Effects of HES 130/0 .4 on no-reflow after myocardial ischemia-reperfu-sion injury in rats
10.3969/j.issn.1000-4718.2016.03.005
- VernacularTitle:羟乙基淀粉对大鼠心肌缺血再灌注后无复流的影响
- Author:
Chongan HUANG
;
Lina HE
;
Jiali SUN
;
Anna YING
;
Yongting YE
;
Qi CAI
;
Linbo YUAN
;
Chunyan HUA
- Publication Type:Journal Article
- Keywords:
Hydroxyethylstarch;
Myocardial reperfusion injury;
No-reflow phenomenon;
Myeloperoxidase;
Calcium ions
- From:
Chinese Journal of Pathophysiology
2016;32(3):411-417
- CountryChina
- Language:Chinese
-
Abstract:
AIM:To observe the effects and mechanisms of hydroxyethylstarch (HES) 130/0.4 on no-reflow phenomenon after myocardial ischemia-reperfusion in rats.METHODS: SD rats were randomly divided into 4 groups:sham operation group , ischemia-reperfusion ( IR, treated with normal saline ) group, normal saline ischemia-reperfusion (NS-IR, treated with NS) group and HES ischemia-reperfusion (HES-IR, treated with HES) group.Myocardial infarct size and no-reflow range were determined by staining methods , and the activities of myocardial enzymes ( CK-MB, cTnI and MPO) were measured .Meanwhile , cardiac microvascular endothelial cells of the rat were cultured and divided into 4 groups:control group, hypoxia/reoxygenation (H/R) group, NS-H/R group and HES-H/R group.Acute ischemia reper-fusion models were simulated , and the concentration of calcium ions was measured .The relative cell activity was evaluated by CCK-8 assay, and the apoptotic rate was detected by flow cytometry .RESULTS:In HES-IR group, the myocardial in-farct size, the no-reflow zone, CK-MB, cTnI and MPO activity were all significantly lower than those in IR group ( P<0.05).In microvascular endothelial cells , the concentration of calcium ions and the apoptotic rate in HES-H/R group were significantly decreased, while the relative cell activity increased compared with H/R group (P<0.05).CONCLUSION:HES reduces no-reflow in acute myocardial ischemia-reperfusion .The mechanism may be involved in the inhibition of both the infiltration of neutrophils and the calcium overload of endothelial cells .
