Ryoji Yokota

Preconditioning improves energy metabolism during reperfusion but does not attenuate myocardial stunning in porcine hearts.

BackgroundIt has been reported that a brief period of coronary occlusion and reperfusion slows the rate of ATP depletion during subsequent sustained ischemia as well as limiting infarct size. However, it has not yet been determined whether ischemic preconditioning also has an effect on the functional and metabolic recovery of stunned myocardium. Our study was designed to address this problem. Methods and ResultsFarm pigs were anesthetized with fluothane and randomly assigned to either a control group or a preconditioned group. The control group (n=15) underwent 15 minutes of coronary occlusion followed by 120 minutes of reperfusion. The preconditioned group (n=14) underwent two episodes of 5-minute occlusion and 5-minute reperfusion followed by 15 minutes of occlusion and 120 minutes of reperfusion. This protocol was designed to exclude the stunning effect of the preconditioning procedure itself as much as possible besides preconditioning the heart. A pair of ultrasonic crystals was implanted in the area at risk perfused by the left anterior descending coronary artery. 31P-nuclear magnetic resonance spectroscopy and sonomicrometry were performed alternately. Regional myocardial blood flow (RMBF) was determined with colored microspheres. At 15 minutes of sustained ischemia, phosphocreatine (Pcr), ATP, and intracellular pH were significantly better preserved in the preconditioned group (Pcr: control/preconditioned, 1±1%/o/14

Blockade of ATP-sensitive K+ channels attenuates preconditioning effect on myocardial metabolism in swine:: Myocardial metabolism and ATP-sensitive K+ channels

1%; ATP:control/preconditioned, 66

Incidence and Clinical Predictors of Stent Restenosis and Early Stent Occlusionin Patients with Acute Myocardial Infarction Treated by Bare Metal Stents:Importance of Infarct Location and Serum Creatinine Level

2%1/74

Ischemic preconditioning elevates cardiac stress protein but does not limit infarct size 24 or 48 h later in rabbits.

2%; pH:control/preconditioned, 632

Expression of heat shock protein after ischemic preconditioning in rabbit hearts

0.07/6.52

Transient adenosine infusion before ischemia and reperfusion protects against metabolic damage in pig hearts

0.05; P<.05). After reperfusion, ATP increased progressively and was almost normalized at 120 minutes of reperfusion in the preconditioned group (control/ preconditioned, 73

Preconditioning with 15-minute ischemia extends myocardial infarct size after subsequent 30-minute ischemia in rabbits

4%/95

Nitric oxide inhibition improved myocardial metabolism independent of tissue perfusion during ischemia but not during reperfusion.

3%; P<.05). Overshoot of Pcr (which indicates that the energy generating system is operating better than energy utilizing system) persisted in preconditioned hearts but disappeared rapidly in controls (control/preconditioned, 104

Dilazep dihydrochloride prolongs the infarct size-limiting effect of ischemic preconditioning in rabbits

3%/o/130

Oxygen radicals mediate ultrastructural and metabolic protection of preconditioning in vivo in pig hearts.

3% after 120 minutes of reperfusion). There was no significant difference in percent segment shortening (%SS), RMBF, and hemodynamics between the two groups throughout the experiment (%SS: control/preconditioned, 29.8