Senescent rat hearts exhibited greater contractile impairment during reperfusion following ischemia compared to adult hearts (p<0.05), without further deterioration of metabolic efficiency.
Does aging worsen functional impairment and oxygen consumption during reperfusion following myocardial ischemia in rat hearts?
Aging exacerbates postischemic contractile dysfunction in rat hearts without further deteriorating the already impaired aerobic metabolic efficiency seen in adult hearts.
p-value: p=<0.05
It has been suggested that aging may enhance the deleterious effects of myocardial ischemia-reperfusion. This study evaluates the relationship between oxygen consumption and functional impairment during reperfusion following myocardial ischemia in adult and senescent rat hearts. Global ischemia induced a marked impairment of contractile function which was significantly higher in senescent than in adult hearts. During reperfusion postischemic dysfunction was more evident in senescent hearts: at the 10th minute, the developed pressure recovered less (p < 0.05) and end-diastolic pressure increased more (p < 0.05) in senescent than in adult hearts. However, oxygen consumption per unit of work was significantly higher throughout 60 min of reperfusion when compared to controls with no significant difference between adult and senescent hearts. This study demonstrates that following ischemia and reperfusion depression of function and inappropriately high oxygen consumption were observed in both adult and senescent hearts. However, aging was associated with greater contractile impairment, which occurred in the absence of further deterioration of metabolic efficiency of contraction.
Abete et al. (Tue,) conducted a other in Myocardial ischemia-reperfusion. Aging (senescent vs adult) vs. Adult rat hearts was evaluated on Contractile function and oxygen consumption per unit of work (p=<0.05). Senescent rat hearts exhibited greater contractile impairment during reperfusion following ischemia compared to adult hearts (p<0.05), without further deterioration of metabolic efficiency.
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