Disease relevance of Shock, Hemorrhagic

• Hemorrhagic shock primes for increased expression of cytokine-induced neutrophil chemoattractant in the lung: role in pulmonary inflammation following lipopolysaccharide [1].
• Cyclosporin blocks NF-kappaB activation and protects against hypovolemic hemorrhagic shock [2].
• Recent evidence shows that melatonin is a scavenger of oxyradicals and peroxynitrite and exerts protective effects in septic shock, hemorrhagic shock and inflammation [3].
• In conclusion, the pathogen exclusion properties of both Lactobacillus strains and the reduction of endotoxin-induced inflammation by their DNA in vitro are not prerequisites for a beneficial effect of probiotic therapy on gut barrier function following hemorrhagic shock [4].
• OBJECTIVE: To determine properties of acadesine, the prototype adenosine regulating agent, in an experimental model in which abdominal sepsis is superimposed onto hemorrhagic shock [5].

Psychiatry related information on Shock, Hemorrhagic

• The purpose of this study was to examine the effects of matrix metalloproteinase inhibitor (MMPI) (British Biotech 1101) in vivo on hepatic integrity in a rat model of hemorrhagic shock [6].

High impact information on Shock, Hemorrhagic

• Thyrotropin-releasing hormone improves cardiovascular function in experimental endotoxic and hemorrhagic shock [7].
• Here we postulated that increased endothelial expression of P-selectin in the microvasculature would play an essential role in initiating the inflammatory signaling of hemorrhagic shock [8].
• We have previously demonstrated that the inducible nitric oxide synthase (iNOS) is expressed during hemorrhagic shock [9].
• Protective role of endogenous carbon monoxide in hepatic microcirculatory dysfunction after hemorrhagic shock in rats [10].
• Subepithelial tissue pH of rat gastric mucosa exposed to luminal acid, barrier breaking agents, and hemorrhagic shock [11].

Chemical compound and disease context of Shock, Hemorrhagic

• Subcutaneously administered propantheline bromide (30 mg/kg) or cimetidine (100 mg/kg) had no effect on gastric lesion and PD reduction caused by hemorrhagic shock [12].
• Intravenous infusion of NaHCO3 (0.5 M) also significantly prevented the lesion with a concomitant suppression of the PD reduction in response to hemorrhagic shock, but these effects were significantly reversed by pretreatment of the animals with acetazolamide (50 mg/kg) [12].
• Plasma adenosine concentrations doubled when rats were subjected to 90 min of profound hemorrhagic shock [13].
• This study investigates the role of nitric oxide (NO) and the induction of a calcium-independent NO synthase (NOS) in development of vascular hyporeactivity to norepinephrine (NE) and vascular decompensation associated with hemorrhagic shock (HS) in the anesthetized rat [14].
• Vascular hyporeactivity to vasoconstrictor agents and hemodynamic decompensation in hemorrhagic shock is mediated by nitric oxide [14].

Biological context of Shock, Hemorrhagic

• Thus, activation of P-selectin protein on the microvascular endothelium is essential for the initial upregulation of the inflammatory response occurring in hemorrhagic shock [8].
• CONCLUSIONS: These results suggest that hemorrhagic shock may lead to early bacterial translocation in the intestinal wall and transient access of gut-derived LPS and LPS-induced mediators into the circulation predominantly via the portal circulation [15].
• Lymphatic division before hemorrhagic shock prevented shock-induced increases in lung permeability to Evans blue dye and alveolar apoptosis and reduced pulmonary MPO levels [16].
• CONCLUSIONS: Using HTS instead of RL to resuscitate hemorrhagic shock diminishes vascular permeability in vivo by altering PMN-EC interactions [17].
• Endothelin blockade lowers total peripheral resistance in hemorrhagic shock recovery [18].

Anatomical context of Shock, Hemorrhagic

• Because of evidence that Metiamide, an H2-receptor antagonist, strongly inhibits gastric acid secretion, the present study was designed to test the hypothesis that Metiamide will prevent bile salt-induced stress ulcers during hemorrhagic shock [19].
• Airspace instillation of dibutyryl cAMP, a stable analog of cAMP, restored the normal fluid transport capacity of the alveolar epithelium after prolonged hemorrhagic shock, whereas direct stimulation of adenyl cyclase by forskolin had no effect [20].
• In rats submitted to hemorrhagic shock, pretreatment with hemoglobin (Hb) increased HO-1 mRNA expression in macrophages [21].
• A free radical scavenger, edaravone (MCI-186), diminishes intestinal neutrophil lipid peroxidation and bacterial translocation in a rat hemorrhagic shock model [22].
• OBJECTIVE: To determine the effects of a hydroxyethyl starch-deferoxamine conjugate on hepatic microcirculation in an isobaric, anesthetized rat model of hemorrhagic shock and asanguineous resuscitation [23].

Gene context of Shock, Hemorrhagic

• Chymostatin, a serine protease inhibitor that does not prevent the activation of NF-kappaB, had no effect on the organ injury/failure caused by hemorrhagic shock [24].
• We showed that antecedent hemorrhagic shock enhanced LPS-induced TLR2 upregulation in AMphi [25].
• Hemorrhagic shock resulted in increased plasma and myocardial TNF-alpha (4.9- and 4.5-fold, respectively) at 30 min and induced myocardial contractile depression at 4 h [26].
• Prolonged periods of hemorrhagic shock are associated with the induction of a calcium-independent isoform of NOS in a variety of organs and in the vascular smooth muscle [27].
• Signaling for myocardial depression in hemorrhagic shock: roles of Toll-like receptor 4 and p55 TNF-alpha receptor [26].
• Exposure to CpG-ODN prior to hemorrhagic shock significantly augmented shock-induced release of IFN-gamma, tumor necrosis factor-alpha (TNF-alpha) (P < 0.05), interleukin (IL)-6 (P < 0.05), and nitrite levels (P < 0.05), while there was a defective IL-10 response (P < 0.05) [28].

Analytical, diagnostic and therapeutic context of Shock, Hemorrhagic

• The present study evaluated the effect of the benzothiazepine Ca2+ channel blocker diltiazem (DZ) on altered hepatocellular Ca2+ regulation and oxidant injury during hemorrhagic shock/resuscitation [29].
• These data show that the attempt of the rat splanchnic bed to compensate for hemorrhagic shock by increasing release of PGI2 (potent vasodilator) was abolished during reperfusion of blood [30].
• Effect of glucagon and blood transfusion on liver metabolism in hemorrhagic shock [31].
• We then studied the influence of cold versus warm gastric lavage on the severity of gastric mucosal injury and on the rate of breakdown of gastric mucosal adenosine phosphates during hemorrhagic shock [32].
• An increased understanding of the role played by Nramp1 is particularly important in the liver, as this organ is subjected to a wide variety of injuries during hemorrhagic shock, partial resections, and transplantation [33].

References