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myocardial damage
Greater myocardial damage in SHRSP than in Wistar rats following the equal increase in OH· production above the basal level suggests the existence of deficit of the antioxidant defense in the hypertrophied myocardium.
      
Local myocardial damage due to current flow through the heart is the probable cause of the extrasystoly.
      
Background Perioperative myocardial damage is an important determinant for postoperative cardiac function and recovery.
      
Cardiac troponin I (cTNI) is a specific marker for myocardial damage.
      
The coronary angiography demonstrated intact coronary circulation and a broad area of myocardial damage of the left ventricular lateral wall.
      
This increased blood glucose level on the one hand is due to preexisting diabetes mellitus or metabolic syndrome, but on the other hand may be a marker of larger myocardial damage with excess katecholamine release.
      
For the quantitative evaluation of myocardial damage induced by isoprenaline (ISO) a method based on the uptake of203Hg-labelled Mercurascan (MSC) in the heart was used.
      
The extent of myocardial damage was determined morphometrically.
      
These findings indicate the massive intracellular calcium influx by the calcium reintroduction and the myocardial damage induced by the calcium overload as observed in isolated whole hearts.
      
Myocardial damage by ventricular fibrillation in isolated perfused rat hearts, and its underlying mechanisms
      
Protective effect of taurine against isoprenaline-induced myocardial damage
      
Implantation of ultrasonic crystals is associated with reversible and irreversible myocardial damage which might limit the interpretation of the obtained results, in particular during acute experiments.
      
We therefore developed a sonomicrometric device which can be easily and quickly implanted, and thus reduces the reversible myocardial damage induced by prolonged surgical implantation.
      
On the other hand, chlorpromazine (30 mg/kg) and mepacrine (50 mg/kg) partially prevented myocardial damage through the preservation of myocardial phospholipid composition, total phosphorus and CK activity.
      
These results show a clear correlation between the development of irreversible myocardial damage and increased sarcolemmal membrane permeability.
      
Thus, exercise training reduces myocardial damage caused by isoproterenol, but the evidence does not support the hypothesis that prostacyclin mediated this effect of training.
      
Further research is needed to determine the extent to which exercise training-induced alterations in sensitivity to PGI2 or TXA2 affect myocardial damage from isoproterenol.
      
These results indicate that myocytic mitochondria are especially vulnerable to oxygen radicals, and further that myocytic mitochondrial ultrastructural changes may be a crucial step in the development of oxygen radical-induced myocardial damage.
      
Cardiac TnT can be used as a useful biochemical marker for hemodynamics and myocardial damage after reperfusion.
      
The number of cells with such deposits was markedly increased after 30 min of ischemia (19%), as well as after 20 min of ischemia followed by reperfusion (17%), prior to the development of irreversible myocardial damage.
      
 

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