Aging might increase myocardial ischemia / reperfusion-induced apoptosis in humans and rats

Liu, Miaobing; Zhang, Ping; Chen, Mulei; Wu-ning, Zhang; Yu, Liping; Yang, Xinchun; Fan, Qingyu

doi:10.1007/s11357-011-9259-8

Cited by 65 publications

(60 citation statements)

References 28 publications

(24 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Aging has been found to reduce the angiogenic response to ischemic injury in animal models 24 and result in greater ischemia reperfusion injury and apoptosis. 25,26 A loss of cardioprotection and a decreased response to ischemic precondition have also been noted with aging, 27,28 although this has not been consistent across all studies. 29 In addition, relative to older adult donors, younger adult donors have been associated with some studies with a decreased incidence of cardiac allograft vasculopathy and improved long-term survival.…”

Section: Discussionmentioning

confidence: 99%

Pediatric Heart Transplantation From Donors With Depressed Ventricular Function

Rossano

Lin

Paridon

et al. 2013

Circ: Heart Failure

View full text Add to dashboard Cite

Background— Wait-list mortality for children awaiting heart transplantation remains high. Potential donor hearts with depressed ventricular function are often declined. We aimed to test the hypothesis that pediatric heart transplant recipients of grafts with depressed ventricular function would have comparable survival with those with normal function. Methods and Results— A retrospective study was performed for pediatric heart transplants from the United Network of Organ Sharing Database from October 26, 1999, to June 30, 2011. Patients were grouped based on accepted donor left ventricular ejection fraction (LVEF): normal function (LVEF ≥55%), mildly depressed function (LVEF 45%–54%), or moderately-to-severely depressed function (LVEF <45%). During the study period, there were 3672 pediatric heart transplants; 3306 (90%) had a LVEF reported. Ventricular function was mildly depressed in 245 (7%) and moderately-to-severely depressed in 172 (5%). Patients receiving grafts with moderately-to-severely depressed function were more likely to be younger and weigh less ( P <0.001 for both) than those receiving grafts with normal function. Median graft survival from accepted donors with normal ventricular function (10.6 years) was similar to survival from accepted donors with mildly depressed ventricular function (9.7 years; P =0.24) and from accepted donors with moderately-to-severely depressed ventricular function (9.1 years; P =0.13). On propensity-matched analysis, donor ventricular function was not associated with graft survival. Conclusions— The use of donors with depressed ventricular function is uncommon in pediatric heart transplantation (<15% of all transplants), yet graft survival does not differ significantly from accepted donors with normal ventricular function. Hearts from donors with depressed ventricular function may be considered in selected patients.

show abstract

Section: Discussionmentioning

confidence: 99%

Pediatric Heart Transplantation From Donors With Depressed Ventricular Function

Rossano

Lin

Paridon

et al. 2013

Circ: Heart Failure

View full text Add to dashboard Cite

show abstract

“…It has also been reported that older guinea pig, rat, and mouse hearts are less sensitive to cardioprotective strategies such as ischemic or anesthetic preconditioning compared with younger hearts (5,7,31,33,34). Other reports indicate that aging exacerbates apoptosis (25) and cardiac damage after ischemia (18); however, not all studies have observed increased infarct size in aged rats (32,34).…”

mentioning

confidence: 99%

Reduced mitochondrial Ca²⁺ loading and improved functional recovery after ischemia-reperfusion injury in old vs. young guinea pig hearts

Rhodes

Camara

Heisner³

et al. 2012

American Journal of Physiology-Heart and Circulatory Physiology

View full text Add to dashboard Cite

Oxidative damage and impaired cytosolic Ca(2+) concentration ([Ca(2+)](cyto)) handling are associated with mitochondrial [Ca(2+)] ([Ca(2+)](mito)) overload and depressed functional recovery after cardiac ischemia-reperfusion (I/R) injury. We hypothesized that hearts from old guinea pigs would demonstrate impaired [Ca(2+)](mito) handling, poor functional recovery, and a more oxidized state after I/R injury compared with hearts from young guinea pigs. Hearts from young (∼4 wk) and old (>52 wk) guinea pigs were isolated and perfused with Krebs-Ringer solution (2.1 mM Ca(2+) concentration at 37°C). Left ventricular pressure (LVP, mmHg) was measured with a balloon, and NADH, [Ca(2+)](mito) (nM), and [Ca(2+)](cyto) (nM) were measured by fluorescence with a fiber optic probe placed against the left ventricular free wall. After baseline (BL) measurements, hearts were subjected to 30 min global ischemia and 120 min reperfusion (REP). In old vs. young hearts we found: 1) percent infarct size was lower (27 ± 9 vs. 57 ± 2); 2) developed LVP (systolic-diastolic) was higher at 10 min (57 ± 11 vs. 29 ± 2) and 60 min (55 ± 10 vs. 32 ± 2) REP; 3) diastolic LVP was lower at 10 and 60 min REP (6 ± 3 vs. 29 ± 4 and 3 ± 3 vs. 21 ± 4 mmHg); 4) mean [Ca(2+)](cyto) was higher during ischemia (837 ± 39 vs. 541 ± 39), but [Ca(2+)](mito) was lower (545 ± 62 vs. 975 ± 38); 5) [Ca(2+)](mito) was lower at 10 and 60 min REP (129 ± 2 vs. 293 ± 23 and 122 ± 2 vs. 234 ± 15); 6) reduced inotropic responses to dopamine and digoxin; and 7) NADH was elevated during ischemia in both groups and lower than BL during REP. Contrary to our stated hypotheses, old hearts showed reduced [Ca(2+)](mito), decreased infarction, and improved basal mechanical function after I/R injury compared with young hearts; no differences were noted in redox state due to age. In this model, aging-associated protection may be linked to limited [Ca(2+)](mito) loading after I/R injury despite higher [Ca(2+)](cyto) load during ischemia in old vs. young hearts.

show abstract

“…13,26 In mice, regression occurs even after only two weeks of detraining train which indicates that cardiac mass in mice returned to basal state after about 21 days of detraining. 27 According to Liu et al 28 age may contribute to the loss of more than 30% of cardiac myocytes without heart disease, and can lead to myocardial dysfunction or heart failure. 29 In addition, These authors also reported that the expression of protein Bcl-2 and Bax increased in the heart of old Fischer-344 rats under physiological conditions.…”

Section: 18mentioning

confidence: 99%

Effects of anaerobic exercise and detraining on the caspase-3 expression of rat ventricular cardiomyocyte

et al. 2015

View full text Add to dashboard Cite

Background: Anaerobic physical exercise is a high intensity physical exercise performed in a short time. This exercise can stimulate apoptosis in left ventricular cardiomyocytes. The aim of this study is to analyze the apoptosis of cardiomyocytes after anaerobic exercise and detraining.Methods: Thirty two wistar rats Ratus Novergicus 250-350 grams (8-10 weeks old) were divided into the following groups (n = 4) and given naerobic physical exercise four and 12 weeks (group Exc-4, Exc-12) and anaerobic exercise followed by four weeks of detraining (Exc-4-D, Exc-12-D). The control groups were only observed in the same period (group CTL-4, CTL-12, CTL-4-D, CTL-12-D). At the end of observation, the rats were sacrificed and examination of the expression of caspase-3 as an indicator of apoptosis was done using immunohistochemical staining. Data were analyzed with ANOVA test.Results: An increase in expression of caspase-3 in the group Exc-4 (72.03%) compared to the CTL-4 (27.22%), (p < 0,001); and Exc-12 (79.30%) compared to the CTL-12 (30.53%) (p = 0.027). Detraining process showed a significant decline Capase-3 expression (31.12% in exc-4-D and 30.44% in the exc-12-D).Conclusion: Anaerobic physical exercise can increase apoptosis in rat left ventricle cardiomyocyte characterized by increased expression of caspase-3. Detraining can improve heart condition characterized by decreased expression of caspase-3.

show abstract

Aging might increase myocardial ischemia / reperfusion-induced apoptosis in humans and rats

Cited by 65 publications

References 28 publications

Pediatric Heart Transplantation From Donors With Depressed Ventricular Function

Pediatric Heart Transplantation From Donors With Depressed Ventricular Function

Reduced mitochondrial Ca²⁺ loading and improved functional recovery after ischemia-reperfusion injury in old vs. young guinea pig hearts

Effects of anaerobic exercise and detraining on the caspase-3 expression of rat ventricular cardiomyocyte

Contact Info

Product

Resources

About

Aging might increase myocardial ischemia / reperfusion-induced apoptosis in humans and rats

Cited by 65 publications

References 28 publications

Pediatric Heart Transplantation From Donors With Depressed Ventricular Function

Pediatric Heart Transplantation From Donors With Depressed Ventricular Function

Reduced mitochondrial Ca2+ loading and improved functional recovery after ischemia-reperfusion injury in old vs. young guinea pig hearts

Effects of anaerobic exercise and detraining on the caspase-3 expression of rat ventricular cardiomyocyte

Contact Info

Product

Resources

About

Reduced mitochondrial Ca²⁺ loading and improved functional recovery after ischemia-reperfusion injury in old vs. young guinea pig hearts