Shock : molecular, cellular, and systemic pathobiological aspects and therapeutic approaches : the official journal the Shock Society, the European Shock Society, the Brazilian Shock Society, the International Federation of Shock Societies
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Brain death (BD) induces hemodynamic instability with microcirculatory hypoperfusion, leading to increased organ inflammation and dysfunction. This study investigated the effects of 7.5% hypertonic saline solution (HSS) on mesenteric microcirculatory dysfunction and inflammation in a rat model of BD. ⋯ HSS may improve the density of mesenteric perfused small vessels due to its effects on eNOS and endothelin-1 protein expression, and reduces inflammation by decreasing leukocyte adhesion and migration in a rat model of BD.
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Studies have shown that Nod-like receptor protein (NLRP) 3 inflammasome activation contributes to myocardial ischemia/reperfusion (I/R) injury. However, the role and mechanism of NLRP1 inflammasome in myocardial I/R injury remain unknown. Endoplasmic reticulum (ER) stress is involved in the development of myocardial I/R injury. ⋯ NLRP1 inflammasome activation induced by H/R was also suppressed by PDTC. In conclusion, NLRP1 inflammasome activation promotes myocardial I/R injury. ER stress can activate NLRP1 inflammasome via activating the NF-κB signaling pathway.