The Journal of surgical research
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The causes of cardiovascular collapse (CC) during hemorrhagic shock (HS) are unknown. We hypothesized that vascular tone loss characterizes CC, and that arterial pulse pressure/stroke volume index ratio or vascular tone index (VTI) would identify CC. ⋯ Vasodilatation immediately prior to CC in severe HS occurs at the same time as an increase in LIR, suggesting loss of tone as the mechanism causing CC, and energy failure as its probable cause.
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Neuroinflammatory response triggered by surgery has been increasingly reported to be associated with postoperative cognitive dysfunction. Proinflammatory cytokines, such as interleukin 1β (IL-1β) and tumor necrosis factor α (TNF-α), play a pivotal role in mediating surgery-induced neuroinflammation. The role of cyclooxygenase-2 (COX-2), a critical regulator in inflammatory response, in surgery-induced neuroinflammation is still unknown. The aim of the study was to investigate the changes of COX-2 expression and prostaglandin E2 (PGE2) production in the hippocampus in aged rats following partial hepatectomy. The effects of selective COX-2 inhibitor (parecoxib) on hippocampal proinflammatory cytokine expression were also evaluated. ⋯ COX-2 may play a critical role in surgery-induced neuroinflammation. The COX-2 inhibitor may be a promising candidate for treatment of neuroinflammation caused by surgical trauma.
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This study aimed to evaluate the differential protective effects of isoflurane or sevoflurane on lung inflammation in a rat model of cecal ligation and puncture (CLP) induced sepsis. ⋯ Both sevoflurane and isoflurane attenuated inflammatory response, lipid peroxidation, and oxidative stress. Furthermore, sevoflurane was more effective in modulating sepsis induced inflammatory response at the chosen concentration in sepsis model.
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Sepsis is associated with high morbidity and mortality, and survivors can present with cognitive dysfunction. The present study was performed to investigate the effects of hydrogen-rich saline (HRS) on oxidative stress in the brain, cognitive dysfunction, and mortality in a rat model of sepsis. ⋯ These findings indicate that HRS could attenuate the consequences of sepsis induced by cecal ligation and puncture in rats, at least in part, by the inhibition of oxidative stress.
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We observed that centhaquin, a cardiovascular active agent, reduces blood lactate levels. Because blood lactate is an important indicator of end-organ perfusion, we determined the resuscitative effect of centhaquin in hemorrhaged rats. ⋯ Centhaquin significantly improved the resuscitative effect of hypertonic saline by increasing CO, reducing blood lactate, and improving survival time of hemorrhaged rats.