Cellular edema and alterations in metabolite content in the ischemic and reperfused canine heart following different forms of cardiac arrest.
This study investigates firstly how far cellular edema correlates with parameters of the anaerobic energy turnover independent of the method used for cardiac arrest, and secondly to what extent cellular edema developing during reversible global ischemia is reduced after reperfusion. Canine hearts were arrested 1. by aortic cross clamping (ACC), 2. by coronary perfusion with St. Thomas solution, or 3. HTK (histidine tryptophan ketoglutarate) solution (Custodiol). Samples for biochemical and structural analysis were taken at different times during ischemia and after reperfusion with Tyrode solution. Cellular edema determined morphometrically and given as volume ratio of sarcoplasm and mitochondria to myofibrils (Vvsp + V vmi/Vvmf) varies significantly in the differently arrested hearts. Reperfusion after a decrease in ATP to 4 mumol/gww (revival time) leads to a nearly complete structural recovery. The relationship between cellular edema and defined over-all metabolite tissue concentrations and extracellular pHe values shows: 1. during the decrease of creatine phosphate to 3 mumol/gww, cellular edema does not change; it is, however, significantly higher after ACC and St. Thomas than after HTK perfusion; 2. at each lactate concentration, cellular edema differs significantly depending on the form of cardiac arrest; 3. during the decrease of ATP and pHe cellular edema increases and is comparable at concentrations < 4 mumol/gww and at pHe values < 6.5 independent of the form of cardiac arrest; 4. beyond 10 mumol/gww of inorganic phosphate (Pi), increasing values for cellular edema correspond to defined Pi values in the differently arrested hearts. Thus, the ratio VVSp+ VVMi/VVMf is a powerful parameter for the determination of cellular edema during ischemia, as well as for correlations with metabolic parameters.
Schmiedl
A
A
Department of Anatomy, University of Göttingen, FRG.
Schnabel
P A
PA
Richter
J
J
D000818:Animals; D001011:Aorta; D001639:Bicarbonates; D002122:Calcium Chloride; D009202:Cardiomyopathies / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D002314:Cardioplegic Solutions; D003250:Constriction; D004285:Dogs; D004487:Edema / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D005947:Glucose; D006324:Heart Arrest, Induced / Q000379:methods; D008274:Magnesium; D008353:Mannitol; D017202:Myocardial Ischemia / Q000209:etiology* / Q000378:metabolism* / Q000473:pathology; D015425:Myocardial Reperfusion; D009206:Myocardium / Q000378:metabolism; D010477:Perfusion; D011189:Potassium Chloride; D011343:Procaine; D012965:Sodium Chloride
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