title: Ultrastructural effects induced by global ischaemia on the AV node compared with the working myocardium. A qualitative and morphometric investigation on the canine heart.
abstract: The cardiac conduction system is considered to be particularly resistant to ischaemia. Nevertheless, following open heart surgery with short periods of ischaemia disturbances in AV conduction or ventricular arrhythmia have been reported. We compared the ultrastructure of AV node and working myocardium following 30 min global ischaemia at 25 degrees C, during pure ischaemia and with HTK cardioplegia qualitatively and morphometrically. After 30 min of pure ischaemia, interstitial and intracellular oedema together with considerable changes in organelles in AV nodes predominate over mainly cellular oedema in working myocardium. Sometimes irregular overcontractions of sarcomeres occur in the AV node, though very seldom in working myocardium. In pure ischaemia, mitochondrial swelling is comparable in both types of tissue. Following HTK cardioplegia and 30 min ischaemia, cellular oedema and mitochondrial swelling are significantly reduced in AV nodal cells and working myocardium, but remain more extensive in the AV nodes. Irregularities in the contractile state of sarcomeres are not observed. The extent of the ultrastructural alterations corresponds to the degree of metabolic change in the working myocardium. Thus, despite considerable differences during pure ischaemia and HTK cardioplegia, ultrastructurally the AV nodal cells do not display a greater resistance to ischaemia than working myocardium.
authors.affiliation: Abteilung Vegetative Physiologie und Pathophysiologie, Universität Göttingen, FRG.
authors.forename: P A
authors.initials: PA
authors.lastname: Schnabel
authors.forename: J
authors.initials: J
authors.lastname: Richter
authors.forename: M M
authors.initials: MM
authors.lastname: Gebhard
authors.forename: G
authors.initials: G
authors.lastname: Mall
authors.forename: A
authors.initials: A
authors.lastname: Schmiedl
authors.forename: H J
authors.initials: HJ
authors.lastname: Clavien
authors.forename: H J
authors.initials: HJ
authors.lastname: Bretschneider
mesh_terms: D000818:Animals; D001283:Atrioventricular Node / Q000473:pathology / Q000648:ultrastructure*; D002314:Cardioplegic Solutions / Q000494:pharmacology; D003327:Coronary Disease / Q000473:pathology*; D004285:Dogs; D005947:Glucose / Q000494:pharmacology; D006329:Heart Conduction System / Q000648:ultrastructure*; D008353:Mannitol / Q000494:pharmacology; D008854:Microscopy, Electron; D008933:Mitochondrial Swelling; D009206:Myocardium / Q000473:pathology / Q000648:ultrastructure*; D009210:Myofibrils / Q000648:ultrastructure; D010477:Perfusion; D011189:Potassium Chloride / Q000494:pharmacology; D011343:Procaine / Q000494:pharmacology; D012016:Reference Values; D013997:Time Factors
chemical_list: C039984:Bretschneider cardioplegic solution; D002314:Cardioplegic Solutions; D008353:Mannitol; D011343:Procaine; D011189:Potassium Chloride; D005947:Glucose