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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The hemodynamic response to progressive blood loss passes through three distinct phases: an initial normotensive compensatory phase, a secondary hypotensive decompensatory phase, and a posthemorrhage recompensatory phase. The role of cardiac vagal and cardiac spinal signals in triggering the different phases of the response to hemorrhage was evaluated in the unanesthetized, freely moving rat by observing the effects on the response to 30% blood loss of prior cardiac vagal deafferentation (bilateral vagal rhizotomy) or prior cardiac spinal deafferentation (bilateral stellate ganglionectomy). In comparison to control animals, it was found that (i) cardiac spinal deafferentation significantly delayed the onset of the decompensatory phase, and (ii) cardiac vagal deafferentation slightly potentiated the decompensatory phase and impaired the recompensatory phase. These results indicate that it is cardiac spinal signals, rather than cardiac vagal signals, which in the conscious rat contribute to the triggering and progression of the decompensatory response to blood loss.
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The objective of this study was to investigate the effects of pyruvate-containing fluids on peritoneal resuscitation (PR), following intravenous fluid resuscitation from hemorrhagic shock (HS) in rats. ⋯ Peritoneal resuscitation with hyperosmolar fluids attenuated visceral vasoconstriction and splanchnic hypoperfusion and improved the intestinal barrier protein and organ function following conventional fluid resuscitation from severe HS in rats. Pyruvate was superior to lactate in PDS as PR fluids, and 2.2% pyruvate was the optimal fluid in PR.
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Zinc is a trace element vital for immune function during host response to infection. The proinsulin C-peptide has been shown to exert beneficial effects through activation of the anti-inflammatory peroxisome proliferator-activated receptor γ (PPARγ) in experimental endotoxemia. Some in vitro activities of C-peptide appear dependent on the presence of zinc. ⋯ Combination of zinc supplementation with C-peptide posttreatment significantly improved survival rate (61%) similarly to antibiotic treatment (60%), ameliorated lung architecture and liver function, reduced tissue neutrophil infiltration, and increased bacterial clearance when compared with vehicle, C-peptide, or zinc treatment alone. These beneficial effects were associated with restored lung nuclear expression of PPARγ and reduction of phosphorylated extracellular signal-regulated kinases 1 and 2 and nuclear factor κB activities in comparison to vehicle or single treatment protocols. Our data demonstrate that short-term zinc prophylaxis before the infectious insult is a requisite for the anti-inflammatory properties of C-peptide by facilitating modulation of inflammatory pathways.
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Mechanical ventilation can cause structural and functional disturbances in the lung termed ventilator-induced lung injury (VILI). The aim of this study was to evaluate whether BML-111, a lipoxin receptor agonist, could attenuate VILI. Following induction of anesthesia and tracheostomy, Sprague-Dawley rats were ventilated with low tidal volume (6 mL/kg) or high tidal volume (20 mL/kg, HVT) for 4 h. ⋯ Administration with BML-111 suppressed the decrement of the nuclear factor κB (NF-κB) inhibitor IκB-α, diminished NF-κB activation, and reduced activation of mitogen-activated protein kinase in VILI. This study indicates that BML-111 attenuated VILI via a NF-κB and mitogen-activated protein kinase dependent mechanism. BML-111 may be a promising strategy for alleviation of VILI in patients subjected to mechanical ventilation.