Abstract
ObjectiveTo ascertain if levosimendan postconditioning can alleviate lung ischemia–reperfusion injury (LIRI) in rats.MethodOne hundred rats were divided into five groups: Sham (sham), ischemia–reperfusion group (I/R group), ischemic postconditioning (IPO group), levosimendan postconditioning (Levo group) and combination postconditioning group of levosimendan and 5-Hydroxydecanoic acid (Levo+5-HD group). The apoptotic index (AI) of lung tissue cells was determined using the terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. Expression of active cysteine aspartate specific protease-3 ( active caspase-3), Bcl-2 and Bax in lung tissue was determined by immunohistochemical staining. The morphopathology of lung tissue was observed using light and electron microscopy.ResultsAI values and expression of active caspase-3, Bcl-2 and Bax of lung tissue in I/R and Levo+5-HD groups were significantly higher than those in the sham group ( P<0.05). AI values and expression of active caspase-3 and Bax were significantly lower, whereas that of Bcl-2 was higher significantly in the Levo group, compared with I/R and Levo+5-HD groups (P<0.05). Significant differences were not observed in comparisons between I/R and Levo+5-HD groups as well as IPO and Levo groups.ConclusionLIRI can be alleviated by levosimendan, which simulates an IPO protective function. A postulated lung-protective mechanism of action could involve opening of mitochondrial adenosine triphosphate-sensitive potassium channels, relieving Ca2+ overload, upregulation of expression of Bcl-2, and downregulation of expression of active caspase-3 and Bax.
Highlights
Acute lung injury (ALI) is caused by ischemia–reperfusion during cardiopulmonary bypass (CPB)
Despite improvements in CPB, ALI remains the main cause of increasing postoperative mortality and increased duration of hospitalization [1, 2]
Some studies have reported that specific openers of mitoKATP channels protect skeletal muscle and the liver from ischemia– reperfusion injury through alleviation of apoptosis [11, 12]
Summary
Acute lung injury (ALI) is caused by ischemia–reperfusion during cardiopulmonary bypass (CPB). Despite improvements in CPB, ALI remains the main cause of increasing postoperative mortality and increased duration of hospitalization [1, 2]. Ischemic postconditioning (IPO) has been suggested to be a new method to protect organs from ischemia–reperfusion injury [7,8,9]. Recent studies [9, 10] have shown that one of the main protective mechanisms of IPO is to activate mitochondrial adenosine triphosphate (ATP)-sensitive potassium (mitoKATP) channels. Some studies have reported that specific openers of mitoKATP channels protect skeletal muscle and the liver from ischemia– reperfusion injury through alleviation of apoptosis [11, 12]. There are few reports focusing on the protective function of IPO in LIRI
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