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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There are very few data regarding the effects of norepinephrine uptitration on global and regional hemodynamics in cardiogenic shock. We studied 25 patients with shock secondary to myocardial infarction successfully treated with percutaneous coronary intervention. Before the inclusion, 16 of 25 patients presented a cardiac arrest in the presence of medical staff. ⋯ The StO2 recovery slope and delta StO2, respectively, increased from 3.0% ± 1.3%/s to 3.6% ± 1.3%/s and 10% ± 3% to 14% ± 4%, whereas StO2 did not change (83% ± 6% to 83% ± 7%). After H1, norepinephrine was decreased to basal values, and all variables returned to baseline. In conclusion, a short-term increase in MAP with norepinephrine in resuscitated cardiogenic shock complicated by postreperfusion disease is associated with better cardiac performance and improved microcirculatory variables.
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Sepsis-induced inflammation in the gut/peritoneal compartment occurs early in sepsis and can lead to acute lung injury (ALI). We have suggested that inflammatory ascites drives the pathogenesis of ALI and that removal of ascites with an abdominal wound vacuum prevents ALI. We hypothesized that the time- and compartment-dependent changes in inflammation that determine this process can be discerned using principal component analysis (PCA) and Dynamic Bayesian Network (DBN) inference. ⋯ These combined in vivo and in silico studies suggest that in this clinically realistic paradigm of sepsis, endotoxin drives the inflammatory response in the ascites, interplaying with lung dysfunction in a feed-forward loop that exacerbates inflammation and leads to endothelial dysfunction, systemic spillover, and ALI; PST partially modifies this process.