Fine structural alteration in the atrioventricular junctional conduction tissues of the dog heart during severe ischaemia.

To define the fine structural changes produced in the atrioventricular junctional conduction tissues by severe ischaemia, 3 sets of specimens from 37 dogs were examined by light and electron microscopy using a large specimen resin-embedding method. Surgical control material was taken from 18 open-chest animals maintained under anaesthesia for up to 6 h, autolysis control material from 10 excised normal hearts maintained at 37 degrees C in vitro for up to 4 h, and ischaemic material from 8 animals in which the septal and distal left circumflex coronary arteries were occluded for 15 min to 3 h. Surgical control material was found to be within normal limits, whereas both autolysed and ischaemic showed initially mild fine structural alteration, which increased progressively in severity with time and was comparable in both sets. All cell types showed loss of glycogen granules, mitochondrial swelling, dilatation of sarcoplasmic reticulum vesicles, clumping of nuclear chromatin and ultimately varying degrees of generalised cell swelling. Intramitochondrial dense inclusions also were prominent in autolysis but not ischaemia. These changes progressed faster in nodal cells than in His bundle/bundle branch cells, which retained considerable quantities of glycogen for at least 60 min. The slower development of irreversible alteration in His-Purkinje cells suggests that they may be relatively more resistant to ischaemia, whilst the low incidence of intramitochondrial dense inclusions in vivo suggests a beneficial effect of collateral blood flow.