Post-ischaemic organ dysfunction: A review

Homer‐Vanniasinkam, Shervanthi; Crinnion, J. N.; Gough, Michael

doi:10.1016/s1078-5884(97)80191-8

Cited by 106 publications

(76 citation statements)

References 76 publications

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“…A severe complication of GI/R, most likely due to changes in intestinal permeability, is multiorgan failure, also referred to as remote or secondary organ injury (2,4,5). Significant elevations of serum FITC-dextran concentrations were observed in WT and C1q KO, but not C2/fB KO, mice after GI/R.…”

Section: Discussionmentioning

confidence: 99%

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Gastrointestinal Ischemia-Reperfusion Injury Is Lectin Complement Pathway Dependent without Involving C1q

Hart

Ceonzo

Shaffer

et al. 2005

The Journal of Immunology

182

163

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Complement activation plays an important role in local and remote tissue injury associated with gastrointestinal ischemia-reperfusion (GI/R). The role of the classical and lectin complement pathways in GI/R injury was evaluated using C1q-deficient (C1q KO), MBL-A/C-deficient (MBL-null), complement factor 2- and factor B-deficient (C2/fB KO), and wild-type (WT) mice. Gastrointestinal ischemia (20 min), followed by 3-h reperfusion, induced intestinal and lung injury in C1q KO and WT mice, but not in C2/fB KO mice. Addition of human C2 to C2/fB KO mice significantly restored GI/R injury, demonstrating that GI/R injury is mediated via the lectin and/or classical pathway. Tissue C3 deposition in C1q KO and WT, but not C2/fB KO, mice after GI/R demonstrated that complement was activated in C1q KO mice. GI/R significantly increased serum alanine aminotransferase, gastrointestinal barrier dysfunction, and neutrophil infiltration into the lung and gut in C1q KO and WT, but not C2/fB KO, mice. MBL-null mice displayed little gut injury after GI/R, but lung injury was present. Addition of recombinant human MBL (rhuMBL) to MBL-null mice significantly increased injury compared with MBL-null mice after GI/R and was reversed by anti-MBL mAb treatment. However, MBL-null mice were not protected from secondary lung injury after GI/R. These data demonstrate that C2 and MBL, but not C1q, are necessary for gut injury after GI/R. Lung injury in mice after GI/R is MBL and C1q independent, but C2 dependent, suggesting a potential role for ficolins in this model.

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Section: Discussionmentioning

confidence: 99%

“…Clinically, GI/R is commonly associated with sepsis, hemorrhagic shock, vascular surgery, small bowel transplantation (2,3), and multiple organ failure (4,5). The complement system is a key component in GI/R, resulting in local intestinal and secondary tissue injury (6 -11).…”

Section: G Astrointestinal Ischemia-reperfusion (Gi/r)mentioning

confidence: 99%

Gastrointestinal Ischemia-Reperfusion Injury Is Lectin Complement Pathway Dependent without Involving C1q

Hart

Ceonzo

Shaffer

et al. 2005

The Journal of Immunology

182

163

View full text Add to dashboard Cite

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“…GASTROINTESTINAL ISCHEMIA-reperfusion (GI/R) is a common clinical problem in the settings of sepsis, hemorrhagic shock, vascular surgery, and small bowel transplantation (17,21). GI/R causes gut dysfunction characterized by histological evidence of impaired gut motility, increased intestinal permeability, and mucosal injury (18).…”

mentioning

confidence: 99%

“…The exogenous administration of SOD in a rat model of gastric ischemia-reperfusion increases luminal NO levels, suggesting that SOD-mediated protection is afforded by decreasing the local concentra-tion of superoxide that is available to react with NO (53). Because endogenous SOD levels are not adequate to quench the sudden surge in superoxide levels after reperfusion, attention has been directed toward the delivery of exogenous SOD (21,39). To date, factors mediating the regulation of endogenous SOD after ischemia-reperfusion have not been identified.…”

mentioning

confidence: 99%

Role for complement in mediating intestinal nitric oxide synthase-2 and superoxide dismutase expression

Montalto

Hart

Jordan

et al. 2003

American Journal of Physiology-Gastrointestinal and Liver Physi

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. Role for complement in mediating intestinal nitric oxide synthase-2 and superoxide dismutase expression. Am J Physiol Gastrointest Liver Physiol 285: G197-G206, 2003. First published March 13, 2003 10.1152/ajpgi.00029.2003.-Inducible nitric oxide synthase (iNOS) and superoxide dismutase (SOD) play an important role in the pathology of ischemia-reperfusion. This study sought to determine if the proinflammatory effects of complement modulate iNOS and SOD in the rat after gastrointestinal ischemia and reperfusion (GI/R). An inhibitory or noninhibitory anti-complement component 5 (C5) monoclonal antibody (18A or 16C, respectively) was administered before GI/R. RT-PCR revealed a significant increase in intestinal iNOS mRNA compared with sham after GI/R that was attenuated significantly by 18A. Immunohistochemistry demonstrated increased iNOS protein expression within the intestinal crypts after GI/R. Cu/Zn SOD (mRNA and protein) was unaffected by GI/R, whereas Cu/Zn SOD activity was reduced significantly. Mn SOD protein expression was decreased significantly by GI/R. Anti-C5 preserved Cu/Zn SOD activity and Mn SOD protein expression. Staining for nitrotyrosine showed that anti-C5 treatment reduced protein nitration in the reperfused intestine. Immunohistochemistry demonstrated prominent phosphorylated (p) inhibitory factor-B (I B)-␣ staining of intestinal tissue after GI/R, whereas anti-C5 reduced p-I B-␣ expression. These data indicate that complement may mediate tissue damage during GI/R by increasing intestinal iNOS and decreasing the activity and protein levels of Cu/Zn SOD and Mn SOD, respectively. ischemia-reperfusion; inhibitory factor-B; interleukin-1␤ GASTROINTESTINAL ISCHEMIA-reperfusion (GI/R) is a common clinical problem in the settings of sepsis, hemorrhagic shock, vascular surgery, and small bowel transplantation (17, 21). GI/R causes gut dysfunction characterized by histological evidence of impaired gut motility, increased intestinal permeability, and mucosal injury (18). Numerous mediators have been implicated in GI/R injury, including cytokines (8,15,43,54,55) NF-B is maintained in a latent form in the cytoplasm of cells where it is complexed to inhibitory factor-B (I B) proteins (24). Upon activation of NF-B, I B is phosphorylated (p) by I B kinases at two conserved serine residues in the NH 2 terminus, which targets the protein for ubiquination and degradation by the proteosome. This rapidly frees NF-B to translocate to the nucleus, where it upregulates the transcription of a variety of adhesion molecules (ICAM-1 and VCAM-1), cytokines (TNF, IL-1, and IL-6), and enzymes (iNOS; see Refs. 24 and 37).NO has been implicated as a mediator of tissue damage in several models of intestinal disease, including reperfusion injury (26,47,48). NO can be produced by three nitric oxide synthase (NOS) isoforms (neuronal NOS, iNOS, and endothelial NOS). Specific inhibition of iNOS has been shown to attenuate NO production significantly and decrease intestinal injury, indicating that iNOS mediates the excessive p...

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“…Once critical situations such as shock, multiple organ dysfunction syndrome (MODS), and systemic inflammatory response syndrome (SIRS) occur, skeletal muscle and the gastrointestinal system fall into hypoperfusion state earlier than other important organs. It is thought that ischemia is caused by microvascular dysfunction (20,21). Therefore, the higher the H-FABP level, the greater the degree of invasiveness of myocardial and/or skeletal muscle damage and the poorer the prognosis.…”

Section: Discussionmentioning

confidence: 99%

Relationship between Heart-Type Fatty Acid-Binding Protein Levels and the Risk of Death in Patients with Serious Condition on Arrival at the Emergency Department

et al. 2005

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Objective Although heart-type fatty acid-binding protein (H-FABP) is a cardiac marker useful for early diagnosis of acute myocardial infarction (AMI), few data are available on its prognostic value. The objective of this study is to clarify the prognostic value of H-FABP in patients with a serious condition. Methods and PatientsWe conducted a prospective study of 617 patients who presented to the emergency department with a serious condition. The H-FABP levels on arrival at the emergency department were divided into four groups using their quartiles. The endpoint was death from any causes in-hospital.Results H-FABP ranged from 1.2 to 2,300 ng/ml, with a median of 19.9 ng/ml, a 25%-value of 6.7 ng/ml and 75%-value of 54.0 ng/ml. The unadjusted rate of the mortality increased progressively with increasing H-FABP quartile point (11% for quartile-I, 22% for quartile-II, 36% for quartile-III, and 38% for quartile-IV; p<0.001). After adjustment for age, gender, systolic blood pressure and the presence or absence of cardiovascular disease, H-FABP was the independent factor to predict the mortality.Conclusion H-FABP has proven to be an independent factor for prognosis in patients with a serious condition on arrival at the emergency department. (Internal Medicine 44: 1039-1045, 2005)

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Post-ischaemic organ dysfunction: A review

Cited by 106 publications

References 76 publications

Gastrointestinal Ischemia-Reperfusion Injury Is Lectin Complement Pathway Dependent without Involving C1q

Gastrointestinal Ischemia-Reperfusion Injury Is Lectin Complement Pathway Dependent without Involving C1q

Role for complement in mediating intestinal nitric oxide synthase-2 and superoxide dismutase expression

Relationship between Heart-Type Fatty Acid-Binding Protein Levels and the Risk of Death in Patients with Serious Condition on Arrival at the Emergency Department

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