The Mechanism of Sevoflurane Preconditioning-Induced Protections against Small Intestinal Ischemia Reperfusion Injury Is Independent of Mast Cell in Rats
The study aimed to investigate whether sevoflurane preconditioning can protect against small intestinal ischemia reperfusion (IIR) injury and to explore whether mast cell (MC) is involved in the protections provided by sevoflurane preconditioning. Sprague-Dawley rats exposed to sevoflurane or treated with MC stabilizer cromolyn sodium (CS) were subjected to 75-minute superior mesenteric artery occlusion followed by 2-hour reperfusion in the presence or absence of MC degranulator compound 48/80 (CP). Small intestinal ischemia reperfusion resulted in severe intestinal injury as demonstrated by significant elevations in intestinal injury scores and p47phox and gp91phox, ICAM-1 protein expressions and malondialdehyde and IL-6 contents, and MPO activities as well as significant reductions in SOD activities, accompanied with concomitant increases in mast cell degranulation evidenced by significant increases in MC counts, tryptase expression, and β-hexosaminidase concentrations, and those alterations were further upregulated in the presence of CP. Sevoflurane preconditioning dramatically attenuated the previous IIR-induced alterations except MC counts, tryptase, and β-hexosaminidase which were significantly reduced by CS treatment. Furthermore, CP exacerbated IIR injury was abrogated by CS but not by sevoflurane preconditioning. The data collectively indicate that sevoflurane preconditioning confers protections against IIR injury, and MC is not involved in the protective process. 1. Introduction Small intestinal ischemia reperfusion (IIR) injury occurs frequently in many clinical conditions, including bowel transplantation [1] and liver transplantation, as well as all kinds of shock [2]. Although the advanced treatments have been applied in clinical, the mortality associated with IIR is still high [3]. Mast cells are widely present throughout gastrointestinal tract; previous studies including ours have demonstrated that mast cells play a critical role in the pathogenesis of IIR injury [4, 5], and mast cell inhibition provides a promising therapeutic method against IIR injury. Sevoflurane, a novel inhaled anesthetic, has been widely used in patients undergoing surgery. In addition to its anesthesia effect, several studies so far have demonstrated that sevoflurane preconditioning confers protections against hypoxic and ischemic cerebral and spinal cord injuries [6, 7], moreover, sevoflurane preconditioning also provides promising benefits against ischemia/reperfusion injury in the heart and kidneys [8, 9]. The protective mechanisms were associated with the
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