[Intravenous treatment with streptokinase of acute myocardial infarction. II. Effect of patency of the artery supplying the infarction area on the infarction size and post-infarction impairement of left-ventricular function]. / Dozylne leczenie streptokinaza swiezego zawalu serca. II. Wplyw droznosci tetnicy zaopatrujacej obszar zawalu na mase zawalu i pozawalowy ubytek czynnosci lewej komory.

153 patients with a first acute myocardial infarction underwent the study. 90 of them received 1.000.000 units of streptokinase intravenously, followed by intravenous heparin administration for 5-7 days. The control group consisted of 63 remaining. In all patients serum CK-MB activity was determined every 4 hours for 72 hours: the infarct mass was calculated from the obtained curves. In 118 patients selective coronarography and left ventriculography was performed in the 2-nd or 3-rd week of hospitalisation. Left ventricular ejection fraction (E.F.) and dyssynergy index were calculated from ventriculographic data. Coronarography revealed a patent infarct-related artery in 76.7% of patients treated with streptokinase and in 44.4% of the control group (p less than 0.001). Among patients with a patent infarct-related artery an early peak of serum CK-MB activity (suggesting early recanalisation) occurred in 72.2% of streptokinase patients but in only 42.1% of the control group. Patients with a patent infarct-related artery had a significantly lower infarct mass (45 +/- 28 g vs 56 +/- 30 g), a lower left ventricular dyssynergy index (229 +/- 243 vs 348 +/- 247) and a significantly higher E.F. (63 +/- 12% vs 54 +/- 15%) compared with patients with an occluded artery.

[Intravenous streptokinase treatment of acute myocardial infarction. I. Effect of the treatment on the course of infarction and the patency of the artery supplying the infarction area]. / Dozylne leczenie streptokinaza swiezego zawalu serca. I. wplyw leczenia na przegieg zawalu i droznosc tetnicy zaopatrujacej obszar zawalowy.

128 consecutive patients with a first myocardial infarction, admitted within 4 hours after the onset of an angina pain, were divided into two groups according to the history of the peptic ulcer. Group I (with a negative history, n = 72) received intravenously 1,000,000 units of streptokinase followed by intravenous heparin infusion for 5-7 days. Group II (with a positive history, n = 56) was the control one. In hospital mortality was 2.8% in group I and 5.3% in group II (N. S.). Coronarography performed during second or third week of hospitalization revealed the patency of a coronary artery supplying an infarcted region twice as frequent in group I than in group II (78% vs 41%, p less than 0.001). Percentage of patients with the early serum peak of CKMB activity (from 8 to 12 hours from the start of therapy) suggesting early recanalization of a coronary artery supplying an infarcted region was significantly higher in group I (44.7% and 70.1%) than in group II (7.8% and 19.5%). Both differences between groups were significant (p less than 0.001). Early serum peak of CKMB activity (from 8 to 12 hours from start of treatment) was stated respectively in 46.5% and 81.4% of patients of group I in which subsequent coronarography revealed the patency of a coronary artery supplying the infarcted region.

Interaction of zinc ions with DNA-dependent RNA polymerases A, B and C isolated from calf thymus.

Purified DNA-dependent RNA polymerases A, B and C isolated from calf thymus contain a significant amount of zinc. Atomic absorption spectroscopy revealed the presence of 6.7, 5.35 and 2.6--4.1 g-atoms of zinc per mole of polymerase A, B and C, respectively. These enzymes are inhibited by treatment with 1,10-phenanthroline at concentrations varying from 10(-5) to 10(-4) M. However, the addition of zinc ions does not restore fully the activity of 1,10-phenanthroline treated enzymes. Exogenous zinc ions reduce in vitro an overall RNA synthesis catalysed by RNA polymerases from calf thymus. In addition to the sites which bind zinc in a specific and stoichiometric way these enzymes possess other classes of binding sites with high and low affinity. Occupancy by exogenous zinc of these additional binding sites inhibit polymerase activity.