title: The contraction state of myofibrils during global ischemia and after reperfusion following different forms of cardiac arrest. Correlation with metabolic parameters in the canine heart.
abstract: This study was undertaken in order to obtain information on the mode of reaction of the contractile apparatus after different forms of cardiac arrest, global ischemia and reperfusion, as well as on possible correlations between the contraction state of myofibrils and biochemical parameters. During the survival time, before the level of 3 mumol/gww creatine phosphate (CP) is reached, the contraction state shows only minor changes. During the revival time in which ATP tissue concentrations decay to 4 mumol/gww, the contribution of ATP, lactate, anorganic phosphate (Pa) and acidosis to the degree of relaxation depends on the method of cardiac arrest. At defined biochemical values, the degree of relaxation is comparable after aortic cross clamping (ACC) and St. Thomas perfusion, but significantly different compared to HTK perfusion. Thus, during the revival time, the relaxation of sarcomeres depends predominantly on the composition of the solutions used for cardiac arrest. The re-entry of contraction below 3 mumol/gww ATP is correlated with the ATP concentration, independent of the form of cardiac arrest. Reperfusion after HTK or St. Thomas cardioplegia and reversible ischemia leads to the focal formation of contraction bands, which do not occur during ischemia. This contraction state is significantly more pronounced after reperfusion of St. Thomas arrested hearts. Thus, the contraction state of myofibrils is influenced not only by alterations in metabolite concentrations, but also by the composition of cardioplegic solutions and by the characteristic conditions (sufficient energy, oxygen and Calcium) during reperfusion.
authors.affiliation: Department of Anatomy, University of Göttingen, FRG.
authors.forename: A
authors.initials: A
authors.lastname: Schmiedl
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: H J
authors.initials: HJ
authors.lastname: Bretschneider
mesh_terms: D000255:Adenosine Triphosphate / Q000032:analysis / Q000378:metabolism; D000818:Animals; D002118:Calcium / Q000032:analysis / Q000378:metabolism; D004285:Dogs; D004734:Energy Metabolism; D006323:Heart Arrest / Q000201:enzymology / Q000378:metabolism* / Q000503:physiopathology*; D007773:Lactates / Q000032:analysis / Q000378:metabolism; D009119:Muscle Contraction / Q000502:physiology*; D009132:Muscles / Q000737:chemistry / Q000378:metabolism / Q000502:physiology; D017202:Myocardial Ischemia / Q000201:enzymology / Q000378:metabolism* / Q000503:physiopathology*; D015425:Myocardial Reperfusion; D009210:Myofibrils / Q000737:chemistry / Q000378:metabolism / Q000502:physiology*; D010100:Oxygen / Q000032:analysis / Q000378:metabolism; D010725:Phosphocreatine / Q000032:analysis / Q000378:metabolism
chemical_list: D007773:Lactates; D010725:Phosphocreatine; D000255:Adenosine Triphosphate; D010100:Oxygen; D002118:Calcium