Inhibition of p53 by pifithrin-alpha reduces myocyte apoptosis and leukocyte transmigration in aged rat hearts following 24 hours of reperfusion.

Ischemic heart disease is a common age-related disease. Apoptotic cell death and inflammation are the major contributors to I/R injury. The mechanisms that trigger myocyte apoptosis and inflammation during myocardial I/R (MI/R) remain to be elucidated.

Pifithrin-alpha attenuates p53-mediated apoptosis and improves cardiac function in response to myocardial ischemia/reperfusion in aged rats.

Ischemic cardiovascular disease is a common age-related disease. The p53-dependent cardiac myocyte apoptosis induced by myocardial ischemia/reperfusion (MI/R) is an important feature in the progression of ischemic heart disease. In the present studies, we hypothesized that inhibition of p53-dependent myocyte apoptosis may improve cardiac dysfunction in aged rats after MI/R.

Attenuation of antioxidative capacity enhances reperfusion injury in aged rat myocardium after MI/R.

Mortality due to ischemic cardiovascular diseases is significantly higher in elderly than in young adults. Myocardial ischemia-reperfusion (MI/R) can induce oxidative stress and an inflammatory response. We hypothesized that increased vulnerability of aged myocardium to reperfusion injury could be caused by decreased antioxidative capacity, rather than increased oxidant production, after MI/R.

Age-related difference in myocardial function and inflammation in a rat model of myocardial ischemia-reperfusion.

Objective: Aging is associated with a reduced tolerance to myocardial ischemia reperfusion injury when compared to the young adult. However, there is very little information in the literature regarding age-related changes in myocardial function and inflammation during myocardial ischemia-reperfusion (MI/R) in vivo.

Methods: We examined age-related differences in myocyte apoptosis and the inflammatory response in a rat model of myocardial ischemia-reperfusion (MI/R).

L-NAME enhances microcirculatory congestion and cardiomyocyte apoptosis during myocardial ischemia-reperfusion in rats.

Besides necrosis, apoptosis is the other major mode of cardiomyocyte loss in ischemic cardiovascular disease. In the present study, we examined the hypothesis that nitric oxide (NO) protects myocardial function by improving myocardial microcirculation and attenuating cardiomyocyte apoptosis in a rat model of myocardial ischemia/reperfusion (MI/R). The left main coronary artery of anesthetized male rats was ligated for 40 min, followed by 4 h reperfusion.