22 research outputs found
The level of hypotension during hemorrhagic shock is a major determinant of the post-resuscitation systemic inflammatory response: an experimental study
<p>Abstract</p> <p>Background</p> <p>To evaluate whether the level of hypotension during hemorrhagic shock may influence the oxidative and inflammatory responses developed during post-ischemic resuscitation.</p> <p>Methods</p> <p>Fifteen rabbits were equally allocated into three groups: sham-operated (group sham); bled within 30 minutes to mean arterial pressure (MAP) of 40 mmHg (group shock-40); bled within 30 minutes to MAP of 30 mmHg (group shock-30). Shock was maintained for 60 min. Resuscitation was performed by reinfusing shed blood with two volumes of Ringer's lactate and blood was sampled for estimation of serum levels aminotransferases, creatinine, TNF-α, IL-1β, IL-6, malondialdehyde (MDA) and total antioxidant status (TAS) and for the determination of oxidative burst of polymorhonuclears (PMNs) and mononuclear cells (MCs).</p> <p>Results</p> <p>Serum AST of group shock-30 was higher than that of group shock-40 at 60 and 120 minutes after start of resuscitation; serum creatinine of group shock-30 was higher than group shock-40 at 120 minutes. Measured cytokines, MDA and cellular oxidative burst of groups, shock-40 and shock-30 were higher than group sham within the first 60 minutes after start of resuscitation. Serum concentrations of IL-1β, IL-6 and TNF-α of group shock-30 were higher than group shock-40 at 120 minutes (p < 0.05). No differences were found between two groups regarding serum MDA and TAS and oxidative burst on PMNs and MCs but both groups were different to group sham.</p> <p>Conclusion</p> <p>The level of hypotension is a major determinant of the severity of hepatic and renal dysfunction and of the inflammatory response arising during post-ischemic hemorrhagic shock resuscitation. These findings deserve further evaluation in the clinical setting.</p
Nitrosative and Oxidative Stresses Contribute to Post-Ischemic Liver Injury Following Severe Hemorrhagic Shock: The Role of Hypoxemic Resuscitation
Purpose: Hemorrhagic shock and resuscitation is frequently associated with liver ischemia-reperfusion injury. The aim of the study was to investigate whether hypoxemic resuscitation attenuates liver injury. Methods: Anesthetized, mechanically ventilated New Zealand white rabbits were exsanguinated to a mean arterial pressure of 30 mmHg for 60 minutes. Resuscitation under normoxemia (Normox-Res group, n = 16, PaO2 = 95–105 mmHg) or hypoxemia (Hypox-Res group, n = 15, PaO 2 = 35–40 mmHg) followed, modifying the FiO 2. Animals not subjected to shock constituted the sham group (n = 11, PaO 2 = 95–105 mmHg). Indices of the inflammatory, oxidative and nitrosative response were measured and histopathological and immunohistochemical studies of the liver were performed. Results: Normox-Res group animals exhibited increased serum alanine aminotransferase, tumor necrosis factor- alpha, interleukin (IL)-1b and IL-6 levels compared with Hypox-Res and sham groups. Reactive oxygen species generation, malondialdehyde formation and myeloperoxidase activity were all elevated in Normox-Res rabbits compared with Hypox-Res and sham groups. Similarly, endothelial NO synthase and inducible NO synthase mRNA expression was up-regulated and nitrotyrosine immunostaining increased in animals resuscitated normoxemically, indicating a more intense nitrosative stress. Hypox-Res animals demonstrated a less prominent histopathologic injury which was similar to sham animals. Conclusions: Hypoxemic resuscitation prevents liver reperfusion injury through attenuation of the inflammatory respons
Fasciitis and Septic Shock Complicating Retrocecal Appendicitis
Introduction: A case of fasciitis and septic shock complicating
retrocecal appendicitis is presented. Case report: A 52-year-old man
presented to the Emergency Department with lumbar pain, fever of recent
onset and subsequently developed septic shock attributed to fasciitis of
abdominal, flank and groin region. On intensive care unit, he was
managed with broad-spectrum intravenous antibiotics and surgical
debridement. An abdominal computed tomography scan confirmed the
findings of fasciitis and was negative for intra-abdominal pathology. In
the following days, an enterocutaneous fistula with foul smelling fluid
was noted. A new surgical exploration revealed the presence of a
ruptured retrocecal appendix, and right hemicolectomy was performed. The
postoperative period was long but uneventful. Conclusion: Retrocecal
appendicitis can rarely be presented as deteriorating
cellulitis-fasciitis in the right abdominal, flank or groin region, with
or without abdominal symptoms
Hypoxemic resuscitation after hemorrhagic shock is accompanied by reduced serum levels of angiopoietin-2
Background: To investigate whether angiopoietin-2 (Ang2) and vascular
endothelial growth factor (VEGF) are implicated in the hypoxemic
resuscitation from hemorrhagic shock. Methods: Twenty rabbits were
subjected to hemorrhagic shock after blood exsanguination; resuscitation
was performed by infusion of the shed blood in ten rabbits under
normoxemic conditions (NormoxRes) and in 10 under hypoxemic conditions
(HypoxRes); four rabbits were subjected to sham operation. Serum was
drawn at serial time intervals: serum was applied for stimulation of
U937 monocytes. Results: Serum concentrations of Ang2 were higher in the
NormoxRes group compared to the HypoxRes group at 90 min (p: 0.049) and
at 120 min (p: 0.028). Serum concentrations of VEGF did not differ
between groups. Concentrations of VEGF in the supernatants of U937
stimulated with sera of all groups were below detection limit The wet to
dry. lung ratio of the HypoxRes group was significantly lower than the
NormoxRes group (p < 0.0001). Conclusions: Hypoxemic resuscitation from
hemorrhagic shock is a process accompanied by reduced serum levels of
Ang2. These findings add significantly to our understanding of that
experimental treatment strategy of resuscitation. (C) 2009 Elsevier Ltd.
All rights reserved
Administration of Human Protein-C concentrate prevents apoptotic brain cell death after experimental sepsis
Activated Protein C renders anti-apoptotic properties in neurons and
endothelial cells. The aim of the present study was to evaluate the in
vivo cytoprotective role of Protein C zymogen (PC) administration in
septic rat brain. Male Wistar rats (n = 60) were subjected to sepsis via
Cecal Ligation and Puncture (CLP). Animals were randomly divided either
to receive 100 IU/kg human PC concentrate at 1, 7 and 13 h post CLP (CLP
+ PC group) or placebo treatment (CLP group). At pre-specified time
points (6, 12, 24, 36, 48 and 60 h post CLP) five animals from either
group were euthanized and the brain tissue was removed. Apoptosis in
both neurons (Neu-N+) and astroglia (GFAP+) was assessed by flow
cytometry using 7-aminoactinomycin D (7AAD). Immunohistochemical
detection of cleaved caspase 3, bax, bcl-2, cytochrome c and caspase 8
was also performed. PC treated animals had significantly reduced
apoptosis in neurons at 6 and 24 h post CLP (p = 0.04 and p = 0.016
respectively) and necrosis at 6, 12 and 60 h post CLP (p=0.008, p=0.012
and p=0.032 respectively). Astrocyte necrosis was also decreased in
septic rats receiving PC (6, 12 and 60 h post CLP p=0.008, p=0.016 and
p=0.008 respectively). In addition, active caspase 3, bax, cytochrome c
and caspase 8 expression was significantly decreased during early sepsis
(6-36 h) while bcl-2 expression was increased (24 h p=0.001 and 60 h
p=0.001) in the PC treated animals compared to placebo. PC concentrate
administration in experimental sepsis produced a time dependent
inhibition of apoptosis in rat neurons and astrocytes. The inhibition of
sepsis related apoptosis concerned both the mitochondrial and caspase 8
dependent pathways. (C) 2009 Elsevier B.V. All rights reserved
Reasons of PEG failure to eliminate gastroesophageal reflux in mechanically ventilated patients
AIM: To investigate factors predicting failure of percutaneous endoscopic gastrostomy (PEG) to eliminate gastroesophageal reflux (GER)