scholarly journals Sensitivity to Perioperative Ischemia/Reperfusion Injury in Male and Female Donor Myocardium

2017 ◽  
pp. 949-957 ◽  
Author(s):  
M. SMETANA ◽  
J. BESIK ◽  
I. NETUKA ◽  
J. MALY ◽  
J. MALUSKOVA ◽  
...  
Keyword(s):  
Cell Death ◽  
Cardiac Troponin ◽  
Caspase 3 ◽  
Troponin T ◽  
Apoptotic Cell ◽  
Ischemia Reperfusion ◽  
Cardiac Troponin T ◽  
Male And Female ◽  
Ventricular Mass ◽  
Apoptosis Markers

Many functions of the cardiovascular apparatus are affected by gender. The aim of our study was find out whether markers of cell death present in the donor myocardium differ in male and female hearts. The study involved 81 patients undergoing heart transplantation from September 2010 to January 2013. Patients were divided into two groups: male allograft (n=49), and female allograft (n=32). Two types of myocardial cell death were analyzed. High-sensitive cardiac troponin T as a necrosis marker and protein bcl-2, caspase 3 and TUNEL as apoptosis markers were measured. We observed a significantly higher level of high-sensitive cardiac troponin T after correcting for predicted ventricular mass in female donors before transplantation as well as in the female allograft group after transplantation throughout the monitored period (P=0.011). There were no differences in apoptosis markers (bcl-2, caspase 3, TUNEL) between male and female hearts before transplantation. Both genders showed a significant increase of TUNEL-positive myocytes one week after transplantation without differences between the groups. Moreover, there were no differences in caspase 3 and bcl-2 expression between the two groups. Our results demonstrated the presence of necrotic and apoptotic cell death in human heart allografts. High-sensitive cardiac troponin T adjusted for predicted ventricular mass as a marker of myocardial necrosis was higher in female donors, and this gender difference was even more pronounced after transplantation.

scholarly journals Upregulation of Restrictive N-Terminal Truncation of Cardiac Troponin T in Ischemia-Reperfusion Preserves Ventricular Function

2012 ◽  
Vol 102 (3) ◽  
pp. 561a
Author(s):  
Han-Zhong Feng ◽  
Heidi L. Lujan ◽  
Karin Przyklenk ◽  
Stephen E. DiCarlo ◽  
J.-P. Jin
Keyword(s):  
Ventricular Function ◽  
Cardiac Troponin ◽  
Troponin T ◽  
Ischemia Reperfusion ◽  
Cardiac Troponin T

scholarly journals Biomarkers of Cellular Apoptosis and Necrosis in Donor Myocardium Are Not Predictive of Primary Graft Dysfunction

2016 ◽  
pp. 251-257 ◽  
Author(s):  
O. SZARSZOI ◽  
J. BESIK ◽  
M. SMETANA ◽  
J. MALY ◽  
M. URBAN ◽  
...  
Keyword(s):  
Cell Death ◽  
Prospective Study ◽  
Reperfusion Injury ◽  
Caspase 3 ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Transplant Recipients ◽  
Primary Graft Dysfunction ◽  
Graft Dysfunction ◽  
Apoptosis Markers

Primary graft dysfunction (PGD) is a life-threatening complication among heart transplant recipients and a major cause of early mortality. Although the pathogenesis of PGD is still unclear, ischemia/reperfusion injury has been identified as a predominant factor. Both necrosis and apoptosis contribute to the loss of cardiomyocytes during ischemia/reperfusion injury, and this loss of cells can ultimately lead to PGD. The aim of our prospective study was to find out whether cell death, necrosis and apoptosis markers present in the donor myocardium can predict PGD. The prospective study involved 64 consecutive patients who underwent orthotopic heart transplantation at our institute between September 2010 and January 2013. High-sensitive cardiac troponin T (hs-cTnT) as a marker of minor myocardial necrosis was detected from arterial blood samples before the donor’s pericardium was opened. Apoptosis (caspase-3, active + pro-caspase-3, bcl-2, TUNEL) was assessed from bioptic samples taken from the right ventricle prior graft harvesting. In our study, 14 % of transplant recipients developed PGD classified according to the standardized definition proposed by the ISHLT Working Group. We did not find differences between the groups in regard to hs-cTnT serum levels. The mean hs-cTnT value for the PGD group was 57.4±22.9 ng/l, compared to 68.4±10.8 ng/l in the group without PGD. The presence and severity of apoptosis in grafted hearts did not differ between grafts without PGD and hearts that subsequently developed PGD. In conclusion, our findings did not demonstrate any association between measured myocardial cell death, necrosis or apoptosis markers in donor myocardium and PGD in allograft recipients. More detailed investigations of cell death signaling pathways in transplanted hearts are required.

scholarly journals 6-Gingerol Activates PI3K/Akt and Inhibits Apoptosis to Attenuate Myocardial Ischemia/Reperfusion Injury

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Xiangwei Lv ◽  
Tongtong Xu ◽  
Qi Wu ◽  
Yao Zhou ◽  
Guidong Huang ◽  
...  
Keyword(s):  
Cardiac Troponin ◽  
Caspase 3 ◽  
Ischemia Reperfusion Injury ◽  
Troponin T ◽  
Ischemia Reperfusion ◽  
Histopathological Changes ◽  
Myocardial Apoptosis ◽  
Creatine Kinase Mb ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion

6-Gingerol (6-G) is known to alleviate myocardial ischemia/reperfusion injury. However, the underlying molecular mechanisms of 6-G myocardial protection are not known. In this study, the protective effect of 6-G on ischemia/reperfusion (I/R) damage and whether such a mechanism was related to apoptosis inhibition and activation of phosphoinositide 3-kinases (PI3K)/serine/threonine kinase (Akt) signaling pathway were investigated. Rats were subjected to I/R in the presence or absence of 6-G and the changes of cardiac function, infarct size and histopathological changes, and the levels of cardiac troponin T, creatine kinase-MB, and myocardial apoptosis were examined. The expression of caspase-3, PI3K, p-Akt, and Akt was also determined. We found that 6-G (6 mg/kg) pretreatment significantly improved heart function and ameliorated infarct size and histopathological changes and cardiac troponin T and creatine kinase-MB levels induced by I/R. Moreover, pretreatment with 6-G significantly inhibited myocardial apoptosis and caspase-3 activation induced by I/R. 6-G also upregulated expression of PI3K, p-Akt, and Akt in myocardial tissues. Taken together, these findings suggest that 6-G inhibits apoptosis and activates PI3K/Akt signaling in response to myocardial I/R injury as a possible mechanism to attenuate I/R-induced injury in heart. These results might be important for developing novel strategies for preventing myocardial I/R injury.

Cardioprotective Effect of Saffron Extracts against Acute Doxorubicin Toxicity in Isolated Rabbit Hearts Submitted to Ischemia-Reperfusion Injury

2014 ◽  
Vol 69 (11-12) ◽  
pp. 459-470 ◽  
Author(s):  
Nathalie Chahine ◽  
Hassane Makhlouf ◽  
Laurent Duca ◽  
Laurent Martiny ◽  
Ramez Chahine
Keyword(s):  
P38 Mapk ◽  
Cardiac Troponin ◽  
Ischemia Reperfusion Injury ◽  
Troponin T ◽  
Mapk Pathway ◽  
Ischemia Reperfusion ◽  
Myocardial Damage ◽  
Crocus Sativus ◽  
Cardiac Troponin T ◽  
Protective Effects

Abstract Doxorubicin (DOX) is an anthracycline antibiotic routinely used as a chemotherapeutic agent for the treatment of solid tumours. However, DOX possesses an acute and cumulative cardiotoxicity due to free radical production. The present study was designed to investigate the possible protective effects of saffron (Crocus sativus) extracts against DOX-induced acute cardiotoxicity in isolated rabbit hearts submitted to 30 min global ischemia followed by 40 min reperfusion. DOX was delivered during reperfusion, without or with saffron given 5 min before ischemia or at reperfusion. Cardiodynamic, biochemical, and histopathological parameters were determined. In addition, to determine the expression of the AKT/mTOR/4EBP1 pathway, the levels of p38 MAPK and cardiac troponin T in heart homogenates were visualized by Western blotting. DOX administration during 40 min of reperfusion increased ischemic tissue damage, but did not act synergistically. Administration of saffron extracts during the first minutes of reperfusion significantly reduced oxidative myocardial damage, but was less effective when given before ischemia. Subsequent Western blot analysis revealed that saffron administration preserved cardiac troponin T proteins, inhibited the p38 MAPK pathway, and activated the AKT/mTOR/4EBP1 pathway in reperfusion- and DOX-treated rabbit hearts. In conclusion, saffron extracts, acting through antioxidant and antiapoptotic mechanisms, exhibited a protective effect against DOX-induced cardiotoxicity under ischemic condition.

Cardiac Troponin I and cardiac Troponin T increases in pigs during ischemia-reperfusion damage

2000 ◽  
Vol 52 (2) ◽  
pp. 157-159 ◽  
Author(s):  
T. Bertsch ◽  
C. Janke ◽  
C. Denz ◽  
M. Weiss ◽  
T. Luiz ◽  
...  
Keyword(s):  
Cardiac Troponin ◽  
Troponin I ◽  
Troponin T ◽  
Ischemia Reperfusion ◽  
Cardiac Troponin I ◽  
Cardiac Troponin T ◽  
Reperfusion Damage

Exercise Training Increases Serum Cardiac Troponin T Independent of Left Ventricular Mass

2021 ◽  
Author(s):  
Zhaowei Kong ◽  
Haifeng Zhang ◽  
Jinlei Nie ◽  
Li Wen ◽  
Qingde Shi ◽  
...  
Keyword(s):  
Exercise Training ◽  
Left Ventricular Mass ◽  
Cardiac Troponin ◽  
Troponin T ◽  
Left Ventricular ◽  
Control Group ◽  
Cardiac Troponin T ◽  
Obese Women ◽  
Ventricular Mass ◽  
2D Echocardiography

AbstractThe purpose of this study was to determine whether exercise training mediated cardiac troponin T (cTnT) and whether this was associated with increases in left ventricular mass (LVM). Fifty-four sedentary obese women were randomised to high-intensity interval training (HIIT, repeated 4–min cycling at 90% V̇O2max interspersed with 3–min rest), work-equivalent continuous aerobic training (CAT, continuous cycling at 60% V̇O2max) or a control group (CON). Resting serum cTnT was assessed using a high-sensitivity assay before and after 12 weeks of training. LVM was determined from 2D echocardiography at the same timepoints. Both HIIT and CAT induced a similar elevation (median 3.07 to 3.76 ng.l−1, p<0.05) in resting cTnT compared with pre-training and the CON (3.49 to 3.45 ng.l−1, p>0.05). LVM index in HIIT increased (62.2±7.8 to 73.1±14.1 g.m−2, p<0.05), but not in CAT (66.1±9.7 to 67.6±9.6 g.m−2, p>0.05) and CON (67.9±9.5 to 70.2±9.1 g.m−2, p>0.05). Training-induced changes in resting cTnT did not correlate with changes in LVM index (r=−0.025, p=0.857). These findings suggest that twelve weeks of either HIIT or CAT increased resting cTnT, but the effects were independent of any changes in LVM in sedentary obese women.

Sign in / Sign up

Export Citation Format

Share Document