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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No drug therapy has demonstrated improved survival following cardiac arrest (CA) of cardiac or noncardiac origin. In an effort to translate the cardiorescue properties of Adenocaine (adenosine and lidocaine) and magnesium sulfate (ALM) from cardiac surgery and hemorrhagic shock to resuscitation, we examined the effect of ALM on hemodynamic rescue and coagulopathy following asphyxial-induced CA in the rat. ⋯ Small bolus of 0.9% NaCl ALM improved survival and hemodynamics following nonhemorrhagic, asphyxial CA and corrected prolonged clot times and clot retraction compared with controls.
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It has been shown that the innate immune system mediates acute lung inflammation triggered by intestinal trauma. Sexual dimorphism modulates the profile of TH1 and TH2 lymphocytes, and accordingly sex hormones may modulate acute lung inflammation by intestinal ischemia/reperfusion (I/R). Studies indicate that female rats are relatively resistant to organ injury caused by hemorrhagic shock and that the gut of female is more resistant than that of the male to deleterious effects of ischemic injury. At the present study, we investigated the effect of estradiol (E(2)) on the lung inflammation after intestinal I/R and its interaction with the nitric oxide (NO) pathway. ⋯ Estradiol treatment is able to reduce lung inflammation due to intestinal I/R, but with the concomitant blockade of NOS activity, this effect is abolished. Nitric oxide probably reduces the vascular deleterious effects of intestinal I/R, and E(2) pretreatment reduces lung inflammation after intestinal I/R and exerts these effects by modulating eNOS protein expression in the lungs.