已建立的β -肾上腺素受体阻断治疗对急性心肌梗死后胞质酶和溶酶体酶释放的影响。

E Welman, K M Fox, A P Selwyn, B J Carroll
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引用次数: 8

摘要

1. 对45例急性心肌梗死患者进行了连续静脉血采集。其中10名患者在胸痛发作时正在接受-肾上腺素受体阻断药物,并在冠状动脉护理病房住院期间继续服用这些药物。测定血浆中肌酸激酶及其mb同工酶(CK-MB)的活性。溶酶体酶β - n -乙酰氨基葡萄糖酶也被检测。2. 在35例未经治疗的患者中,发现肌酸激酶活性在胸痛发作后平均21.3 +/- 1.3 h达到最大值,而在接受β -肾上腺素受体阻断药物治疗的患者中,肌酸激酶活性峰值出现在24.4 +/- 0.7 h。CK-MB活性峰值也从对照组的18.1 +/- 1.6 h延迟到治疗组的22.4 +/- 1.2 h。4. 溶酶体酶表现出与CK-MB相似的变化模式。对照组患者胸痛发作后18.0 +/- 1.0 h血浆活性达到最大值。在接受治疗的患者中,溶酶体酶活性直到24.2 +/- 1.2 h才达到峰值。急性心肌梗死后血浆酶变化的时间变化与β受体拮抗剂可能延缓心肌缺血期间组织损伤的提示一致。
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The effect of established beta-adrenoreceptor-blocking therapy on the release of cytosolic and lysosomal enzymes after acute myocardial infarction in man.

1. Serial venous blood samples were obtained from 45 patients with acute myocardial infarction. Ten of these patients were receiving beta-adreno-receptor-blocking drugs at the time of onset of chest pain and continued on these drugs during their stay in the coronary care unit. The activities of creatine kinase and its MB-isoenzyme (CK-MB) were assayed in the plasma. A lysosomal enzyme, beta-N-acetylglucosaminidase, was also assayed. 2. In the 35 untreated patients it was found that creatine kinase activity was maximal at a mean time of 21.3 +/- 1.3 h after the onset of chest pain, whereas in the patients receiving beta-adrenoreceptor-blocking drugs peak activity of the enzyme occurred at 24.4 +/- 0.7 h. 3. Peak CK-MB acitivity was also delayed from 18.1 +/- 1.6 h in the control group to 22.4 +/- 1.2 h in the treated patients. 4. The lysosomal enzyme showed a similar pattern of changes to that of CK-MB. Maximum activity in plasma occurred at 18.0 +/- 1.0 h after the onset of chest pain in the control group of patients. In the treated patients peak lysosomal enzyme activity was not found until 24.2 +/- 1.2 h. 5. These alterations in the time-course of plasma enzyme changes after acute myocardial infarction are consistent with the suggestion that beta-receptor antagonists may delay tissue damage during myocardial ischaemia.

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Proceedings of the Fifth Meeting of the International Society of Hypertension, Paris, 12-14 June 1978. Brain catecholamines and catecholamine-synthesizing enzymes in renovascular hypertension in the rat. Enhanced hypothalamic noradrenaline biosynthesis in Goldblatt I renovascular hypertension. Definitive evidence for renin in rat brain by affinity chromatographic separation from protease. Renal release of active and inactive renin in essential and renovascular hypertension.
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