Disease relevance of Shock, Traumatic

• Treatment of tumor necrosis factor alpha (TNF-alpha)-primed mice with anti-Ly-6G antibodies reproduced many of the features of septic or traumatic shock including microvessel obstruction and coagulation, severe vasculitis, respiratory difficulties, and vascular leakage [1].
• CONCLUSIONS: High adenosine plasma concentrations are found in patients with septic shock but not during traumatic shock, or in healthy volunteers [2].
• An impairment of NO formation by the ecNOS has been demonstrated in various models of traumatic shock, whereas there is good experimental evidence supporting the hypothesis that an enhanced formation of NO contributes to the pathophysiology of experimental thermal injury and anaphylactic shock [3].
• We observed previously that allopurinol, which was used for the treatment of gout, had a life saving effect after experiment on traumatic shock rats and hemorrhagic shock rabbits [4].
• These properties result in a depletion of plasma fibronectin in certain clinical situations, such as disseminated intravascular coagulation (DIC), traumatic shock and severe burns [5].

High impact information on Shock, Traumatic

• Effect of recombinant soluble P-selectin glycoprotein ligand-1 on leukocyte-endothelium interaction in vivo. Role in rat traumatic shock [6].
• These results indicate that PDT-induced lethality is consistent with a traumatic shock syndrome and suggest that endogenous vasoactive mediators of shock such as prostaglandins, thromboxanes, and histamine are associated with the lethality induced by localized PDT in mice [7].
• Neutrophil CD18 expression and blockade after traumatic shock and endotoxin challenge [8].
• CONCLUSIONS: These results suggest that TF may play an important role in the pathophysiology of severe trauma and that regulatory elements AP-1 and NF-kappaB may be involved in the regulation of TF mRNA expression in traumatic shock [9].
• In addition, PGE1 significantly attenuated plasma MDF activity during traumatic shock (58 +/- 10 vs. 27 +/- 7 U/ml), vehicle vs. drug, respectively (p less than .02) [10].

Chemical compound and disease context of Shock, Traumatic

• Beneficial effects of prostaglandin E1 infusion in experimental traumatic shock [10].
• Protective effects of KW-3635, a novel thromboxane A2 antagonist, in murine traumatic shock [11].
• Increased plasma D-lactate is associated with the severity of hemorrhagic/traumatic shock in rats [12].
• Analysis of potential risks associated with 7.5% sodium chloride resuscitation of traumatic shock [13].
• A case of traumatic shock complicated by methamphetamine intoxication [14].

Biological context of Shock, Traumatic

• Our results suggest that complement activation plays an important role in tissue injury associated with trauma, and that its inhibition at an early step in the complement cascade through a C1 esterase inhibitor is beneficial in rats experiencing traumatic shock [15].
• The present results provide evidence for a P-selectin-dependent mechanism that enhances TF gene expression in traumatic shock [16].
• Our results suggest that a combination of membrane stabilizing and anti-proteolytic effects and inhibition of platelet aggregation may mediate the protective effects of CG-4203 in traumatic shock [17].
• RESULTS: We found that in the experimental animals the RBC aggregability was sharply increased, the RBC deformability significantly decreased, while the systemic hematocrit underwent considerable lowering during the traumatic shock [18].

Anatomical context of Shock, Traumatic

• Moreover, superior mesenteric artery rings isolated from rats in traumatic shock relaxed to the endothelium-dependent vasodilator acetylcholine only 21 +/- 6% of U-46619 induced contraction [19].
• Decreased activity of NADPH oxidase in alveolar macrophages as a result of traumatic shock [20].

Gene context of Shock, Traumatic

• Pulmonary tissue factor mRNA expression during murine traumatic shock: effect of P-selectin blockade [16].
• Because there is evidence that TF is regulated by a P-selectin dependent gene, we examined TF mRNA expression in the lungs during murine traumatic shock in the presence and absence of recombinant soluble P-selectin glycoprotein ligand-1 (rsPSGL.Ig) by using ribonuclease protection assays [16].
• In addition, TRH did not attenuate any of the biochemical indices of the severity of the shock state (i.e., plasma amino-nitrogen concentrations, or plasma cathepsin D and MDF activities) nor did it improve survival time in traumatic shock (2.8 +/- 0.4 vs. 2.0 +/- 0.2 hours) [21].
• Beneficial effects of C1 esterase inhibitor in murine traumatic shock [15].
• We have investigated TRH (2 mg/kg bolus plus 2 mg/kg/hr infusion) in both hemorrhagic (cats) and traumatic shock (rats) [21].

Analytical, diagnostic and therapeutic context of Shock, Traumatic

• The effect of drug therapy without volume restoration in experimental traumatic shock. Part II. Pethidine [22].
• A double-blind clinical study was performed in ten Italian intensive care units on 115 patients with septic, cardiac of traumatic shock, by using acetyl-L-carnitine infusion for 12 hours, with a previous single bolus intravenously [23].

References