Study on Cardiac Responses to Ischemia - Reperfusion Injury in Experimentally Induced Uremic Cardiomyopathy

2013 ◽  
Vol 64 (10-12) ◽  
pp. 939-958
Author(s):  
Faten M. A. Diab ◽  
Magda H. Youssef ◽  
Mona A. Ahmed ◽  
Ramadan A. Saad ◽  
Noha N. Lasheen ◽  
...  
2012 ◽  
Vol 303 (9) ◽  
pp. F1275-F1286 ◽  
Author(s):  
David J. Semple ◽  
Sunil Bhandari ◽  
Anne-Marie L. Seymour

Chronic kidney disease is associated with a unique cardiomyopathy, characterized by a combination of structural and cellular remodeling, and an enhanced susceptibility to ischemia-reperfusion injury. This may represent dysfunction of the reperfusion injury salvage kinase pathway due to insulin resistance. The susceptibility of the uremic heart to ischemia-reperfusion injury and the cardioprotective effects of insulin and rosiglitazone were investigated. Uremia was induced in Sprague-Dawley rats by subtotal nephrectomy. Functional recovery from ischemia was investigated in vitro in control and uremic hearts ± insulin ± rosiglitazone. The response of myocardial oxidative metabolism to insulin was determined by13C-NMR spectroscopy. Activation of reperfusion injury salvage kinase pathway intermediates (Akt and GSK3β) were assessed by SDS-PAGE and immunoprecipitation. Insulin improved postischemic rate pressure product in control but not uremic hearts, [recovered rate pressure product (%), control 59.6 ± 10.7 vs. 88.9 ± 8.5, P < 0.05; uremic 19.3 ± 4.6 vs. 28.5 ± 10.4, P = ns]. Rosiglitazone resensitized uremic hearts to insulin-mediated cardioprotection [recovered rate pressure product (%) 12.7 ± 7.0 vs. 61.8 ± 15.9, P < 0.05]. Myocardial carbohydrate metabolism remained responsive to insulin in uremic hearts. Uremia was associated with increased phosphorylation of Akt (1.00 ± 0.08 vs. 1.31 ± 0.11, P < 0.05) in normoxia, but no change in postischemic phosphorylation of Akt or GSK3β. Akt2 isoform expression was decreased postischemia in uremic hearts ( P < 0.05). Uremia is associated with enhanced susceptibility to ischemia-reperfusion injury and a loss of insulin-mediated cardioprotection, which can be restored by administration of rosiglitazone. Altered Akt2 expression in uremic hearts post-ischemia-reperfusion and impaired activation of the reperfusion injury salvage kinase pathway may underlie these findings.


2015 ◽  
Vol 66 (4-6) ◽  
pp. 289-302
Author(s):  
جيهان إبراهيم السلاموني ◽  
فاتن محمود دياب ◽  
إيناس عبد العزيز عبد الهادي ◽  
غيدة محمد حسن

Surgery Today ◽  
1995 ◽  
Vol 25 (4) ◽  
pp. 343-350 ◽  
Author(s):  
Kenji Karashima ◽  
Yuzo Uchida ◽  
Kazuhide Tohara ◽  
Kenji Kashima ◽  
Shigeo Yokoyama ◽  
...  

2019 ◽  
Vol 124 ◽  
pp. e208-e213 ◽  
Author(s):  
Yasar Karatas ◽  
Mehmet Fatih Erdi ◽  
Bülent Kaya ◽  
Fatih Keskin ◽  
Gökhan Cüce ◽  
...  

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