Armiger L C, Harland-Smith S J, Eagar R L
Department of Pathology, University of Auckland, School of Medicine, New Zealand.
Exp Pathol. 1990;38(2):109-18. doi: 10.1016/s0232-1513(11)80245-8.
The effects of major ischaemic metabolites on the fine structure of false tendon Purkinje cells from the dog heart were investigated in vitro under oxygenated and oxygen-deficient conditions. High levels of potassium ion induced potentially reversible alteration consisting of moderate cell swelling, swelling of sarcoplasmic reticulum, and nuclear swelling with moderate aggregation of chromatin irrespective of gas tension. Other metabolites induced alteration only in oxygen-deficient solutions. Ischaemic levels of lactate and inorganic phosphate both caused mitochondrial swelling, which was most severe in the presence of lactate. At acidic pH intramitochondrial dense inclusions, the hallmark of irreversible injury, also developed. Severe aggregation of nuclear chromatin and gross dilatations of the sarcoplasmic reticulum were focal and much less prominent than in contractile myocardium exposed to excess hydrogen ion. These observations indicate that the efflux of ischaemic metabolites from a developing infarct may be arrhythmogenic by impairing the function of the subjacent Purkinje network without damaging its cell structure, since luminal blood flow ensures it is always adequately oxygenated.
在有氧和缺氧条件下，体外研究了主要缺血代谢产物对犬心脏假腱索浦肯野细胞精细结构的影响。无论气体张力如何，高浓度钾离子都会引起潜在的可逆性改变，包括中等程度的细胞肿胀、肌浆网肿胀以及核肿胀和染色质中度聚集。其他代谢产物仅在缺氧溶液中引起改变。缺血水平的乳酸和无机磷酸盐都会导致线粒体肿胀，在乳酸存在的情况下最为严重。在酸性pH值下，线粒体内致密包涵体（不可逆损伤的标志）也会出现。核染色质的严重聚集和肌浆网的明显扩张是局部性的，并且比暴露于过量氢离子的收缩性心肌中要轻得多。这些观察结果表明，正在形成的梗死灶中缺血代谢产物的外流可能通过损害下方浦肯野网络的功能而致心律失常，而不会破坏其细胞结构，因为管腔内的血流可确保其始终获得充足的氧合。
