title: [Effects of ischemic preconditioning on the hypothermic ischemia/reperfusion injury of immature rabbit hearts].
abstract: OBJECTIVE
  To study effects of ischemic preconditioning on the hypothermic ischemia/reperfusion injury of immature rabbit hearts.
  
  
  METHODS
  The isolated immature rabbit (3-4 weeks) hearts were perfused on Langendorff apparatus. After 30 min perfusing with 37 degrees C K-H perfusate, the hearts in part one were yielded 0, 1, 2 or 3 times of IP respectively before 120 min ischemia at 20 degrees C hypothermia, and the hearts in part two were yielded 0 or 2 times of IP before being arrested by infusion of St. Thomas II crystalloid cardioplegic solution, then the arrested hearts were yielded ischemia for 30, 90 or 120 min at 32 degrees C, 25 degrees C and 2 degrees C hypothermia respectively. Then all the hearts were reperfused for 30 min at 37 degrees C normothermia. Heart rate (HR), left ventricular developed pressure (LVDP), +/- dp/dt(max) were recorded at baseline, preischemic and 1, 3, 5, 10, 20, 30 min after reperfusion. Also contents of ATP and MDA and activity of SOD and Ca(2+) -ATPase of myocardium were measured.
  
  
  RESULTS
  At the end of reperfusion, the recovery rate of left ventricular function in IP2 group were significantly higher than that of control group and IP3 group (P < 0.01, P < 0.05), also the IP2 group showed a higher content of ATP and activity of Ca(2+) -ATPase than control group and IP3 group (P < 0.01, P < 0.05). When the ischemic hearts were at different hypothermia accompanied with CCS, the recovery rate of left ventricular function and contents of ATP in SIP1 and SIP2 group were significantly higher than that of SCon 1 group and SCon 2 group respectively (P < 0.01, P < 0.05), the contents of MDA in the two IP groups were lower than that of the two control groups.
  
  
  CONCLUSIONS
  IP can attenuate the hypothermic ischemia/reperfusion injury of immature rabbit hearts, the cardioprotective effects are dependent on the mode of IP and the possible mechanisms may involve the following aspects: decrease the consumption of ATP, inhibit lipid peroxidation and maintain the activity of Ca(2+) -ATPase of cardiac myocyte.
authors.affiliation: Jiangsu Province Key Laboratory of Anesthesiology, Xuzhou Medical College, Xuzhou 221002, China.
authors.forename: Shan-Shan
authors.initials: SS
authors.lastname: Zhu
authors.forename: Yin-Ming
authors.initials: YM
authors.lastname: Zeng
authors.forename: Zhong-Ming
authors.initials: ZM
authors.lastname: Zhang
authors.forename: Yu-Cai
authors.initials: YC
authors.lastname: Zhang
authors.forename: Peng-Cheng
authors.initials: PC
authors.lastname: Xu
authors.forename: Xiao-Zhou
authors.initials: XZ
authors.lastname: Wang
authors.forename: Jian-Wei
authors.initials: JW
authors.lastname: Fan
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D000252:Calcium-Transporting ATPases / Q000378:metabolism; D007036:Hypothermia, Induced; D066298:In Vitro Techniques; D019194:Ischemic Preconditioning; D015227:Lipid Peroxidation; D015428:Myocardial Reperfusion Injury / Q000517:prevention & control; D011817:Rabbits
chemical_list: D000255:Adenosine Triphosphate; D000252:Calcium-Transporting ATPases