[Role of interleukin-2 in the functional myocardial impairment induced by anoxia and reoxygenation].
To investigate the effect of interleukin-2 (IL-2) on myocardial impairment during ischemia/reperfusion or anoxia/reoxygenation.



Chemical anoxia was introduced in the isolated rat ventricular myocytes by Krebs-Henseleit (K-H) solution containing 10(-3) mol/L sodium dithionite. The video-tracking system and spectrofluorometric method were employed to verify the cell contraction and calcium homeostasis of the single myocyte. Radioimmunoassay was used to analyze the IL-2 levels in myocardium.



The levels of IL-2 in myocardium subjected to ischemia/reperfusion were elevated [(14.34+/-5.99 compared with 22.25+/-3.68)ng/g, P<0.01]. During anoxia, cell contraction and the amplitude of electrically induced calcium transient were depressed and the parameters did not return to the pre-anoxia level during reoxygenation. IL-2 at 200 U/L administered during anoxia aggravated the effect of reoxygenation on cell contraction and calcium transient. After perfusion with IL-2, the malondialdehyde content of myocardial mitochondria was elevated.



Coexistence of IL-2 during anoxia aggravates the effect of reoxygenation on the cell contraction and calcium homeostasis in the isolated rat ventricular myocytes, in which the mitochondrial lipid peroxidation induced by IL-2 is involved.
Cao
Chun-mei
CM
Department of Physiology, College of Medical Sciences, Zhejiang University, Hangzhou 310031, China.
Yao
Hui
H
Xu
Wan-hong
WH
Ye
Zhi-guo
ZG
Chen
Jun-zhu
JZ
Xia
Qiang
Q
D000818:Animals; D002118:Calcium / Q000378:metabolism; D007376:Interleukin-2 / Q000502:physiology*; D015227:Lipid Peroxidation; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D008929:Mitochondria, Heart / Q000378:metabolism; D017202:Myocardial Ischemia / Q000503:physiopathology*; D015428:Myocardial Reperfusion Injury / Q000503:physiopathology*; D051381:Rats; D017207:Rats, Sprague-Dawley
D007376:Interleukin-2; D008315:Malondialdehyde; D002118:Calcium