title: Swelling of capillary endothelial cells and cardiomyocytes in the ischaemic myocardium of artificially arrested canine hearts.
abstract: To establish whether coronary perfusion with cardioplegic solutions results in better intraischaemic structural preservation of endothelial cells than of cardiomyocytes, we determined intraischaemic swelling of these two cell types in hearts differently arrested during global ischaemia at 5 degrees C. Cardiac arrest was induced in situ by aortic cross clamping or by additional coronary perfusion with various cardioplegic solutions. Parameters for cellular swelling were determined, i.e. barrier thickness of capillary endothelial cells and sum of the volume fractions (V(V)) of free sarcoplasm and mitochondria (V(VSp) + V(VMi)) in cardiomyocytes. In order to test the intraischaemic relative increase of cellular volume in both cell types, regression analyses were performed. The results show that the relative intraischaemic volume increase was similar in both cell types after perfusion with histidine-tryptophan-ketoglutarate solution, and significantly less pronounced in capillary endothelial cells after perfusion with University of Wisconsin solution. In hearts arrested with St. Thomas' Hospital solution, a significantly higher volume increase was determined in capillary endothelial cells. Thus, capillary endothelium does not generally show a higher structural preservation than cardiomyocytes during ischaemia. Instead, volume regulation in both types of cells depends on the type of cardioplegic solution used. These results should be taken into consideration in human transplantation medicine.
authors.affiliation: Department of Anatomy, University School of Medicine Hannover, Germany. Schmiedl.Andreas@MH-Hannover.de
authors.forename: A
authors.initials: A
authors.lastname: Schmiedl
authors.forename: P A
authors.initials: PA
authors.lastname: Schnabel
authors.forename: H
authors.initials: H
authors.lastname: Kausch Blecken von Schmeling
authors.forename: K
authors.initials: K
authors.lastname: Marten
authors.forename: J
authors.initials: J
authors.lastname: Richter
mesh_terms: D000241:Adenosine; D000493:Allopurinol; D000818:Animals; D001639:Bicarbonates; D002122:Calcium Chloride; D002196:Capillaries / Q000473:pathology / Q000648:ultrastructure; D002314:Cardioplegic Solutions; D048429:Cell Size; D004285:Dogs; D004730:Endothelium, Vascular / Q000473:pathology / Q000648:ultrastructure; D005260:Female; D005947:Glucose; D005978:Glutathione; D006324:Heart Arrest, Induced; D006801:Humans; D007328:Insulin; D008274:Magnesium; D008297:Male; D008353:Mannitol; D008854:Microscopy, Electron; D008929:Mitochondria, Heart / Q000473:pathology / Q000648:ultrastructure; D008933:Mitochondrial Swelling; D017202:Myocardial Ischemia / Q000473:pathology*; D009206:Myocardium / Q000473:pathology* / Q000648:ultrastructure; D019188:Organ Preservation Solutions; D011189:Potassium Chloride; D011343:Procaine; D011887:Raffinose; D012965:Sodium Chloride
chemical_list: D001639:Bicarbonates; C039984:Bretschneider cardioplegic solution; D002314:Cardioplegic Solutions; D007328:Insulin; D019188:Organ Preservation Solutions; C041711:St. Thomas' Hospital cardioplegic solution; C055206:University of Wisconsin-lactobionate solution; D008353:Mannitol; D012965:Sodium Chloride; D011343:Procaine; D000493:Allopurinol; D011189:Potassium Chloride; D005978:Glutathione; D008274:Magnesium; D005947:Glucose; D000241:Adenosine; D002122:Calcium Chloride; D011887:Raffinose