Interleukin-2 pretreatment improves the contractility of isolated rat ventricular myocytes during hypoxia and reoxygenation
- VernacularTitle:白细胞介素-2预处理对缺氧/复氧心肌细胞收缩功能的影响
- Author:
Huiping WANG
;
Qiang XIA
;
Linlin WANG
;
Chunmei CAO
;
Guohua LIN
;
Zhangqiang CHEN
- Publication Type:Journal Article
- Keywords:
Interleukin-2;
Myocardium;
Receptors, opioid, kappa;
Protein kinase C;
Potassium channels
- From:
Chinese Journal of Pathophysiology
1986;0(03):-
- CountryChina
- Language:Chinese
-
Abstract:
AIM: To investigate the effect and possible mechanisms of interleukin-2 (IL-2) on the cell contractility in cardiomyocytes during hypoxia and reoxygenation.METHODS: Glucose-free Krebs-Henseleit (K-H) solution, gassed with 95% N 2 and 5% CO 2 for hypoxia, were used. The cell contractility were determined after 20 min of hypoxia and 30 min of reoxygenation by the video tracking system. The parameters of cell contractility included peak velocity of cell shortening (+d L /d t max), peak velocity of cell relengthening (-d L /d t max), contraction amplitude (dL) and end-diastolic cell length.RESULTS: It was shown that during hypoxia, the cell contraction was depressed. All the parameters were unable to return to the pre-hypoxia level during reoxygenation. Pretreatment with IL-2 at 2?10 3 U/L attenuated the inhibitory effect of hypoxia/reoxygenation on contractility in single ventricular myocytes. The effect of IL-2 was reduced in the presence of 10 -8 mol/L nor-binaltorphimine (nor-BNI), a selective ?-opioid receptor antagonist. On blockade of protein kinase C with 3?10 -6 mol/L chelerythrine, the effect of IL-2 was significantly attenuated. The effect of IL-2 was also blocked by 10 -4 mol/L 5-hydroxydecanoate (5-HD), a mitochondrial ATP-sensitive potassium (K ATP ) channel blocker. CONCLUSIONS: The results of the present study provide evidence that pretreatment with IL-2 at 2?10 3 U/L attenuates the effect of hypoxia/reoxygenation on cell contraction in the isolated ventricular myocytes. The ?-opioid receptor mediates the effect of IL-2, in which activation of PKC and opening of mitochondrial ATP-sensitive potassium (mito K ATP ) channel are involved.
