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Background Uncontrolled hemorrhage (UH) remains the most common cause of death on the battlefield. This study examined the pathophysiological characteristics of UH in rats acutely exposed to high altitude. Material and methods Rats raised at sea level were randomly divided into two groups. Rats in the high-altitude group were exposed to hypobaric hypoxia in a hypobaric chamber (simulating 4000 m above sea level) for 2 d and then were performed a hemorrhagic shock protocol in the hypobaric chamber. Rats that underwent the same hemorrhage procedure at sea level were used as control. Anesthetized rats were bled to maintain their mean arterial pressure at 45 mmHg for 1 h. The distal quarter of the tail was amputated to allow free blood loss. After 1 h, the tail cut was ligated to induce hemostasis. mean arterial pressure, acid–base balance, blood loss, and survival were recorded. Rats were killed, and tissues were obtained for histological analysis. Results Rats in the high-altitude group suffered less uncontrolled blood loss, more severe acidosis (lower pH and base excess), and inferior tissue oxygen supply (lower oxygen saturation and higher arterial lactate concentration) during the hemorrhage periods compared with the control group. Survival rates were significantly lower in the high-altitude group than those in the control group ( P < 0.05), which was consistent with the results of pathological tissue injury. Conclusions In this rat model of hemorrhagic shock, acute high-altitude exposure resulted in decreased UH but more serious hemorrhagic shock injuries than that at sea level. [ABSTRACT FROM AUTHOR]

Abstract: Nitric oxide (NO), an endothelial-derived relaxing factor, plays important roles in a variety of pathophysiological conditions such as hemorrhagic shock (HS). So far, the impact of NO administration in HS treatment has been controversial. Through literature review, we summarize here the biphasic effects of NO in early and late phases of HS. Evidence suggests that NO administration is beneficial in the early stage while detrimental in the late stage of HS. We further propose inhalation of NO as a novel therapeutic strategy for the treatment of HS in the early stage. [Copyright &y& Elsevier]

Abstract: Background: Hemorrhagic shock is associated with severe rheological abnormalities. We hypothesized that in the setting of hemorrhagic shock, resuscitation can alter hemorheological characteristics dramatically, and different fluids cause different effects. The aim of this study was to investigate whether the type of fluid administered has an impact on hemorheological characteristics at the early stage of resuscitation in a rodent model of hemorrhagic shock. Methods: Animals were randomized into five groups: (1) sham hemorrhage (SHAM); (2) shock and sham resuscitation (SHOCK); (3) shock and resuscitation with normal saline 32ml/kg (NS); (4) shock and resuscitation with 7.5% hypertonic saline 4ml/kg (HS); (5) shock and resuscitation with 7.5% hypertonic saline/6% Dextran 70 4ml/kg (HSD). Hemorheological characteristics were measured at 60min after resuscitation. Results: Results showed that NS resuscitation deteriorated red blood cell (RBC) deformability compared with the SHOCK group. The HS group showed improved RBC deformability compared with the NS group, although the differences were not statistically significant. There were significant improvements of RBC deformability at all shear rates in the HSD group compared with the NS group. Whole blood and plasma viscosities decreased significantly in the SHOCK group compared with the SHAM group. At shear rates of 60 and 150s−1, the NS group decreased whole blood viscosity compared with the SHOCK group. The HSD group showed elevated plasma viscosity compared with the SHOCK, NS and HS groups. Conclusion: These results suggested that at the early stage of hemorrhagic shock resuscitation, hypertonic–hyperoncotic resuscitation could improve RBC deformability compared with isotonic crystalloid resuscitation. Dextran 70 could elevate plasma viscosity to nearly baseline level. These effects of hypertonic–hyperoncotic resuscitation could be beneficial to maintain microcirculation. [Copyright &y& Elsevier]

Background Oxidative stress induced by hemorrhagic shock (HS) is known to initiate a systemic inflammatory response, which leads to subsequent acute lung injury. This study is aimed to assess the efficacy of exendin-4 (Ex-4) in attenuating lung injury in a rat model of HS and resuscitation (HS/R). Methods HS was induced in sodium pentobarbital–anesthetized adult male Wistar rats by withdrawing blood to maintain a mean arterial pressure of 30-35 mm Hg for 50 min. Then, the animals received Ex-4 (5 μg/kg) or vehicle (saline) intravenously and were resuscitated with a volume of normal saline 1.5 times that of the shed blood volume. Mean arterial pressure was measured throughout the experiment, and acid-base status, oxidative stress, inflammation, and lung injury were evaluated at 2 h after resuscitation. Results Ex-4 infusion reduced the methemoglobin content, the malondialdehyde content, the myeloperoxidase activity, and the expression of tumor necrosis factor-α and interleukin-6 in the lungs. The histologic injury was also markedly decreased in the Ex-4 group compared with the vehicle group. Conclusions Ex-4 ameliorates the oxidative stress, inflammatory response, and subsequent acute lung injury occurring after HS/R. Although future studies are required to elucidate the underlying mechanism, our results indicate that Ex-4 infusion may be a promising strategy for improving lung injury in the treatment of HS. [ABSTRACT FROM AUTHOR]

Hemorrhagic shock/resuscitation involves overwhelming reactive oxygen species (ROS) that cause oxidative stress, inflammation, and subsequent tissue injury. We investigated the effects of the potent antioxidant carboxyfullerene (C 3 ) on acute liver injury during hemorrhage shock/resuscitation. C 3 infusion reduced the alanine aminotransferase (ALT) activity, methemoglobin content, malondialdehyde content, myeloperoxidase activity and expression levels of tumor necrosis factor -α and interleukin-6; it increased superoxide dismutase activity in the liver. The histologic injury score and apoptotic index were also markedly decreased after C 3 treatment compared with the vehicle group. Additionally, C 3 -treated rats showed a significant decrease in nuclear factor-κB DNA binding capacity, which was preceded by reduced phosphorylation of the nuclear factor κB (NF-κB) p65 subunit in the liver. C 3 nanoparticles ameliorate oxidative stress, the inflammatory response, and subsequent acute liver injury after hemorrhagic shock/resuscitation. These protective effects appear to be mediated through the inhibition of the nuclear factor-κB pathway. C 3 treatment may be a promising strategy to improve tissue injury in hemorrhagic shock/resuscitation. [ABSTRACT FROM AUTHOR]