Abstract

 
 
 
 Purpose: To study the effect of dexmedetomidine pretreatment on a rat model of myocardial ischemia-reperfusion injury (IRI)
 Methods: Three groups of SD rats (n = 48; mean body weight = 275 ± 25 g) were used (16 rats each): sham, IRI, and dexmedetomidine groups. Ischemia-reperfusion injury (IRI) was established via ligation of left anterior coronary artery. Rats in dexmedetomidine group were treated with single i.p. injection of dexmedetomidine (100 μg/kg) 30 min before induction of IRI. Serum levels of IL-1β, IL-6 and TNF-α were determined by enzyme-linked immunosorbent assay (ELISA). Western blotting was used to determine the protein expressions of bcl-2 and bax, while histopathological changes in rat myocardial tissue were determined with H&E staining.
 Results: Serum TNF-α, IL-1β and IL-6 levels were significantly up-regulated in IRI rats, relative to sham rats, but were decreased by dexmedetomidine (p < 0.05). Dexmedetomidine significantly reduced the level of malondialdehyde (MDA) in myocardial tissues of IRI rats, but it increased superoxide dismutase (SOD) activity (p < 0.05). It also markedly increased bcl-2 protein level, while the protein expression of bax was decreased (p < 0.05). Results of H & E staining showed that dexmedetomidine significantly mitigated IRI-induced damage.
 Conclusion: Dexmedetomidine mitigates myocardial IRI in rats through suppression of inflammatory and apoptotic changes, and enhancement of physiological antioxidant potential. This finding may be useful for the management of myocardial ischemia-reperfusion injury.
 
 
 
Highlights
Organs and tissues differ in their ischemic tolerance
Ischemia-reperfusion injury (IRI), a common pathological event during anesthesia, refers to blood re-flow caused by ischemia of myocardial tissue/cells, which leads to myocardial tissue injury [5,6]
The cells were neatly and compactly arranged, with large and Effect of dexmedetomidine on levels of inflammatory cytokines in rat serum As shown in Table 1, the cytokine levels were markedly higher in IRI rat than in sham operation rats
Summary
Organs and tissues differ in their ischemic tolerance. Prolonged and persistent ischemia causes severe necrosis in tissues [1,2,3]. The present research was aimed at investigating the influence of dexmedetomidine pretreatment on myocardial IRI in rats. Pathological changes in rat myocardial tissue were recorded and analyzed with ImageJ analysis software. Protein expression levels of bcl-2 and bax in ischemic myocardial tissues of rats were measured with Western blotting. Rat myocardial tissue was homogenized in PBS and lysed with ice-cold RIPA buffer mixed with PMSF (1:10, v: v). Myocardial tissue cells of IRI rats were highly disorganized and vacuolated, with pyknotic nuclei. Ischemic myocardial tissue of each rat was homogenized with ice-cold PBS and spun at 3500 rpm for 10 min to obtain a clear supernatant. Pretreatment of IRI rats with dexmedetomidine markedly increased the protein expression of bcl, but it reduced bax protein expression (Figure 2).
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