Articles: sepsis.
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Apoptosis (A O) is a pathological process by which cells undergo a form of inducible nonnecrotic cellular suicide. In vitro studies suggest that changes in the rate of macrophage (Mo) A O may be associated with elevated proinflammatory cytokine secretory capacity, such as interleukin-1 beta (IL-1 beta) (via IL-1 converting enzyme activation). Furthermore, it has been reported that Mo are activated during early (0-4 hours) experimental septic insult to act as sources of proinflammatory cytokines, such as IL-1. ⋯ At 24 hours (late) after the onset of sepsis, the ex vivo extent of A O in PMo was increased but it was decreased in KMo. However, the addition of LPS in vitro results in a marked increase in both septic PMo and KMo A O. This latter result suggests that the inability of Mo to release cytokines in response to stiumulants, such as LPS during late sesis (24 hours), may be because of induciton of accelerated A O in these Mo populations.
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Low dose ATP-MgCl2 is reported to cause selective pulmonary vasodilation during hypoxic and thromboxane mimetic-induced constriction. In addition, it has been shown to increase cardiac output and improve cellular function during circulatory shock. Based on these properties we hypothesized that ATP-MgCl2 might ameliorate the cardiopulmonary manifestations of sepsis secondary to group B streptococci (GBS). ⋯ Also dynamic lung compliance was higher (p < 0.001) and pulmonary airway resistance lower (p < 0.001) in treated animals. Median survival in control animals was 153 min, whereas all treated animals survived to 240 min (p < 0.001). These data demonstrate that ATP-MgCl2 ameliorates the deleterious cardiopulmonary manifestations of GBS sepsis and results in improved survival in a young animal model.