注射内毒素(ET)后5分钟内血中即出现以血小板为主的微聚物,同时血中血小板、嗜中性白细胞、血压及中心静脉压均下降,血球压积增加,肺中出现微血栓,动物呈呼气性呼吸困难。此变化迅即缓解,动物于 ET 后30′～120′内上述指标逐渐部分恢复。4～6小时内血中又再度出现大量不易解聚的微聚物,上述指标变化加重而导致大部分动物于6小时内死亡,对照组无上述变化。此实验说明微聚物形成在内毒素休克发生中具有重要意义。