Cardioprotection of adenosine treatment in cadaver donor rats with warm ischemia.
10.3969/j.issn.1672-7347.2010.08.019
- Author:
Dongkai WU
1
;
Shengxi CHEN
;
Wanjun LUO
;
Haihe JIANG
Author Information
1. Department of Cardiothoracic Surgery, Xiangya Hospital, Central South University, Changsha 410008, China.
- Publication Type:Journal Article
- MeSH:
Adenosine;
pharmacology;
Animals;
Cardiotonic Agents;
pharmacology;
Heart;
drug effects;
Heart Transplantation;
Male;
Myocardial Reperfusion Injury;
prevention & control;
Organ Preservation;
methods;
Random Allocation;
Rats;
Rats, Sprague-Dawley;
Warm Ischemia;
methods
- From:
Journal of Central South University(Medical Sciences)
2010;35(8):885-891
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To determine the cardioprotection of adenosine treatment in cadaver donor rats with warm ischemia.
METHODS:Rats were randomly divided into 7 groups. Group C was a control group. Group I(5), I(15), and I(30): The donor hearts from the cadaver rats that died of acute hemorrhagic shock and within warm ischemic durations of 5, 15, and 30 min, respectively, and the donor hearts were perfused with STH-1 for 30 min before cervical heterotopic heart transplantation. Group A(5), A(15), and A(30) were adenosine treatment groups and the donor hearts were obtained as mentioned above and perfused with STH-1 plus adenosine (adenosine concentration 1.2 mmol/L) before cervical heterotopic heart transplantation. We detected the change of the grafts including ultrastructure, the level of ATP, SOD, and MDA, NF-kappaB mRNA, TNF-alpha, and IL-6 24 h after the transplantation.
RESULTS:At the same time point, compared with Group I(5), I(15), and I(30), Group A(5), A(15), and A(30) showed increased ATP and SOD in the myocardial tissues, and decreased MDA, NF-kappaB mRNA, TNF-alpha, and IL-6 (P<0.05).
CONCLUSION:Adenosine treatment can protect the graft in cadaver donor rats with warm ischemia. The mechanism may improve the myocardial energy metabolism, attenuate lipid peroxidation injury, suppress the expression of NF-kappaB mRNA, and decrease the inflammatory damage of TNF-alpha and IL-6.
