title: Patterns of structural deterioration due to ischemia in Purkinje fibres and different layers of the working myocardium.
abstract: Cellular and mitochondrial swelling are regarded as typical intra-ischemic alterations ("IIA"), contraction band lesions (CBL), in contrast, as products of post-ischemic reperfusion. The occurrence of both types of structural deterioration was investigated in Purkinje fibres and subendocardial and intramural working myocardium: initially after St. Thomas- or HTK cardioplegia, then during ensuing global ischemia up to the "practical limit of resuscitability", and following post-ischemic reperfusion. Generally, Purkinje fibres are not better preserved than neighbouring working myocardium. Comparing St. Thomas- and HTK cardioplegia, considerable quantitative, but not qualitative differences in the reaction patterns of different cell types or layers arise. Immediately after cardioplegia, CBL are completely lacking in both cell types. During ischemia, CBL occur occasionally in Purkinje fibres and seldom in subendocardial working myocardium, "IIA" predominate. During post-ischemic reperfusion "IIA" tend to reverse in all layers, whereas CBL are found to remain in the subendocardial cell types. In intramural layers, CBL occur only during reperfusion. Thus, we deduce that cardioplegia only modulates the severity of "IIA" and the frequency of CBL, but cannot abolish the particular sensitivity of subendocardial Purkinje fibres to global ischemia. Prerequisites for the development of irreversible CBL are on the one hand ischemic metabolic alterations and corresponding energy deficits, and, on the other hand, a supply of oxygen. The oxygen may be inadequately supplied via diffusion during ischemia or may be subsequently provided by reperfusion.
authors.affiliation: Department of Physiology, Georg-August-University, Göttingen, Germany.
authors.forename: P A
authors.initials: PA
authors.lastname: Schnabel
authors.forename: J
authors.initials: J
authors.lastname: Richter
authors.forename: A
authors.initials: A
authors.lastname: Schmiedl
authors.forename: F
authors.initials: F
authors.lastname: Bach
authors.forename: U
authors.initials: U
authors.lastname: Bartels
authors.forename: B
authors.initials: B
authors.lastname: Ramsauer
authors.forename: M M
authors.initials: MM
authors.lastname: Gebhard
authors.forename: H J
authors.initials: HJ
authors.lastname: Bretschneider
mesh_terms: D000818:Animals; D001639:Bicarbonates; D002122:Calcium Chloride; D002314:Cardioplegic Solutions; D004285:Dogs; D004699:Endocardium / Q000648:ultrastructure; D005947:Glucose; D006324:Heart Arrest, Induced; D008274:Magnesium; D008353:Mannitol; D015428:Myocardial Reperfusion Injury / Q000473:pathology*; D009206:Myocardium / Q000648:ultrastructure*; D011189:Potassium Chloride; D011343:Procaine; D011690:Purkinje Fibers / Q000648:ultrastructure*; D012965:Sodium Chloride
chemical_list: D001639:Bicarbonates; C039984:Bretschneider cardioplegic solution; D002314:Cardioplegic Solutions; C041711:St. Thomas' Hospital cardioplegic solution; D008353:Mannitol; D012965:Sodium Chloride; D011343:Procaine; D011189:Potassium Chloride; D008274:Magnesium; D005947:Glucose; D002122:Calcium Chloride