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对40例急性心肌梗死（AMI）患者血浆内皮素（endothelin－1，ET－1）水平检测结果显示，AMI患者就诊时血浆ET－1水平明显高于健康人水平，差异显著（P＜0．01）。就诊后1小时（h）即发病后5．07±3．08h，血浆ET-1水平达高峰（27．892±6．96gp／ml）。尿激酶静脉溶栓治疗20例病人的血浆ET-1峰值较20例非溶栓治疗的ET－1峰值低（26．145±3．90pg／ml对29．587±6．08pg／ml），且下降较快（P＜0．01）。溶栓治疗后，血流再通组与血流未再通组的ET－1时间活性差异有统计学意义（P＜0．05），说明缺血再灌流ET-1释放减少。有合并症（心力衰竭，心源性休克）AMI病人的血浆ET-1较无合并症者更呈现持续性增高，在就诊后72小时仍高；而无合并症者此时已接近正常值（19．3±6．29pg／ml）。两组比较，有显著性差异。
The plasma level of endothelin-1 (ET-1) in 40 patients with acute myocardial infarction (AMI) showed that the plasma level of ET-1 at the time of visit was significantly higher than that of healthy people (P <0. 01). One hour after treatment (h), ie 5.07 ± 3.08 h after onset, the plasma ET-1 level reached the peak (27.892 ± 6.96 gp / ml). The peak of plasma ET-1 in 20 patients with urokinase thrombolytic therapy was lower than that of 20 patients without thrombolysis (26.145 ± 3.90pg / ml vs 29.587 ± 6.08pg / ml) And decreased rapidly (P <0.01). After thrombolytic therapy, there was a significant difference in the ET-1 activity between the recanalization group and the non-recanalization group (P <0.05), indicating that the release of ET-1 was reduced after ischemia-reperfusion. In patients with AMI (heart failure, cardiogenic shock), plasma ET-1 showed a persistent increase compared with non-comorbid patients, and still remained high at 72 hours after treatment; at this time, patients without complications were close to normal ( 19.3 ± 6.29 pg / ml). There was a significant difference between the two groups.