Establishment of an experimental mouse model of trauma-hemorrhagic shock.
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This study established an experimental mouse model of trauma-hemorrhagic shock (THS). THS-induced mice (C57BL/6J, n=33) were subjected to femoral fracture, ischemia for 90 min, and resuscitation for 15 min. The sham-operated mice (C57BL/6J, n=33) underwent the same anesthetic and surgical procedures, but neither trauma-hemorrhage nor fluid resuscitation were performed. Mean arterial pressure (MAP) and microvascular tissue perfusion over the small intestine, liver, and left kidney were longitudinally measured in all mice. Blood was collected for analysis at baseline and 3, 6, 12, and 24 h post resuscitation, and the small intestine, liver, and left kidney were resected for hematoxylin and eosin staining 24 h post resuscitation. Compared with the sham group, MAP and microvascular tissue perfusion over the small intestine, liver, and left kidney were all significantly reduced in the THS group at the end of hemorrhage. Following resuscitation, no significant differences were observed between the groups. THS induction was associated with significantly increased plasma concentrations of Cr, AST, CPK, IL-6, IL-10, and TNF-alpha from the baseline values by two- to three-fold after the hemorrhage phase, and THS-induced mice demonstrated significantly increased histological injury scores. The rapid drop in MAP and microvascular tissue perfusion observed following THS induction, and the gradual recovery post resuscitation, reflects the successful establishment of a THS experimental mouse model. (+info)
Paraoxonase 1 (PON1) C/T-108 association with longitudinal mean arterial blood pressure.
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Exercise-induced acute changes in systolic blood pressure do not alter choroidal thickness as measured by a portable spectral-domain optical coherence tomography device.
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Continuous venovenous hemodiafiltration in patients with multiple organ dysfunction syndrome in an intensive care unit.
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INTRODUCTION: Continuous venovenous hemodiafiltration, generally used in patients with acute renal failure, enables elimination of humoral mediators of systemic inflammatory response and sepsis from blood. This effect should improve treatment results in patients with multiple organ dysfunction, but evidence of improved survival is insufficient. OBJECTIVES: Describe the effect of continuous venovenous hemodiaflitration on patients with multiple organ dysfunction syndrome in terms of systemic and brain hemodynamics, oxygenation, metabolism and status on ICU separation. METHODS: An observational case series was done of 18 patients (11 men and 7 women) aged 24-78 years with multiple organ dysfunction syndrome treated with continuous venovenous hemodiafiltration in the Medical-Surgical Research Center's ICU in Havana. General, systemic and brain hemodynamic, oxygenation and metabolic variables were assessed immediately before and 12 hours after starting the procedure; vital status on separation from intensive care was recorded. For analysis, patients were grouped by whether cause of multiple organ dysfunction syndrome was septic or nonseptic. Variable means before and after treatment were compared using the Wilcoxon matched pairs test. Standardized mortality ratios were calculated for both groups, with survival efficacy defined by a ratio of <0.9. RESULTS: After 12 hours continuous venovenous hemodiafitration, the septic group showed clinical improvement, with statistically significant improvement in all variables except mean arterial pressure and brain hemodynamics. Survival to discharge from ICU was 64%, with a standardized mortality ratio of 0.66. In the nonseptic group, survival was 0% and ratio was 2.13; temperature was the only variable found to improve significantly. CONCLUSIONS: Continuous venovenous hemodiafltration improved clinical parameters and survival in patients with multiple organ dysfunction of septic origin. Further studies are needed with larger numbers of patients to corroborate these results. (+info)
Plasma endothelin-1 and vascular endothelial growth factor levels and their relationship to hemodynamics in idiopathic pulmonary fibrosis.
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BACKGROUND: Pulmonary hypertension (PH) is associated with a poor prognosis in idiopathic pulmonary fibrosis (IPF). Endothelin-1 (ET-1) and vascular endothelial growth factor (VEGF) are important in both fibrosis and vascular remodeling. OBJECTIVES: We sought to determine the relationship between ET-1 and VEGF levels and hemodynamics in patients with IPF. We hypothesized that higher levels of ET-1 and VEGF would be associated with higher pulmonary artery pressures (PAP) and pulmonary vascular resistance (PVR) in patients with IPF. METHODS: We performed a cross-sectional analysis of 52 adults with IPF enrolled in a prospective cohort with available clinical data, platelet-free plasma, and hemodynamics. ET-1 and VEGF levels were measured via immunoassay. The associations of ET-1 and VEGF with PAP and PVR were examined using generalized additive models adjusted for age, gender, race/ethnicity, and forced vital capacity (% predicted). RESULTS: Sixteen of 52 (30.8%) had PH (mean PAP >/=25 mm Hg). After multivariable adjustment, higher ET-1 levels were significantly associated with higher systolic (p = 0.01), diastolic (p = 0.02), and mean (p = 0.01) PAP and possibly higher PVR (p = 0.09). There were no significant associations between VEGF levels and hemodynamics. CONCLUSIONS: Higher levels of ET-1 were associated with higher PAP and possibly higher PVR in participants with IPF. In a subgroup of patients, ET-1 may be a contributor to pulmonary vascular disease burden in IPF. (+info)
Melanocortin 3/4 receptors in paraventricular nucleus modulate sympathetic outflow and blood pressure.
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