European journal of cardio-thoracic surgery : official journal of the European Association for Cardio-thoracic Surgery
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Eur J Cardiothorac Surg · Aug 2008
Comparative StudyCa2+ sensitizer superior to catecholamine during myocardial stunning?
After open-chest cardiac surgery, ventricular function remains depressed (myocardial stunning). Catecholamines (epinephrine) improve ventricular function by increasing the intracellular Ca(2+) concentration. In parallel, the oxygen consumption is increased, so that the hitherto intact myocardium can be jeopardized. In the very insufficient ventricle, epinephrine can even become ineffective. Since Ca(2+) sensitizers provide another therapeutic avenue, the effects of epinephrine and levosimendan on postischemic hemodynamics were investigated. ⋯ In contrast to epinephrine, levosimendan improves ventricular function without increasing oxygen demand, thereby considerably improving external efficiency. Even during epinephrine resistance in extremely dysfunctional hearts, levosimendan successfully improves ventricular function.
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Eur J Cardiothorac Surg · Aug 2008
Clinical TrialThe effect of off-pump coronary artery bypass grafting on platelet activation in patients on aspirin therapy until surgery day.
Antiplatelet therapy is a class I indication in perioperative care after coronary artery bypass grafting to prevent graft occlusion. We sought to determine whether continuation of aspirin until surgery day suppresses platelet activity in the early period after off-pump coronary artery bypass grafting (OPCAB). ⋯ Aspirin therapy continued until surgery day does not protect against acute platelet activation in patients after OPCAB.
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Eur J Cardiothorac Surg · Aug 2008
Effects of hydrogen sulphide on ischaemia-reperfusion injury and ischaemic preconditioning in the isolated, perfused rat heart.
Hydrogen sulphide (H(2)S) protects the heart against ischaemia-reperfusion injury caused by low flow or local ischaemia. We hypothesised that: (1) H(2)S protects against global ischaemia-reperfusion injury of the heart, (2) H(2)S plays a mechanistic role in ischaemic preconditioning, and (3) H(2)S acts by phosphorylation of protein kinases. ⋯ Endogenous H(2)S production protects against global ischaemia, and H(2)S may be a part of the endogenous cell defence. However, endogenous H(2)S did not appear to be important in ischaemic preconditioning, and protein kinases were not important for the effect of H(2)S. Exogenous H(2)S may provide myocardial protection, possibly acting by expression of heat shock protein 72.