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File Download Severe sepsis and drotrecogin alfa (activated) use: results from the PROGRESS registry R Beale, St Thomas' Hospital F Brunkhorst, Friedrich-Schiller University Greg Martin, Emory University M Williams, Lilly Research Laboratories D Nelson, Lilly Research Laboratories J Janes, Lilly Research Laboratories Journal Title: Critical Care Nursing Quarterly Volume: Volume 11, Number Suppl 2 Publisher: BioMed Central | 2007-03-22, Pages P64-P64 Type of Work: Article | Final Publisher PDF Publisher DOI: 10.1186/cc5224 Permanent URL: https://pid.emory.edu/ark:/25593/s7f9v Final published version: http://dx.doi.org/10.1186/cc5224 Copyright information: © 2007 BioMed Central Ltd. Accessed September 25, 2021 9:59 PM EDT Available online http://ccforum.com/supplements/11/S2 Critical Care Volume 11 Suppl 2, 2007 27th International Symposium on Intensive Care and Emergency Medicine Brussels, Belgium, 27–30 March 2007 Published online: 22 March 2007 These abstracts are available online at http://ccforum.com/supplements/11/S2 © 2007 BioMed Central Ltd P1 cells with sodium sulfide (60–300 µM) reduced the loss of cell Infusion of sodium sulfide improves myocardial and viability elicited by the nitric oxide donor compound (3 mM) or by endothelial function in a canine model of cardiopulmonary peroxynitrite (3 mM), as measured by the MTT method. Sodium bypass sulfide did not affect cell viability in the concentration range tested. In mice subjected to bacterial lipopolysaccharide (LPS, 5 mg/kg C Szabó1, G Veres2, T Radovits2, M Karck2, G Szabó2 i.p.), treatment of the animals with sodium sulfide (0.2 mg/kg/hour 1Ikaria Inc., Seattle, WA, USA; 2University of Heidelberg, Germany for 4 hours, administered in Alzet minipumps) reduced the LPS- Critical Care 2007, 11(Suppl 2):P1 (doi: 10.1186/cc5161) induced increase in plasma IL-1β and TNFα levels. These responses were attenuated when animals were pretreated with the Hydrogen sulfide is produced endogenously by a variety of heme oxygenase inhibitor tin-protoporphyrin IX (6 mg/kg). The enzymes involved in cysteine metabolism. Clinical data indicate current results point to the cytoprotective and anti-inflammatory that endogenous levels of hydrogen sulfide are diminished in effects of hydrogen sulfide, in cells exposed to nitrosative stress, various forms of cardiovascular diseases. The aim of the current and in animals subjected to endotoxemia. study was to investigate the effects of hydrogen sulfide supple- mentation on cardiac function during reperfusion in a clinically P3 relevant experimental model of cardiopulmonary bypass. Twelve Epithelial cell apoptosis is similar but hypoxic-inducible anesthetized dogs underwent hypothermic cardiopulmonary factor expression is weaker in acute acalculous bypass. After 60 minutes of hypothermic cardiac arrest, reper- cholecystitis than in calculous cholecystitis fusion was started after application of either saline vehicle (control, n = 6), or the sodium sulfide infusion (1 mg/kg/hour, n =6). M Vakkala1, J Laurila1, J Saarnio2, V Koivukangas2, H Syrjälä3, Biventricular hemodynamic variables were measured by combined T Karttunen4, Y Soini4, T Ala-Kokko1 pressure–volume–conductance catheters. Coronary and pulmonary 1Department of Anesthesiology, 2Department of Surgery, blood flow, vasodilator responses to acetylcholine and sodium- 3Department of Infection Control and 4Department of Pathology, nitroprusside and pulmonary function were also determined. Oulu University Hospital, Oulu, Finland Administration of sodium sulfide led to a significantly better Critical Care 2007, 11(Suppl 2):P3 (doi: 10.1186/cc5163) recovery of left and right ventricular systolic function (P < 0.05) after 60 minutes of reperfusion. Coronary blood flow was also Introduction It has been previously shown that the two forms of significantly higher in the sodium sulfide-treated group (P < 0.05). acute cholecystitis, acute acalculous cholecystitis (AAC) and acute Sodium sulfide treatment improved coronary blood flow, and calculous cholecystitis (ACC), have significantly different preserved the acetylcholine-induced increases in coronary and histopathological features suggesting that AAC is a manifestation pulmonary blood (P < 0.05). Myocardial ATP levels were markedly of systemic critical illness whereas ACC is a local disease of the improved in the sulfide-treated group. Thus, supplementation of gallbladder. A balance between cell proliferation and cell death is sulfide improves the recovery of myocardial and endothelial essential for cell homeostasis. The purpose of this study was to function and energetic status after hypothermic cardiac arrest compare the markers of apoptosis, cell proliferation, and during cardiopulmonary bypass. These beneficial effects occurred expression of hypoxic-inducible factor alpha (HIF-1α) in AAC, ACC without any detectable adverse hemodynamic or cardiovascular and normal gallbladders. effects of sulfide at the dose used in the current study. Methods The AAC group consisted of 30 patients who underwent open cholecystectomy due to acute acalculous cholecystitis during P2 their ICU stay. The ACC group consisted of 21 hospitalized Cytoprotective and anti-inflammatory effects of hydrogen patients who underwent cholecystectomy due to acute calculous sulfide in macrophages and mice cholecystitis. The control group consisted of nine samples taken from normal gallbladders extirpated during pancreatic tumor C Szabo, L Kiss, E Pankotai surgery. The immunohistochemical analysis was done according to University of Medicine and Dentistry of New Jersey, Newark, NJ, USA the manufacturer’s recommendations and they consisted of Ki-67 Critical Care 2007, 11(Suppl 2):P2 (doi: 10.1186/cc5162) (proliferation), M30 (apoptosis) and HIF-1α antibodies. Cell proliferation and degree of apoptosis were expressed as the The aim of the current study was to test potential cytoprotective percentage of positive cells. HIF-1α expression was expressed as and anti-inflammatory effects of the novel biological mediator absent or weak (Score 1) or strong (Score 2). hydrogen sulfide in murine models. Murine J774 macrophages Results Apoptosis (median, 25th, 75th percentiles) was significantly were grown in culture and exposed to cytotoxic concentrations of increased in AAC 1.3% (1.0%, 3.3%), P = 0.001 and ACC 0.93% nitrosoglutathione, or peroxynitrite (a reactive species formed from (0.40%, 3.25%), P = 0.011 compared with controls 0.32% (0.20%, the reaction of nitric oxide and superoxide). Pretreatment of the 0.40%). Proliferation rate was also significantly increased in AAC S1 Critical Care March 2007 Vol 11 Suppl 2 27th International Symposium on Intensive Care and Emergency Medicine 8.0% (4.0%, 17.0%), P < 0.001 and ACC 14% (7.5%, 26.5%), Figure 1 (abstract P5) P = 0.001 compared with controls 1.0% (1.0%, 3.0%). Strong HIF- 1α staining was observed in 100% of ACC, in 57% of AAC and in 44% of control specimens (P < 0.001). Strong HIF-1α expression was associated with increased cell proliferation (P = 0.002). Conclusions Cell proliferation and apoptosis were increased in AAC and ACC. The expression of hypoxic-inducible factor was, however, stronger in ACC compared with AAC. P4 2+ Effect of prostaglandin E2 on ATP-induced Ca responses in human THP-1 monocytic cells M Goto1, M Murakawa1, J Kimura1, I Matsuoka2 1Fukushima Medical University, Fukusima, Japan; 2Takasaki University of Health and Welfare, Gunma, Japan Critical Care 2007, 11(Suppl 2):P4 (doi: 10.1186/cc5164) Introduction To clarify the relation between ATP and prostaglandin E2 (PGE2) in the immunologic system, we investigated the acute and chronic effects of PGE2 on activation of purinergic signaling in monocytes by measuring the ATP-induced elevation of intracellular 2+ Ca ([Ca]i) in fura-2-loaded THP-1 monocytes. Method THP-1 monocytes were grown for about 2 days. To γ examine the chronic effects, PGE2 and dibutyryl cAMP (dbcAMP) sepsis [1]. IFN plays a critical role in host defense by promoting were added and incubated for another day. The cell suspensions Th1 phenotype and bacterial clearance. Low IFNγ levels are were washed, loaded with fura-2-AM, and transferred into a quartz associated with the Th2 phenotype consistent with critical illness cuvette and placed in the thermostat-regulated sample chamber of anergy [2]. It has been reported that 100 and 300 mM ATP a dual excitation beam spectrophotometer. To examine the acute increased LPS/PHA-stimulated IL-10 secretion in human blood [3]. γ effects, ATP was added immediately after PGE2 and dbcAMP into Higher IL-10/IFN ratio shifts the immune phenotype from Th1 to the cuvette. In the chronic experiment, ATP alone was added into Th2 response. We studied the effect of ATP on LPS-stimulated the cuvette. Fura-2 fluorescence emission was measured at IL-10 and IFNγ secretion in a standardized ex-vivo whole human 510 nm. The [Ca]i was calculated from the ratio of the blood culture. fluorescence at the two excitation wavelengths. Methods Venous blood from 10 healthy volunteers was drawn into Results ATP induced a transient increase in [Ca]i followed by a tubes containing 10 ng LPS/ml (ILCSÒ; EDI GmBH, Reutlingen, sustained elevation of [Ca]i. Acutely, PGE2 inhibited both the Germany) and incubated with or without 100 mM ATP, respectively, transient and sustained ATP-induced elevations of [Ca]i. However, at 37°C for 24 hours. The supernates were separated and frozen this acute inhibitory effect diminished gradually with time and at –20°C. Cytokine levels were analysed on a robotic workstation chronic PGE2 accelerated the transient and sustained ATP- (epMotion 5075; Eppendorf AG, Hamburg, Germany) in duplicate induced [Ca]i elevations for 24 hours. Both the acute and chronic using the ELISA Cytokine kit (Luminex; Biosource Int., Camarillo, 2+ effects of PGE2 were mimicked by dbcAMP. In Ca -free solution, CA, USA). γ ATP did not induce the sustained elevation of [Ca]i in control cells Results Added ATP reduced the mean concentration of IFN in LPS- or cells pretreated for 24 hours with dbcAMP. This indicates that stimulated blood from 1,206 ± 1,667 pg/ml to 140 ± 128 pg/ml; 2+ the ATP-induced sustained elevation of [Ca]i was due to Ca P = 0.006.
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