Kubat K, Smedts F
Department of Pathology, University Hospital Nijmegen, The Netherlands.
Mod Pathol. 1993 Nov;6(6):743-7.
The detection of recent myocardial damage by means of the macroscopic lactate dehydrogenase reaction (LDHr) linked to nicotinamide adenine dinucleotide diaphorase (NADHd), conducted in a liquid medium is greatly insensitive to postmortal autolysis. In 10 heart cones (i.e., cardiac ventricles severed underneath the coronary sulcus) stored at 6 degrees C for up to 114 h after death, no autolytic artifacts appeared on freshly cut apical surfaces of transverse myocardial slices. In 10 cones kept at room temperature for up to 95 h after death, no artifacts appeared in eight cases; in two cases the LDHr was impaired by postmortal bacterial spread and decomposition of the myocardium. Intravital perfusion of injured myocardium increases the sensitivity of the LDHr. Postmortal stand-still of circulation is decisive in preserving dehydrogenase activities in undamaged myocardium. An artificial decrease in enzyme activity always appeared on the nonrecent, basally facing cut surfaces of slices exposed to air and fluid oozing out of the myocardium for long periods, even if the exposed surface of the cone was kept at 6 degrees C and wrapped in plastic. In normal practice, when bodies are stored in a refrigerating unit, the LDHr may still indicate myocardial damage more than 114 h after death.
通过与烟酰胺腺嘌呤二核苷酸黄递酶(NADHd)相关的宏观乳酸脱氢酶反应(LDHr)在液体介质中检测近期心肌损伤,对死后自溶极不敏感。在10个心脏锥体(即冠状动脉沟下方切断的心室)于死后在6℃保存长达114小时后,横向心肌切片新切的顶端表面未出现自溶假象。在10个锥体于死后在室温下保存长达95小时后,8例未出现假象;2例中LDHr因死后细菌扩散和心肌分解而受损。活体灌注受损心肌可提高LDHr的敏感性。死后循环停止对保存未受损心肌中的脱氢酶活性起决定性作用。即使锥体暴露表面保持在6℃并用塑料包裹,长时间暴露于空气和从心肌渗出的液体中的切片非近期、面向基部的切割表面上总会出现酶活性的人为降低。在常规实践中,当尸体存放在冷藏单元中时,LDHr在死后114小时以上仍可能表明心肌损伤。