摘要
作者用循环式血液灌注装置,发现呋喃二氢吡啶Ⅰ20μmol/L能使离体兔心局部缺血再灌损伤时,乳酸脱氢酶、谷草转氨酶释放量明显减少;心肌镁含量从对照的0.41±0.07mg/g干重组织升高到0.89±0.16mg/g干重组织(P<0.01,n=6),锌含量和心肌含水量分别从对照的0.09±0.02 mg/g干重组织和82.68％±0.84％下降到0.06±0.01mg/g干重组织和80.19％±0.99％(P均<0.01,n=6)。并预防缺血、再灌时心律失常的发生。说明:该药保护缺血心肌损伤与其对心肌组织镁、锌含量的影响有关。
A recirculating nonpulsatile perfusion circuit was used in isolated rabbit hearts; it was found that furyl-dihydropyridine I 20 μmol/L could inhibit the leakage of myocardial lactate dehydrogenase, glutamic-oxalacetic transaminase; decrease the myocardial zinc and water content from 0.09 ± 0.02 mg/g dry weight and 8268 ± 0.84% to 0.06 ± 0.01 mg/g dry weight and 80.19 ± 0.99% (P<0.01, n=6); increase the magnesium from 0.41 ± 0.07 mg/g dry weight to 0.89 ± 0.16 mg/g dry weight (P<0.01, n=6), thus prevent ischemic-reperfused arrhythmias. These results indicate that the mechanisms of furyl-dihydropyridine I in protecting the ischemic-reperfused myocardium might be associated with change of magnesium and zinc content in myocardium.
出处
《第四军医大学学报》
1991年第2期86-88,共3页
Journal of the Fourth Military Medical University
关键词
呋喃二氢吡啶
再灌注损伤
镁
锌
furyl-dihydropyridine I
calcium channel blockers
ischemic-reperfused injury
lactate dehydrpgenase
giutamic-oxalacetic transaminase
magnesium
zinc
water
