Protective effects of vasoactive intestinal peptide on intestinal lesions induced by endotoxic shock in rat / 中华儿科杂志

<p><b>OBJECTIVE</b>Vasoactive intestinal peptide (VIP) is a neuro-peptide that can modulate immunity in several aspects. Previous reports showed that VIP attenuates the deleterious consequences of severe infection and septic shock by regulating production of inflammatory cytokines in immune activated cells. Intestine is one of the major organ of immune system and it may trigger multiple organ dysfunction syndrome in sepsis. The present study was planned to study the change of serum TNF-alpha, IL-1beta, IL-10 level and histopathological alteration of intestinal tract, and protective effects of VIP on endotoxic shock in rat.</p><p><b>METHODS</b>Twenty eight SD rats were randomly divided into 3 groups, including control group (8 rats), LPS shock group (10 rats), and LPS + VIP group (10 rats). Endotoxic shock model was established by administration of a single dose of 10 mg/kg LPS in LPS shock group, a bolus of 5 nmol VIP intravenous injection following LPS in LPS + VIP group. The rats in the control group were given the same volume of normal saline injection. Blood samples were taken at time points of 1, 2, 4, and 6 hours after intervention from each group for measuring the level of TNF-alpha, IL-1beta and IL-10 by ELISA. Pathological changes of the intestine were observed by light microscope and electron microscope at the animals death or at the end of the experiment.</p><p><b>RESULTS</b>Serum TNF-alpha, IL-1beta and IL-10 levels elevated at each time point in LPS shock group and LPS + VIP group (P < 0.05 or P < 0.01). TNF-alpha concentration reached the peak level 2 h after LPS injection; IL-1beta and IL-10 increased continuously till the end of the experiment. In LPS + VIP group, TNF-alpha and IL-1beta elevated slightly and IL-10 increased significantly as compared with LPS shock group (P < 0.01). Leukocyte infiltration, ischemia, segmental hemorrhage or necrosis appeared in intestine under light microscope and cell swelling, cytoplasmic vacuoles and organelle damage were observed under electron microscope. However, pathological changes in LPS + VIP group were milder than those in LPS group.</p><p><b>CONCLUSIONS</b>VIP improved endotoxic shock-associated histopathological alteration of intestine, down-regulated pro-inflammatory cytokines production and up-regulated anti-inflammatory cytokines. These effects may suggest a protective mechanism of VIP in septic shock. VIP is a potential immunoregulatory substance in treatment of septic shock.</p>

Cause and mortality analysis of acute intracranial hypertension and cerebral edema in pediatric intensive care unit / 中华儿科杂志

<p><b>OBJECTIVE</b>Acute intracranial hypertension/cerebral edema (ICH/CE) is an increase in brain volume caused by an absolute increase in cerebral tissue water content. Severe ICH/CE is often associated with a higher mortality and higher neurological consequence rate in intensive care unit. However, little relevant information is available on critical condition of central nervous system in children. The aim of this survey was to study the causes, clinical epidemiology and risk factors of critical illness with ICH/CE in pediatric intensive care unit (PICU).</p><p><b>METHODS</b>Case records of critically ill patients with ICH/CE admitted to PICU in Children's Hospital Affiliated to Shanghai Jiaotong University during the period from January, 1999 to December, 2003 were reviewed for causes, case fatality rate, prognosis and relationship with multiple organ dysfunction syndrome (MODS). Univariate analyses were performed to identify risk factors associated with ICH/CE.</p><p><b>RESULTS</b>During the 5 years, 1446 cases with critical illnesses were admitted and ICH/CE developed in 216 patients. The leading causes of ICH/CE were central nervous system infection (27.8%), accidental injuries (22.4%), and sepsis (10.2%). The overall mortality of the patients with ICH/CE was 29.2%. The mortality showed no significant change during the years from 1999 to 2003 (chi(2) = 0.371, P = 0.985). There was no significant difference in mortality of patients with ICH/CE between those with and without neurological diseases (chi(2) = 0.546, P = 0.460). Univariate analyses involving 12 factors indicated the following risk factors: younger age, number of failed organ, lower pediatric critical illness score, underlying diseases, abnormal respiration and change in size of pupil (P < 0.05 or < 0.001). The following factors were not associated with higher risk of death from ICH/CE: sex, organ of primary disease, Glasgow coma score (</= 7 versus > 7) on admission, elevated blood pressure and anterior fontanelle change (P > 0.05).</p><p><b>CONCLUSIONS</b>The mortality of ICH/CE remains high since 1999. Central nervous system infection, accidental injuries, and sepsis were leading causes of ICH/CE in PICU of the hospital. Children who had ICH/CE due to younger age, lower pediatric critical illness score, and complicated with MODS had a higher mortality rate.</p>