犬急性肺血栓栓塞部分血管活性物质的实验研究

目的　探讨内皮素(ET)、一氧化氮(NO)、肾上腺髓质素(ADM)和C型利钠肽(CNP)在肺血栓栓塞时的变化及对血流动力学的影响。方法　14只健康杂种犬随机分为肺栓塞组和对照组。栓塞组注射自体血栓,对照组注射温生理盐水。每只犬在注栓前、注栓后的半小时、1、2、4及6h各时点记录血流动力学指标和进行动脉血气分析,收集动脉血标本,检测ET、CNP、ADM和NO的变化。结果　组织病理符合肺血栓栓塞的改变;栓塞组在栓塞后动脉血气血氧分压较栓塞前及对照组明显降低(P <0 .0 5 ) ;栓塞组在栓塞后平均肺动脉压(MPAP)和肺血管阻力(PVR)较栓塞前及对照组明显升高(P<0 .0 5 ) ;与对照组比较,ET和NO在栓塞后2、4及6h明显升高(P <0 .0 5 )。ADM在栓塞后1、2h明显升高(P <0 .0 5 ) ;CNP在栓塞后2h明显升高(P <0 .0 5 )。结论　血管活性物质ET、NO、ADM和CNP参与急性肺血栓栓塞的病理生理过程。     

急性肺栓塞大鼠血管内皮功能动态观察

目的探讨急性肺栓塞大鼠血浆内皮素(ET)、NO水平的动态变化,了解血管内皮功能的改变。方法雄性SD大鼠32只,随机分为对照组、栓塞24h组、栓塞1周组、栓塞2周组,每组8只。医用明胶海绵微粒制备大鼠急性肺栓塞模型,测定血浆ET、NO,HE染色。结果与对照组比较,栓塞24h组、栓塞1周组、栓塞2周组大鼠血浆ET水平呈持续升高状态,NO水平呈持续降低状态。光镜下观查,栓塞2周组大鼠肺动脉内明胶海绵多数溶解。结论急性肺栓塞大鼠血浆ET和NO水平与肺血管内皮功能损伤有关。     

急性肺栓塞大鼠肺表面活性物质的变化

目的探讨急性肺栓塞大鼠肺表面活性物质的变化情况。方法32只雄性SD大鼠以随机数字表法分为对照组、栓塞24h组、栓塞1周组、栓塞2周组,每组8只;以明胶海绵溶液经大鼠颈静脉注入制备大鼠肺栓塞模型,经右心导管测定肺动脉压、心率、呼吸频率,并行动脉血气分析。上述4组大鼠分别于肺动脉栓塞后2周、24h、1周、2周时处死,取肺组织制备病理切片,HE染色光镜下观察肺组织病理变化;逆转录聚合酶链反应、Western-blot法测定肺表面活性物质相关蛋白A(SPA)mRNA及蛋白水平。结果对照组、栓塞24h组、栓塞1周组、栓塞2周组大鼠肺动脉压平均值分别为(14.2±4.1)、(26.1±7.5)、(26.1±6.8)、(29.0±8.2)mm Hg(1mm Hg=0.133kPa),肺栓塞后大鼠肺动脉压升高(F值为3.09,P<0.05);心率分别为(415±15)、(451±35)、(463±29)、(446±14)次/min(F值为2.24,P<0.05);动脉血氧分压分别为(94.1±8.8)、(80.5±5.8)、(80.4±13.8)、(73.4±14.3)mm Hg(F值为1.25,P<0.05)。实验大鼠肺组织病理切片光镜检查,栓塞24h组可见肺组织多个血管腔有明胶海绵栓塞,栓塞1周组栓子部分溶解,栓塞2周组栓子基本溶解。大鼠肺栓塞后2周内肺组织SPA mRNA及蛋白水平显著下降,对照组、栓塞24h组、栓塞1周组、栓塞2周组肺组织SPA mRNA水平分别为1.43±0.51、0.83±0.33、0.91±0.33、0.87±0.35(F值为2.92,P<0.05);蛋白水平分别为1.00±0.00、0.44±0.18、0.44±0.33、0.52±0.32(F值为3.49,P<0.05)。结论大鼠急性肺栓塞后SPA水平显著降低,这可能与急性肺栓塞大鼠动脉低氧血症的发生有关。     

新活素对急性心肌梗死患者内皮功能影响的临床研究

目的探讨急性心肌梗死患者在常规治疗的基础上加用新活素对血管内皮功能的影响。方法选择急性心肌梗死患者60例,随机分为实验组30例及对照组30例。对照组患者给予常规药物治疗,实验组患者在常规治疗基础上即刻静脉注射新活素。治疗前及治疗后2周超声观察肱动脉内皮依赖性舒张功能(FMD)的变化。2组分别在治疗前及治疗后2周采集静脉血,所有标本收集后统一检测。ELISA测定2组患者治疗前及治疗后血清NO及内皮素1含量。结果实验组治疗后FMD较对照组明显升高(15.09±1.13 vs 9.14±2.82,P<0.05);实验组治疗后血清NO含量较治疗前明显升高[(45.09±5.65)μmol/L vs(37.67±5.43)μmol/L,P<0.05],内皮素1含量较治疗前明显降低[(72.08±20.94)ng/L vs(84.56±23.83)ng/L,P<0.05];实验组治疗后血清NO含量较对照组明显升高,内皮素1含量较对照组明显降低。结论新活素能够通过增加血液中NO含量,降低内皮素1含量,改善急性心肌梗死患者的血管内皮功能,是其治疗急性心肌梗死的机制之一。     

实验性急性肺栓塞溶栓疗法与动脉血浆内皮素水平变化

目的：自体血栓注入法建立急性肺栓塞动物模型，探讨内皮素在急性血栓栓塞性肺动脉高压中的作用和溶栓疗法对肺动脉释放内皮素的影响。方法：14只杂种犬，自体血栓注入法建立急性肺栓塞模型。模型犬随机分入溶栓组和对照组，溶栓组7只犬给予尿激酶20000U/kg，100ml液体稀释后30分钟静脉滴入，对照组同期输入等量的生理盐水。分别于注栓前、溶栓前（对照组同期）、溶栓后（对照组同期）血液动力学测定，采动脉血放免法测定血浆内皮素水平。结果：溶栓组犬静注尿激酶30分钟后，伴随肺动脉压力和肺血管阻力的显著性下降，动脉血浆内皮素水平显著升高，溶栓后30小时为99.25±12.90pg/L，与注栓前51．63±10．09pg/L比较P＜005，与对照组同期值55．93±2.10pg/L比较P＜001，对照组犬栓塞后4小时内肺动脉压力和肺血管阻力无显著变化，内皮素水平亦无显著性改变。结论：内皮素可能与急性血栓栓塞性肺动脉高压的形成有关，动脉血浆内皮素水平的增加可能是血管再通的一个标志。     

实验性肺栓塞溶栓血管紧张素I和血管紧张素Ⅱ变化的意义

目的 探讨兔实验性肺栓塞症（PTE）溶栓前后血管紧张素Ⅰ（ANGⅠ）和血管紧张素Ⅱ（ANGⅡ）变化及其临床意义。方法 健康中国大耳白兔30只,按照随机数字法将实验动物分为肺栓塞组,对照组和溶栓组,每组10只。栓塞组和溶栓组自颈静脉注入自体小血凝块建立家兔急性肺栓塞模型,溶栓组从耳静脉注入尿激酶。结果 栓塞组兔的肺表面凸凹不平,有散在苍白病灶,并可见点片状出血灶,镜下肺动脉血管内可见有注入的血凝块,血管壁炎症细胞浸润及间质出血。栓塞后5d处死的家兔可见栓塞灶内有肉芽组织形成。肺栓塞后ANGⅠ 1h开始持续升高,2h达高峰;溶栓组2h后变化无显著差异;栓塞组ANGⅡ 1h明显升高并持续,与栓塞前相比均有显著差异。溶栓组1h开始升高2h达高峰,此后开始下降至与栓塞前相比无显著差异。结论 PTE兔4h内ANGⅠ和ANGⅡ有不同程度的升高,溶栓后明显降低,故PTE的溶栓或一般治疗中用拮抗剂（ACEI）或受体拮抗剂（ARB）是有益的。     

急性冠状动脉综合征患者介入术前后血小板活化及血管内皮功能的变化

目的观察急性冠状动脉综合征患者介入治疗后血小板活化指标CD62p、CD63及糖蛋白Ⅱb/Ⅲa受体复合物及内皮功能的改变。方法60例急性冠状动脉综合征患者在冠状动脉介入术前和术后即刻以及次日采用流式细胞仪检测血小板活化指标CD62p、CD63及糖蛋白Ⅱb/Ⅲa受体复合物;双抗体夹心固相酶联免疫吸附试验测定血浆假血友病因子的表达水平;放射免疫测定法测定血浆内皮素1表达水平;酶法测定血浆一氧化氮的含量;彩色多谱勒超声诊断仪测量内皮依赖性血管舒张功能。选择健康体检者和稳定型心绞痛患者各30例作对照,观察急性冠状动脉综合征患者冠状动脉介入前后指标的变化并与对照组比较。结果与健康对照组和稳定型心绞痛组比,急性冠状动脉综合征组CD62p、CD63及糖蛋白Ⅱb/Ⅲa受体复合物明显增高(P<0.05或0.01);急性冠状动脉综合征患者介入术后即刻CD62p、CD63和糖蛋白Ⅱb/Ⅲa受体复合物与术前相比明显增高(P<0.01),但术后24h较术前无明显变化(P>0.05)。与健康对照组和稳定型心绞痛组比,急性冠状动脉综合征组假血友病因子、内皮素1的表达水平明显增高(P<0.01),内皮依赖性血管舒张功能和一氧化氮降低(P<0.05或<0.01);急性冠状动脉综合征患者介入术后即刻血浆假血友病因子和内皮素1水平升高(P<0.05或P<0.01),内皮依赖性血管舒张功能和一氧化氮水平降低(P<0.05),且介入术后24h假血友病因子水平也较术前升高(P<0.05),内皮依赖性血管舒张功能降低(P<0.05),但内皮素1和一氧化氮水平与术前差异无显著性(P>0.05)。结论血小板活化和内皮功能的损伤在急性冠状动脉综合征发生和发展过程中起重要的作用,冠状动脉介入术后血管内皮受到一定损伤,血小板有一定程度的激活。     

急性肺栓塞大鼠血清血管紧张素转换酶1的变化

目的探讨急性肺栓塞大鼠血清血管紧张素转换酶1的变化。方法雄性SD大鼠24只,随机分为对照组,栓塞后24 h组,栓塞后1周组,每组8只;以明胶海绵溶液经颈静脉注入制备大鼠肺栓塞模型,对照组注入同等体积生理盐水。3组大鼠分别于1周(对照组)、栓塞后24 h、栓塞后1周时处死。经右心导管测定肺动脉压、心率、呼吸频率,取动脉血行动脉血气分析及血清血管紧张素转换酶1活性测定;取肺组织制备病理切片,HE染色光镜下观察肺动脉栓塞情况。结果对照组,栓塞24 h组,栓塞1周组大鼠肺动脉平均压分别为(14.2±4.1)mm Hg(1 mm Hg=0.133 kPa)(、26.1±7.5)mm Hg(、26.1±6.8)mm Hg(P<0.05);动脉血氧分压分别为(94.1±8.8)mm Hg(、80.5±5.8)mm Hg(、80.4±13.8)mm Hg(P<0.05);3组大鼠血清血管紧张素转换酶1分别为(30.5±7.2)U/L(、53.5±15.9)U/L(、45.8±17.4)U/L(P<0.05)。光镜下观察,栓塞后24 h组肺组织切片均可见多个肺动脉管腔内海绵明胶栓塞,有继发红血栓形成,肺组织充血、水肿、炎性细胞浸润;栓塞后1周组大鼠部分肺动脉管腔内海绵明胶溶解。结论急性肺栓塞大鼠肺动脉压升高的同时,血清血管紧张素转换酶1明显升高,其程度可能与肺血管床阻塞的范围或程度有关。     

长期间歇性低氧对大鼠血压及心血管内皮系统的影响

目的建立间歇性低氧(CIH)大鼠模型,验证CIH对大鼠血压及心血管内皮系统的影响。方法选择雄性Wistar大鼠90只,随机分为4组:CIH组、低氧舱空气对照组(CIA组)和动物房内空白对照组(CON组),每组30只。采用往复循环式小动物低氧舱制作CIH大鼠模型;采用Softron智能无创血压计测量鼠尾血压,检测各组大鼠基线、7、14、21、28d时一氧化氮、内皮素1水平及一氧化氮合酶活性。结果与基线比较,随着时间延长,3组大鼠收缩压升高,舒张压比较,差异无统计学意义(P>0.05)。与CIA组和CON组比较,CIH组大鼠14、21、28d时一氧化氮、一氧化氮合酶水平明显降低,差异有统计学意义(P<0.05),内皮素1水平明显升高,差异有统计学意义(P<0.05,P<0.01)。CIA组与CON组一氧化氮、一氧化氮合酶、内皮素1比较,差异无统计学意义(P>0.05)。结论 CIH可导致大鼠持续性血压升高。CIH可引起一氧化氮合酶活性降低、一氧化氮合成释放减少,内皮素1表达增加。     

血清脂联素和一氧化氮及内皮素在糖尿病周围神经病患者中的相关性研究

目的探讨血清脂联素,NO及内皮素在糖尿病周围神经病(DPN)中的作用及其相关性。方法选择糖尿病患者及健康体检者88例,采用病例-对照方法研究,分为3组,其中DPN患者30例为DPN组,单纯糖尿病患者28例为糖尿病组,健康体检者30例为对照组。采用ELISA法测定受试者血清脂联素水平,硝酸还原酶法测定血清NO水平,放射免疫法测定血浆内皮素水平。进行相关性分析。结果与对照组比较,DPN组及糖尿病组血清脂联素和NO水平明显降低,血浆内皮素水平明显增高,差异有统计学意义(P<0.01)。与糖尿病组比较,DPN组血清脂联素和NO水平明显降低(P<0.05),血浆内皮素水平明显升高(P<0.01)。DPN组脂联素与NO呈正相关(r=0.423,P<0.05),NO与内皮素呈负相关(r=-0.440,P<0.05),脂联素与内皮素不相关(r=-0.159,P>0.05);糖尿病组及对照组中脂联素与NO及内皮素不相关(P>0.05)。结论血清脂联素和NO水平降低及内皮素水平增高可能参与了DPN的发病过程,NO作用可能与脂联素的调控有关。     

内皮素与缺血性脑损伤

作为目前已知的作用最强的血管收缩因子,内皮素广泛分布于中枢神经系统,并于缺血损伤时表达明显增加,可通过多种途径对中枢神经系统产生损伤作用。     

用半定量RT－PCR检测内皮素及其受体mRNAs在不同组织中的表达

本文应用半定量逆转录－多聚酶链反应（ｓｑＲＴ－ＰＣＲ）方法，检测了内皮素（ＥＴ）及其受体（ＥＴＲ）ｍＲＮＡｓ在心、肝、肺、肾等重要生命器官中的表达。结果显示，ＥＴ及ＥＴＲｍＲＮＡｓ均同时广泛表达于心、肝、肺、肾等重要脏器中，而且其表达量均以肺组织最高，其次是心脏和肾脏，而以肝组织表达量最低。结果提示，ＥＴ可能是生命活动中必不可少的细胞因子，ＥＴ及其受体在部位上的平行分布揭示ＥＴ可能不是一种循环激素，而是以自分泌和（或）旁分泌方式起作用的一种局部介质。肾脏既有中等量的ＥＴ表达，又有中等量的ＥＴＲ表达，证明肾脏也是ＥＴ发挥作用的重要靶器官，提示ＥＴ在肾脏生理和肾脏病理中可能具有重要的意义。     

Therapeutic Role of Bosentan in Hypertension: Lessons from the Model of Perinephritic Hypertension

Since its discovery in 1988, there has been increasing evidence that endothelin-1 (ET-1) plays an important role in the pathophysiology of hypertension and its related end-organ damages. First studies, using ET-1 administration in animals or in humans suspected this role by demonstrating the hypertensive properties of ET-1. The latter, due to stimulation of ET_A receptors inducing sustained vasoconstriction have been reported to follow transient vasodilation linked with activation of an endothelial ET_B receptor releasing nitric oxide (NO). In certain instances, ET_B smooth-muscle receptors might also induce contraction. Cloning of these receptors helped to develop ET-1 receptor antagonists. As soon as one of them became available, bosentan, a dual (ET_A and ET_B) ET-1 receptor antagonist, we tested its effects in the canine model of perinephritic hypertension. Bosentan was found to exert striking hypotensive effects, due to peripheral vasodilation but without affecting cardiac function. In further experiments, we observed that effects of bosentan were additional to those of ACE inhibitors or angiotensin II antagonists. This opened new therapeutic perspectives and also suggested a proper role of ET-1 in hypertension, independent of the renin-angiotensin system. To explain this role, we demonstrated a real imbalance characterized by an impairment of the NO system in favor of the ET-1 pathway. Recent studies suggest that such an imbalance may also occur in human hypertension. Furthermore, the contribution of ET-1 to human hypertension appears more convincing since bosentan was shown to decrease blood pressure in hypertensive subjects. Finally, ET-1 receptor antagonists might be of therapeutic interest to prevent hypertension induced end-organ damages. Whether or not these compounds are able to prevent or to reverse target organ injuries in man remains to be investigated.     

Endothelin system in human persistent and paroxysmal atrial fibrillation

INTRODUCTION: Activation of the endothelin system is an important compensatory mechanism that is activated during left ventricular dysfunction. Whether this system plays a role at the atrial level during atrial fibrillation (AF) has not been examined in detail. The purpose of this study was to investigate mRNA and protein expression levels of the endothelin system in AF patients with and without concomitant underlying valve disease. METHODS AND RESULTS: Right atrial appendages of 36 patients with either paroxysmal or persistent AF were compared with 36 controls in sinus rhythm. The mRNA amounts of pro-endothelin-1 (pro-ET-1), endothelin receptor A (ET-A), and endothelin receptor B (ET-B) were studied by semiquantitative polymerase chain reaction. Protein amounts of the receptors were investigated by slot-blot analysis. mRNA amounts of pro-ET-1 were increased (+40%; P = 0.002) only in AF patients with underlying valve disease. ET-A and ET-B receptor protein amounts were significantly reduced in patients with paroxysmal AF (-39% and -47%, respectively) and persistent AF with underlying valve disease (-28% and -30%, respectively) and in persistent AF without valve disease (-20% and -40%, respectively). ET-A mRNA expression was unaltered in paroxysmal and persistent AF, whereas ET-B mRNA was reduced by 30% in persistent AF with (P < 0.001) or without (P = 0.04) valve disease, but unchanged in paroxysmal AF. CONCLUSION: Substantial changes in gene expression of the endothelin system were observed in human atria during AF, especially in the presence of underlying valve disease. Alterations in endothelin expression associated with AF could play a role in the pathophysiology of AF and the progression of underlying heart disease.     

内皮素受体拮抗剂与急性心肌梗死

内皮素是一种由 2 1个氨基酸残基构成的多肽 ,它通过与内皮素受体结合在急性心肌梗死的病理生理中起着重要的作用 ,比如扩大心肌梗死面积、诱发心律失常、加重心力衰竭等等。而内皮素受体拮抗剂却可阻断内皮素相应受体的生理学作用。     

Is there a role for serum endothelin in predicting the severity of acute pancreatitis?

BACKGROUND: Acute pancreatitis remains a common presentation to acute surgical units and carries significant morbidity and mortality. The progression of the disease to necrotizing pancreatitis and multi-organ dysfunction syndrome (MODS) is associated with a very poor clinical outcome, and persistendy high mortality. Increases in serum endothelin (ET) have been seen in animal models of acute pancreatitis and this study aims to investigate whether there is a change in serum ET-1 in patients with acute pancreatitis and whether any such change is linked to disease severity. METHODS: All patients admitted with acute pancreatitis were prospectively recruited from die emergency admissions at the Norfolk and Norwich University Hospital. Serum ET levels were determined on admission, at 24 hours and 5 days post admission. Healthy adult controls were recruited from dermatology outpatients. RESULTS: A total of 21 patients joined the trial after giving informed consent. There were 3 men and 18 women with a median age of 65 years (range 26-87 years). Serum ET levels were significantly higher in acute pancreatitis patients than in normal controls (P <0. 05). An association was seen between persistendy raised serum ET levels and progression to MODS. CONCLUSIONS: The study does demonstrate a correlation between the circulating levels of ET and acute pancreatitis in humans, although it does not elicit its involvement in the pathogenesis of the disease. The observation that a persistendy high level of circulating ET-1 is associated with progression to MODS may indicate a role for ET in the monitoring of acute pancreatitis patients for recovery or progression to MODS.     

Endothelin and Heart Failure

The availability of potent and orally active nonpeptide endothelin (ET) receptor antagonists has generated a host of information on the pathophysiological role of ET-1 in a number of preclinical models including hypertension, renal failure, heart failure and pulmonary hypertension. Convincing data are available to show that ET-1 receptor antagonists are beneficial in humans as far as reversal of deranged systemic and regional hemodynamics associated with CHF and pulmonary hypertension. As in other disease areas, the issue of whether ET_A-selective or ET_A/B antagonists are more suited for CHF treatment remains unresolved. ET_B receptors may mediate some critical processes in the kidney such as sodium and water excretion in addition to releasing vasodilator substances such as NO and prostacyclin from endothelial cells. In heart failure and chronic renal diseases, preservation of ET_B-mediated responses in the kidney and pulmonary endothelium might be beneficial. On the other hand, blockade of ET_B-mediated vasoconstriction, smooth muscle cell proliferation and fibrosis by ET_B antagonists might be beneficial. In clinical trials so far, the hemodynamic effects of mixed antagonists of ET receptors and ET_A selective antagonists seem equivalent.     

Endothelin and pulmonary arterial hypertension

BACKGROUND AND OBJECTIVES: Pulmonary arterial hypertension (PHT) is a potentially fatal disease. The purpose of this article is to review the current knowledge of the role played by endothelin (ET) in PHT and the relevant drug regimens used in the treatment of this condition. METHODS: A detailed search via MEDLINE (PubMed) was performed by using PHT and ET as the key terms. RESULTS: PHT could be a primary or a secondary diagnosis associated with various heart and lung diseases. PHT appears during the late stage of systemic sclerosis and may complicate other systemic diseases such as systemic lupus erythematosus. The vascular endothelium and activation of various mediators and growth factors such as the ET system are thought to play a crucial role in the development of this condition. The pathologic process progresses very rapidly from vasoconstriction to widespread pulmonary vascular obstruction. The use of high doses of calcium channel blockers is of limited value. Life-long anticoagulant therapy is recommended for the treatment of PHT. Currently, the drug being used in PHT therapy is continuous central-venous prostacyclin infusion. Prostacyclin is a strong vasodilator with antiaggregate and antifibrotic properties and has the potential to reduce endothelial injury and to induce vasculature remodeling. This treatment results in improved functional status and increased life span. Unfortunately, its use is accompanied by various side effects, technical difficulties, and high cost. The role of other therapeutic modalities (inhaled prostacyclin, subcutaneous treprostinil, oral beraprost, sildenafil) in vascular remodeling, and the improvement in functional capacity and survival of patients with PHT, are currently under investigation. Bosentan, administered orally, is a recently developed active ET receptor antagonist. It is a promising new therapeutic tool in the treatment of PHT because of its potent vasodilator, antiproliferative, and vascular remodeling activity. CONCLUSIONS: The revolutionary conceptual shift in understanding the pathogenesis of PHT from a vasoconstrictive process to a vasoproliferative one, has led to a modification in the treatment of this disease from the use of vasodilators to the use of drugs with antiproliferative and vascular remodeling activity. Until now, prostacyclin was the only drug of this type available for the treatment of PHT. ET blockade seems to be a reasonable and potential therapeutic option.     

冠心病患者经皮冠状动脉腔内成形术后血浆内皮素改变及其意义

经皮冠状动脉腔内成形术（ＰＴＣＡ）常导致冠状动脉收缩，其发生机制尚不明了。本研究对经ＰＴＣＡ的１６例冠心病（ＣＨＤ）患者进行血浆内皮素（ＥＴ）水平、平均血压和心率的观察。结果表明，ＰＴＣＡ后股动脉血浆ＥＴ水平无明显改变（Ｐ＞０．０５），冠状窦血浆ＥＴ浓度明显升高（Ｐ＜０．０５），而平均血压和心率在ＰＴＣＡ前后均无明显改变。结果提示，血浆ＥＴ水平升高可能与ＰＴＣＡ时缺血缺氧有关，并且可能是ＰＴＣＡ后冠状动脉收缩的原因之一。     

放射免疫法测定急性心肌梗塞患者血浆内皮素的动态变化

目的：为了探讨内皮素－1（ET－1）在急性心肌梗塞（AMI）病人中的作用及临床意义。方法：采用放射免疫分析法动态测定35例AMI病人血浆ET－1和肿瘤坏死因子（TNF）的含量，并与心肌酶（CPK－MB）浓度做相关分析。结果：AMI病人血浆ET－1水平较对照组显著升高（100．55±22．50ng/LVS58．7±11．62ng/L）6小时后达高峰，随后缓慢降低，直至7日仍比正常值高，溶栓组比非溶栓组血浆ET－1下降快，入院后72小时已降至正常。ET－1与血清TNF－α呈正相关性（r=0．509，P＜0．05），与CPK－MB则无明显相关性。结论：血浆ET－1在AMI的发病中起一定的作用，测定ET－1水平有助于判断病情变化及预后。