RGD Reference Report - Hemodynamic resuscitation with arginine vasopressin reduces lung injury after brain death in the transplant donor. - Rat Genome Database

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Hemodynamic resuscitation with arginine vasopressin reduces lung injury after brain death in the transplant donor.

Authors: Rostron, Anthony J  Avlonitis, Vassilios S  Cork, David M W  Grenade, Danielle S  Kirby, John A  Dark, John H 
Citation: Rostron AJ, etal., Transplantation. 2008 Feb 27;85(4):597-606. doi: 10.1097/TP.0b013e31816398dd.
RGD ID: 329901924
Pubmed: PMID:18347540   (View Abstract at PubMed)
DOI: DOI:10.1097/TP.0b013e31816398dd   (Journal Full-text)


BACKGROUND: The autonomic storm accompanying brain death leads to neurogenic pulmonary edema and triggers development of systemic and pulmonary inflammatory responses. Neurogenic vasoplegia exacerbates the pulmonary injury caused by brain death and primes the lung for ischemia reperfusion injury and primary graft dysfunction in the recipient. Donor resuscitation with norepinephrine ameliorates the inflammatory response to brain death, however norepinephrine has deleterious effects, particularly on the heart. We tested the hypothesis that arginine vasopressin is a suitable alternative to norepinephrine in managing the hypotensive brain dead donor.
METHODS: Brain death was induced in Wistar rats by intracranial balloon inflation. Pulmonary capillary leak was estimated using radioiodinated albumin. Development of pulmonary edema was assessed by measurement of wet and dry lung weights. Cell surface expression of CD11b/CD18 by neutrophils was determined using flow cytometry. Enzyme-linked immunosorbent assays were used to measure the levels of TNFalpha, IL-1beta, CINC-1, and CINC-3 in serum and bronchoalveolar lavage. Quantitative reverse-transcription polymerase chain reaction was used to determine the expression of cytokine mRNA (IL-1beta, CINC-1 and CINC-3) in lung tissue.
RESULTS: There was a significant increase in pulmonary capillary permeability, wet/dry lung weight ratios, neutrophil integrin expression and pro-inflammatory cytokines in serum (TNFalpha, IL-1beta, CINC-1 and CINC-3), bronchoalveolar lavage (TNFalpha and IL-1beta) and lung tissue (IL-1beta and CINC-1) in braindead animals compared to controls. Correction of neurogenic hypotension with either arginine vasopressin or norepinephrine limits edema, reduces pulmonary capillary leak, and modulates systemic and pulmonary inflammatory responses to brain death.
CONCLUSIONS: Arginine vasopressin and norepinephrine are equally effective in treating the hypotensive pulmonary donor in this rodent model.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
ITGAMHumanBrain Death  ISOItgam (Rattus norvegicus)protein:increased expression:neutrophil (rat)RGD 
ItgamRatBrain Death  IEP protein:increased expression:neutrophil (rat)RGD 
ItgamMouseBrain Death  ISOItgam (Rattus norvegicus)protein:increased expression:neutrophil (rat)RGD 

Gene Ontology Annotations    Click to see Annotation Detail View

Cellular Component

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
ItgamRatcell surface  IDA  RGD 

Objects Annotated

Genes (Rattus norvegicus)
Itgam  (integrin subunit alpha M)

Genes (Mus musculus)
Itgam  (integrin alpha M)

Genes (Homo sapiens)
ITGAM  (integrin subunit alpha M)


Additional Information