Myocardial mitochondrial injury induced by pulmonary exposure to particulate matter in rats.

Exposure to air pollution has been associated with acute myocardial ischemia, impaired myocardrial function, and ST-segment depression. Particulate matter (PM)-associated metals, especially vanadium and nickel, have been implicated in observed cardiovascular impairments. We aimed to assess the effect of single intratracheal pulmonary exposure to vanadium-rich respirable oil combustion PM (HP-10) on the intrinsic myocardial ischemic tolerance and mitochondrial integrity in rats.

Successful restoration of function of frozen and thawed isolated rat hearts.

Objective: Long-term organ preservation for transplantation may allow optimal donor-recipient matching with potential reduction in the incidence and severity of rejection. Complete cessation of metabolism may be obtained by freezing. Previous attempts to freeze intact mammalian hearts were limited to -3.

Occult cardiotoxicity: subtoxic dosage of Bis(2-chloroethoxy)methane impairs cardiac response to simulated ischemic injury.

The effect of Bis(2-chloroethoxy)methane (CEM) on myocardial response to ischemia was tested in rats. CEM was dermally applied for 3 days to F344/N male rats, at 0, 100, 400, or 600 mg/kg/d. Subsequently, left ventricular sections were prepared from each rat heart.

Dexrazoxane prevents myocardial ischemia/reperfusion-induced oxidative stress in the rat heart.

Introduction: Dexrazoxane (Dex), used clinically to protect against anthracycline-induced cardiotoxicity, possesses iron-chelating properties. The present study was designed to examine whether Dex could inhibit the ischemia/reperfusion (I/R) induced damage to the rat heart.

Materials And Methods: Isolated perfused rat hearts were exposed to global ischemia (37 degrees C) and 60 min reperfusion.

Apomorphine-induced myocardial protection is due to antioxidant and not adrenergic/dopaminergic effects.

Apomorphine (Apo), a dopaminergic agonist used for treatment of Parkinson disease, is a potent antioxidant. In addition to its antioxidative effects, the dopaminergic and adrenergic effects of Apo were studied. Isolated perfused rat hearts were exposed to 25 min of no-flow global ischemia (37 degrees C) and 60 min of reperfusion (I/R, control).

Impaired mitochondrial response to simulated ischemic injury as a predictor of the development of atrial fibrillation after cardiac surgery: in vitro study in human myocardium.

Objective: Atrial fibrillation occurs in 20% to 40% of patients after cardiac surgery, but its pathophysiology remains unclear. Recent studies demonstrated preexisting histologic markers that portend the development of postoperative atrial fibrillation. In this prospective study, we focused on mitochondrial dysfunction in response to ischemic stress as a potential predictor for postoperative atrial fibrillation.

Apomorphine prevents myocardial ischemia/reperfusion-induced oxidative stress in the rat heart.

This study examined the hypothesis that low-concentration apomorphine improves postischemic hemodynamic and mitochondrial function in the isolated rat heart model by attenuating oxidation of myocardial proteins. Control and apomorphine-treated hearts were subjected to 35 min of perfusion, 25 min of normothermic global ischemia, and 60 min of reperfusion. Apomorphine (2 microM) was introduced into the perfusate for 20 min starting from the onset of reperfusion.

Protection of myocardium by cyclosporin A and insulin: in vitro simulated ischemia study in human myocardium.

Background: The efficacy of myocardial protection by cyclosporin A (CSA) and insulin was tested in human right atrial myocardial slices subjected to simulated ischemia and reoxygenation.

Methods: Slices of right atrial trabeculae were obtained from patients undergoing elective cardiac surgery. Trabeculae were incubated with oxygenated glucose containing phosphate buffered saline (O(2), G-PBS).