Remifentanil but not sufentanil induces cardioprotection in human ischemic heart muscle in vitro.

Background: Previous studies on animal models have suggested that δ-opioid receptor (OR) signaling is the primary pathway responsible for opioids' cardioprotective effect. We hypothesize that the μ-OR's activation protects the human heart muscle.

Methods: We performed the experiments on muscular trabeculae obtained from the right atrial appendages of 104 consecutive patients subjected to coronary artery bypass surgery.

Opioidergic conditioning of the human heart muscle in nitric oxide-dependent mechanism.

Background: Opioidergic conditioning is well documented to trigger cardioprotection against ischemia/ reperfusion (I/R) injury. Previous studies on animal models have suggested that nitric oxide (NO) mediates the beneficial effect of opioids, but the role of NO in humans seems to be controversial.

Objectives: The aim of the study was to assess the influence of NO modulators on opioid-induced cardioprotection in the human myocardium.

Ischemic conditioning of human heart muscle depends on opioid-receptor system.

Background: Despite progress in the invasive treatment of ischemic heart disease, the ability to limit ischemia-reperfusion (I/R) injury remains largely unrealized. Ischemic pre-conditioning (IPC) and post-conditioning (POC) induce the protective mechanisms of resistance against I/R injury. Stimulation of opioid receptors mimic the protective effect of IPC or POC in an animal models.

Effects of endogenous cardioprotective mechanisms on ischemia-reperfusion injury.

Ischemic heart disease have been remarked as a leading cause of morbidity and mortality in adults. Early restoration of cardiac perfusion is necessary to restore perfusion of ischemic heart muscle. Effective revascularization reduce mortality by limiting myocardial necrosis at the acute phase of the cardiac infarction.

'Opioidergic postconditioning' of heart muscle during ischemia/reperfusion injury.

Background: Ischemic preconditioning and postconditioning are the novel strategies of attaining cardioprotection against ischemia/reperfusion (I/R) injury. Previous studies suggested the role of opioid pathway, however the class of opioid receptors responsible for this effect in humans remains unknown. The aim of the study was to assess the influence of opioids on simulated I/R injury outcomes in the hu-man myocardium.

The co-application of hypoxic preconditioning and postconditioning abolishes their own protective effect on systolic function in human myocardium.

Background: Ischemic preconditioning (IPC) and postconditioning (POC) are well documented to trigger cardioprotection against ischemia/reperfusion (I/R) injury, but the effect oftheir both co-application remains unclear in human heart. The present study sought to assessthe co-application of IPC and POC on fragments of human myocardium in vitro.

Methods: Muscular trabeculae of the human right atrial were electrically driven in the organbath and subjected to simulated I/R injury - hypoxia/re-oxygenation injury in vitro.

Effects of pantoprazole on dual antiplatelet therapy in stable angina pectoris patients after percutaneous coronary intervention.

Background: Our aim was to prospectively assess the potential influence of pantoprazole therapy on the antiplatelet effects of acetylsalicylic acid (ASA) and clopidogrel (CLO) in stable angina pectoris (SAP) patients after percutaneous coronary intervention (PCI).

Methods: Forty-four patients with SAP (CCS I-III) and successful PCI with stent implantation were enrolled into the study. The patients were divided into group proton pump inhibitors (PPI): 23 patients with indications for PPI (F/M = 9/14; age = 64 ± 9; standard therapy + 20 mg pantoprazole) and the control group (group C): 21 patients (F/M = 6/15; age = 64 ± 8; standard therapy).