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目的：探讨急性心肌梗塞患者红细胞在旋精氨酸—一氧化氮（Ｌ－Ａｒｇ－ＮＯ）途径变化及临床意义。 方法：１４例急性心肌梗塞患者为急性心肌梗塞组，１０例健康成人为正常对照组，取静脉抗凝血，分离并提纯红细胞，同位素标记法测定~３Ｈ标记左旋精氨酸（~３Ｈ－Ｌ－Ａｒｇ）的转运动力学；分离统化一氧化氮合酶（ＮＯＳ）后测定其含量及活性，放射免疫法测定红细胞环磷酸鸟苷（ｃＧＭＰ）含量。 结果：急性心肌梗塞组患者红细胞①Ｌ－Ａｒｇ的总转运及Ｙ~＋载体的最大转运速率（Ｖｍａｘ）分别较正常对照组降低１４％（Ｐ＜０．０５）及 １８％（Ｐ＜０．０１），米氏常数（Ｋｍ）分别增加３２％及 ４６％（Ｐ＜０．０１）；Ｙ＋Ｌ载体无改变。②ＮＯＳ含量及活性分别较正常对照组降低１３％（Ｐ＜０．０５）及４４％（Ｐ＜０．０１）。③ＣＧＭＰ含量较正常对照组下降２７％（Ｐ＜０．０５）。 结论：急性心肌梗塞患者红细胞Ｌ－Ａｒｇ－ＮＯ途径存在多环节功能障碍，导致一氧化氮（ＮＯ）生成减少，可能会促进急性心肌梗塞的进展。
Objective: To investigate the changes of erythrocytes in L-arginine-nitric oxide (L-Arg-NO) pathway in patients with acute myocardial infarction and its clinical significance. Methods: Fourteen patients with acute myocardial infarction were acute myocardial infarction group and 10 healthy adults were normal control group. The venous anticoagulant blood was taken and the erythrocytes were isolated and purified. 3H-L-arginine (~ 3H-L -Arg). The content and activity of nitric oxide synthase (NOS) were determined and the content of cyclic guanosine monophosphate (cGMP) was determined by radioimmunoassay. Results: The total transport of L-Arg and the maximum transport rate of Y ~ + vector in erythrocytes of acute myocardial infarction group were 14% (P <0.05) and 18% (P <0.01) lower than that of normal control group ), And the Km increased by 32% and 46%, respectively (P <0.01). There was no change in Y + L vector. ②NOS content and activity decreased by 13% (P <0.05) and 44% (P <0.01) respectively compared with the normal control group. ③GMP content decreased 27% (P <0.05) compared with the normal control group. CONCLUSION: There is a multislice dysfunction in erythrocyte L-Arg-NO pathway in patients with acute myocardial infarction, which leads to the decrease of nitric oxide (NO) production and may promote the progression of acute myocardial infarction.