Fedorova O V, Maslova M N, Roukoyatkina N I, Ukhanova M V, Zhabko E P
I M Sechenov Institute of Evolutionary Physiology and Biochemistry, Academy of Science of the USSR, Leningrad.
Cardiovasc Res. 1991 May;25(5):371-7. doi: 10.1093/cvr/25.5.371.
The aim was to look for the presence of circulating factor(s) with Na,K-ATPase inhibitory properties and digoxin like immunoreactivity in patients after acute myocardial infarction.
Venous blood samples were obtained when the patients were admitted and different methods were used to monitor the plasma concentrations of factor(s) with properties of digitalis. SUBJECTS - These were 26 patients of both sexes (mean age 57.7 years, range 40-72) during the first 24 h of a first transmural acute myocardial infarct, 11 male patients with unstable angina pectoris (52.5 years, 45-67), and 18 healthy male controls (25 to 50 years).
There was significant inhibition of ouabain sensitive Na,K-ATPase in intact erythrocytes in patients with myocardial infarction [1.4(SEM 0.15)mumol Pi.mg-1.h-1] compared with patients with unstable angina pectoris [3.1(0.4), p less than 0.01] and healthy controls [3.4(0.25), p less than 0.01]. In myocardial infarction complicated by ventricular fibrillation (n = 5) Na,K-ATPase activity was significantly lower than in the other 21 patients [0.95(0.2) and 1.55(0.11) mumol Pi.mg-1.h-1 respectively, p less than 0.05]. There was no change in erythrocyte Na,K-ATPase activity in myocardial infarction complicated by acute pulmonary oedema, nor was there any difference in activity in erythrocyte ghosts obtained from the patients with myocardial infarction v healthy controls, at 0.47(0.13) v 0.50(0.02) mumol Pi.mg-1.h-1. Boiled plasma supernatants obtained from the patients with myocardial infarction inhibited Na,K-ATPase in erythrocytes from healthy subjects. This inhibitory effect was antagonised by antidigoxin antibody. Plasma inhibitory potency was correlated with erythrocyte Na,K-ATPase activity in the patients with myocardial infarction (r = -0.65, p less than 0.001, n = 23). There was a 2.5-fold increase in plasma digoxin like immunoreactivity in the patients with myocardial infarction [1.65(0.5) ng.ml-1] using DELFIA fluoroimmunoassay as compared with five healthy controls [0.04(0.12), p less than 0.05] and nine patients with unstable angina [0.48(0.11), p less than 0.05]. There was no difference in plasma digoxin like immunoreactivity in myocardial infarction complicated or not by ventricular fibrillation, but there was very low digoxin like immunoreactivity in patients with myocardial infarction complicated by acute pulmonary oedema [0.26(0.08) ng.ml-1, n = 7]. There was no correlation between plasma digoxin like immunoreactivity and either plasma Na,K-ATPase inhibitory potency or erythrocyte Na,K-ATPase activity.
The results show that plasma factor(s) with some of the properties of digitalis are increased in acute myocardial infarction.
旨在探寻急性心肌梗死后患者体内具有钠钾 - ATP酶抑制特性且与地高辛样免疫反应性相关的循环因子的存在情况。
患者入院时采集静脉血样，采用不同方法监测具有洋地黄特性的因子的血浆浓度。
26例急性透壁性心肌梗死患者（男女均有，平均年龄57.7岁，范围40 - 72岁），于发病后24小时内；11例不稳定型心绞痛男性患者（平均年龄52.5岁，范围45 - 67岁）；18例健康男性对照者（年龄范围25至50岁）。
与不稳定型心绞痛患者[3.1(0.4)]和健康对照者[3.4(0.25)]相比，心肌梗死患者完整红细胞中的哇巴因敏感钠钾 - ATP酶受到显著抑制[1.4(标准误0.15) μmol Pi·mg⁻¹·h⁻¹，p < 0.01]。在合并心室颤动的心肌梗死患者（n = 5）中，钠钾 - ATP酶活性显著低于其他21例患者[分别为0.95(0.2)和1.55(0.11) μmol Pi·mg⁻¹·h⁻¹，p < 0.05]。合并急性肺水肿的心肌梗死患者红细胞钠钾 - ATP酶活性无变化，且心肌梗死患者与健康对照者红细胞膜空壳的酶活性也无差异，分别为0.47(0.13)和0.50(0.02) μmol Pi·mg⁻¹·h⁻¹。心肌梗死患者的煮沸血浆上清液可抑制健康受试者红细胞中的钠钾 - ATP酶。这种抑制作用可被抗地高辛抗体拮抗。心肌梗死患者血浆抑制效力与红细胞钠钾 - ATP酶活性相关（r = -0.65，p < 0.001，n = 23）。采用DELFIA荧光免疫分析法检测，心肌梗死患者血浆地高辛样免疫反应性较5例健康对照者[0.04(0.12)]和9例不稳定型心绞痛患者[0.48(0.11)]升高2.5倍（p < 0.05）。合并或未合并心室颤动的心肌梗死患者血浆地高辛样免疫反应性无差异，但合并急性肺水肿的心肌梗死患者血浆地高辛样免疫反应性极低[0.26(0.08) ng·ml⁻¹，n = 7]。血浆地高辛样免疫反应性与血浆钠钾 - ATP酶抑制效力或红细胞钠钾 - ATP酶活性之间无相关性。
结果表明，急性心肌梗死时具有某些洋地黄特性的血浆因子增加。
