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Introduction Resuscitation after hemorrhagic shock (HS) could result in increased pro-inflammatory cytokines and then multiple organ dysfunctions. Calcitriol exerts pleiotropic effects in a wide variety of target tissues and has a role against anti-inflammation. The present study was aimed to investigate the modulatory effects of calcitriol on the pathophysiological and inflammatory markers following HS in rats. Materials and methods By withdrawing 60% of the total blood volume over 30 min via a femoral artery catheter in rats, HS was induced. Afterwards, 10 ng/kg calcitriol was injected intravenously in rats. After performing these procedures, hemodynamic status of mean arterial pressure (MAP) and heart rate (HR) were continuously monitored for 12 h. Hemoglobin, lactic dehydrogenase (LDH), creatine phosphokinase (CPK), liver and renal function were measured at 30 min before the induction of HS and 0, 1, 3, 6, 9, and 12 h after HS, while an equal volume of normal saline as replacement fluid. At 1 and 12 h after inducing HS, serum levels of tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) levels were measured, and the livers, kidneys and lungs were taken out and then examined histo-pathologically at 48 h after inducing HS. Results Hemoglobin and MAP were significantly decreased, liver and renal function were significantly impaired, but HR and the levels of LDH, CPK, TNF-α and IL-6 were significantly increased after HS in rats. After being treated with calcitriol following HS resulted in better survival rate, lower serum levels of TNF-α and IL-6, and lesser hepatic, renal, and pulmonary histo-pathologic scores of injury in rats. Conclusion Being treated with calcitriol after HS could ameliorate the pro-inflammatory reactions by modulating the effects of cytokines, which lead to prevention of subsequent major organ damages. [ABSTRACT FROM AUTHOR]

Abstract: Background: Hypothermia frequently occurs during fluid resuscitation of trauma victims, especially in patients with a major blood loss. Recent studies have suggested that mild hypothermia may ameliorate hemorrhagic shock (HS) induced splanchnic damage. Objective: The aim of the present study is to compare the status of body temperature and splanchnic injury under different resuscitation speeds for HS in conscious rats. Methods: Experimental study in an animal model of HS. Twenty-four male Wistar-Kyoto rats were used in the study. To mimic HS, 40% of the total blood volume was withdrawn. Fluid resuscitation was given 30min after blood withdrawal. The rats were randomly divided into three groups; the control group, the 10-min rapid group, and the 12-h slow group. Results: Levels of blood biochemical parameters, including aspartate transferase (GOT), and alanine transferase (GPT), were measured. Levels of serum tumor necrosis factor α (TNF-α) and interleukin 6 (IL-6) were measured and levels of bronchoalveolar lavage fluid (BALF) TNF-α and nitric oxide (NO) were measured by ELISA. The lung, liver and small intestine were examined for pathological changes 48h after HS. Conclusions: Initially slow rate resuscitation with limited-volume significantly decreased body temperature, serum GOT, GPT, TNF-α, and IL-6 levels, levels of TNF-α, and NO in BALF. Moreover, the slow group had lower injury scores in the lung, liver and small intestine than the rapid group after HS. This finding suggests that mild hypothermia induced by a slow fluid resuscitation rate with limited-volume ameliorates HS-induced splanchnic damage in conscious rats. [Copyright &y& Elsevier]