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ABSTRACT: BACKGROUND: Mast cell activation plays a key role in the process of small intestinal ischemia-reperfusion (IIR) injury; however, the precise role of tryptase released from mast cell on IIR injury remains poorly understood. The aim of this study was to determine the protective role against IIR injury by using tryptase inhibitor protamine after ischemia and to explore the underlying mechanism. METHODS: Adult Sprague-Dawley rats were randomized into sham-operated group (S), sole IIR group (IIR) in which rats were subjected to 75-minute superior mesenteric artery occlusion followed by 4-hour reperfusion, or IIR being respectively treated with mast cell stabilizer cromolyn sodium (CS group), with the mast cell degranulator compound 48/80 (CP group), or with protamine (P group). The previously mentioned agents were, respectively, administered intravenously 5 minutes before reperfusion. The intestine tissue was obtained for histologic assessment and assays for protein expressions of tryptase and mast cell protease 7 and protease-activated receptor 2 (PAR-2). The intestine mast cell number and levels of tumor necrosis factor α and interleukin 8 were quantified. RESULTS: IIR resulted in intestinal injury evidenced as significant increases in Chiu's scores, accompanied with concomitant increases of mast cell counts and intestinal tryptase and mast cell protease 7 protein expressions. IIR also increased intestinal PAR-2 expressions, tumor necrosis factor α, and interleukin 8 levels. Cromolyn sodium and protamine significantly reduced the responses to IIR injury while compound 48/80 further aggravated the previously mentioned biochemical changes. CONCLUSION: Tryptase releasing from mast cell activation participates in IIR injury through PAR-2, and inhibiting tryptase after ischemia provides promising benefits in limiting IIR injury.
The journal of trauma and acute care surgery. 09/2012;
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ABSTRACT: Small intestinal ischemia-reperfusion (IIR) injury may lead to severe local and remote tissue injury, especially acute lung injury (ALI). Mast cell activation plays an important role in IIR injury. It is unknown whether IIR mediates lung injury via mast cell activation.
Adult SD rats were randomized into sham operated group (S), sole IIR group (IIR) in which rats were subjected to 75 min of superior mesenteric artery occlusion followed by 4h reperfusion, or IIR being respectively treated with the mast cell stabilizer Cromolyn Sodium (IIR+CS group), with the tryptase antagonist Protamine (IIR+P group), with the histamine receptor antagonist Ketotifen (IIR+K group), or with the mast cell degranulator Compound 48/80 (IIR+CP group). The above agents were, respectively, administrated intravenously 5 min before reperfusion. At the end of experiment, lung tissue was obtained for histologic assessment and assays for protein expressions of tryptase and mast cell protease 7(MCP7). Pulmonary mast cell number and levels of histamine, TNF-α and IL-8 were quantified.
IIR resulted in lung injury evidenced as significant increases in lung histological scores (P<0.05 IIR vs. S), accompanied with concomitant increases of mast cell counts and elevations in TNF-α and IL-8 concentrations and reductions in histamine levels (all P<0.05 IIR vs. S). IIR also increased lung tissue tryptase and MCP7 protein expressions (all P<0.05, IIR vs. S). Cromolyn Sodium, Ketotifen and Protamine significantly reduced whilst Compound 48/80 aggravated IIR mediated ALI and the above biochemical changes (P<0.05).
Mast cells activation play a critical role in IIR mediated ALI.
Injury 01/2012; 43(8):1250-6. · 1.98 Impact Factor
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ABSTRACT: Mast cell has been demonstrated to be involved in the small intestinal ischemia-reperfusion (IIR) injury, however, the precise role of tryptase released from mast cell on acute lung injury(ALI) induced by IIR remains to be elucidated, our study aimed to observe the roles of tryptase on ALI triggered by IIR and its underlying mechanism. Adult SD rats were randomized into sham-operated group, sole IIR group in which rats were subjected to 75 min superior mesenteric artery occlusion followed by 4 h reperfusion, or IIR being respectively treated with cromolyn sodium, protamine, and compound 48/80. The above agents were, respectively, administrated intravenously 5 min before reperfusion. At the end of experiment, lung tissue was obtained for assays for protein expressions of tryptase and mast cell protease 7 (MCP7) and protease-activated receptor 2 (PAR-2). Pulmonary mast cell number and levels of IL-8 were quantified. Lung histologic injury scores and lung water content were measured. IIR resulted in lung injury evidenced as significant increases in lung histological scores and lung water contents, accompanied with concomitant increases of expressions of tryptase and MCP7, and elevations in PAR-2 expressions and IL-8 levels in lungs. Stabilizing mast cell with cromolyn sodium and inhibiting tryptase with protamine significantly reduced IIR-mediated ALI and the above biochemical changes while activating mast cell with compound 48/80 further aggravated IIR-mediated ALI and the increases of above parameters. Tryptase released from mast cells mediates ALI induced by intestinal ischemia-reperfusion by activating PAR-2 to produce IL-8.
Inflammation 12/2011; 35(3):1144-53. · 1.75 Impact Factor
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ABSTRACT: To determine the prevalence and type of respiratory complications after adenotonsillectomy for obstructive sleep apnea syndrome (OSAS) in otherwise healthy children with a completed preoperative polysomnography evaluation.
Retrospective analysis.
Affiliated Hospital of Medical University, Guangzhou, Guangdong, China.
The retrospective chart review focused on the demographic data and pertinent history, preoperative sleep evaluation, surgical and anesthetic management, and need for postoperative respiratory interventions. Improvements in quality of life after adenotonsillectomy for children with OSAS were evaluated using the OSA-18 survey (an 18-item survey on obstructive sleep apnea) completed before, and within 6 months after, surgery.
The percentage of children undergoing adenotonsillectomy to treat OSAS who experience a postoperative respiratory complication.
Four hundred seventy-five consecutive cases for adenotonsillectomy were identified, and 321 children met the inclusion criteria. Thirty-six cases (11.2%) had postoperative respiratory complications necessitating a medical intervention. Of the 36, 29 children (80.6%) required an oropharyngeal or nasopharyngeal airway. Twenty-five children (69.4%) experienced multiple episodes of desaturation, and 61.1% of cases (n = 22) had respiratory complications in the postanesthesia care unit. Statistic analysis showed that the risk factors for complications were young age, obesity, and high preoperative apnea-hypopnea index. Improvements in quality of life as shown by change scores (preoperative score minus postoperative score) were comparable in two groups (p > .05).
The most important predictors of postsurgical respiratory morbidity were young age, obesity, and the initial severity of OSAS. Surgical therapy yielded significant improvements in quality of life for children with OSAS, and the amelioration was not linked to the occurrence of postoperative respiratory complications.
Journal of otolaryngology - head & neck surgery = Le Journal d'oto-rhino-laryngologie et de chirurgie cervico-faciale 02/2009; 38(1):49-58. · 0.71 Impact Factor
