In our study, the Z-VAD-FMK mw extent of hypoxia induced myocardial hypertrophy was in good agreement with data published by other groups. Additionally, the diameter of individual cardiomyocytes was determined. Hypoxia induced a 20% increase in diameters of cardio myocytes of the right ventricular wall while cardiomyo cytes of the left ventricular wall were unaffected by changes in the oxygen supply. Hypoxia induced hypertro phy of the right ventricle and of individual right ventricu lar cardiomyocytes was attenuated by treatment with rapamycin. In principle, hypertrophy of the right ventricu lar wall in response to hypoxia is caused Inhibitors,Modulators,Libraries by the ability to respond to increased mechanical stretch caused by pul monary vasoconstriction and vascular remodeling.

How ever, the capability of individual cardiomyocytes to sense changes in the oxygen supply and respond with hypertro phy has been suggested, too. In any case, recent data suggest that, in response to certain hypertrophic stimuli, signaling via mTOR is required for activation of protein synthesis and cardiac hypertrophy. Either Inhibitors,Modulators,Libraries mecha nisms may have resulted in attenuation of right ventricu lar hypertrophy and cardiomyocyte diameter. A direct effect of the drug on cardiomyocyte size raises the possi bility of detrimental effects on right ventricular function. However, when load induced left ventricular hypertrophy was induced in mice, rapamycin treatment resulted in a decrease in chamber size and Inhibitors,Modulators,Libraries a normal systolic function of the left ventricle. However, disruption of coordinated cardiac hypertrophy has recently also been shown to con tribute to the transition to heart failure as well.

Conclusion In vascular medicine, local application of rapamycin through drug coated stent placement is currently the favored invasive strategy to prevent restenosis. Sys temic treatment with rapamycin is, furthermore, success fully used to prevent graft rejection and transplant Inhibitors,Modulators,Libraries vasculopathy in de novo heart transplant recipients. Rapamycin may represent a novel therapeutic strategy for pulmonary arterial hypertension in humans as well to delay further progression or even result in regression of pulmonary vascular remodeling. Background Obstructive sleep apnea is a common disorder defined by upper airway obstruction, apnea and nocturnal hypoxia. There is a prevalence of OSA in patients with cor onary artery disease of up to 50%. Beyond this high prevalence, the occurrence of OSA is associated with an advanced state of atherosclerosis Inhibitors,Modulators,Libraries and a worse progno sis in these patients. In the last decade, there is www.selleckchem.com/products/Axitinib.html grow ing evidence that OSA acts as a cardiovascular risk factor, independent of associated traditional risk factors.