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The correction of hypovolemia with acellular fluids results in acute normovolemic anemia. Whether the choice of the infusion fluid has an impact on the maintenance of oxygen (O2) supply during acute normovolemic anemia has not been investigated so far.
Methods:
Thirty-six anesthetized and mechanically ventilated pigs were hemodiluted to their physiological limit of anemia tolerance, reflected by the individual critical hemoglobin concentration (Hbcrit). Hbcrit was defined as the Hb-concentration corresponding with the onset of supply-dependency of total body O2-consumption (VO2). The hemodilution protocol was randomly performed with either Tetrastarch (6% HES 130/0.4, TS-group, n=9), Gelatin (3.5% urea-crosslinked polygeline, GEL-group, n=9), Hetastarch (6% HES 450/0.7, HS-group, n=9) or Ringer's solution (RS-group, n=9). The primary endpoint was the dimension of Hbcrit, secondary endpoints were parameters of central hemodynamics, O2-transport and tissue oxygenation.
Results:
In each animal, normovolemia was maintained throughout the protocol. Hbcrit was met at 3.7+/-0.6 g/dl (RS), 3.0+/-0.6 g/dl (HS P<0.05 vs. RS), 2.7+/-0.6 g/dl (GEL, P<0.05 vs. RS) and 2.1+/-0.4 g/dl (TS, P<0.05 vs. GEL, HS and RS). Hemodilution with RS resulted in a significant increase of extravascular lung water index (EVLWI) and a decrease of arterial oxygen partial pressure (paO2), O2-extraction ratio was increased, when animals of the TS-, GEL- and HS-groups met their individual Hbcrit.
Conclusions:
The choice of the intravenous (i.v) fluid has an impact on the tolerance of acute normovolemic anemia induced by acellular volume replacement. Third-generation Tetrastarch preparations (e.g., HES 130/0.4) appear most advantageous regarding maintenance of tissue oxygenation during progressive anemia. The underlying mechanism includes a lower degree of extravasation and favourable effects on microcirculatory function.
Background: Initiated by a clinical case of critical endotracheal tube (ETT) obstruction, we aimed to determine factors that potentially contribute to the development of endotracheal tube obstruction by its inflated cuff. Prehospital climate and storage conditions were simulated. Methods: Five different disposable ETTs (6.0, 7.0, and 8.0 mm inner diameter) were exposed to ambient outside temperature for 13 months. In addition, every second of these tubes was mechanically stressed by clamping its cuffed end between the covers of a metal emergency case for 10 min. Then, all tubes were heated up to normal body temperature, placed within the cock of a syringe, followed by stepwise inflation of their cuffs to pressures of 3 kPa and >=12 kPa, respectively. The inner lumen of the ETT was checked with the naked eye for any obstruction caused by the external cuff pressure. Results: Neither in tubes that were exposed to ambient temperature (range: -12°C to +44°C) nor in those that were also clamped, visible obstruction by inflated cuffs was detected at any of the two cuff pressure levels. Conclusions: We could not demonstrate a critical obstruction of an ETT by its inflated cuff, neither when the cuff was over-inflated to a pressure of 12 kPa or higher, nor in ETTs that had been exposed to unfavorable storage conditions and significant mechanical stress.
Background Production of interferon (IFN)-gamma is key to efficient anti-tumor immunity. The present study was set out to investigate effects of IFNgamma on the release of the potent pro-angiogenic mediator IL-8 by human A549 lung carcinoma cells.
Methods A549 cells were cultured and stimulated with interleukin (IL)-1beta alone or in combination with IFNgamma. IL-8 production by these cells was analyzed with enzyme linked immuno sorbent assay (ELISA). mRNA-expression was analyzed by real-time PCR and RNase protection assay (RPA), respectively. Expression of inhibitor-kappaBalpha, cellular IL-8, and cyclooxygenase-2 was analyzed by Western blot analysis.
Results Here we demonstrate that IFNgamma efficiently reduced IL-8 secretion under the influence of IL-1beta. Surprisingly, real-time PCR analysis and RPA revealed that the inhibitory effect of IFNgamma on IL-8 was not associated with significant changes in mRNA levels. These observations concurred with lack of a modulatory activity of IFNgamma on IL-1beta-induced NF-kappaB activation as assessed by cellular IkappaB levels. Moreover, analysis of intracellular IL-8 suggests that IFNgamma modulated IL-8 secretion by action on the posttranslational level. In contrast to IL-8, IL-1beta-induced cyclooxygenase-2 expression and release of IL-6 were not affected by IFNgamma indicating that modulation of IL-1beta action by this cytokine displays specificity.
Conclusions Data presented herein agree with an angiostatic role of IFNgamma as seen in rodent models of solid tumors and suggest that increasing T helper type 1 (Th1)-like functions in lung cancer patients e.g. by local delivery of IFNgamma may mediate therapeutic benefit via mechanisms that potentially include modulation of pro-angiogenic IL-8.