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The relationship between cardiovascular collapse in Methicillin‐resistant Staphylococcus aureus‐induced sepsis and excessive expression of reactive nitrogen and oxidative species
Author(s) -
Jonkam Collette,
Zhu Yong,
Traber Daniel,
Bansal Kamna,
Rehberg Sebastian,
Sousse Linda,
Traber Lillian,
Enkhbaatar Perenlei
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.628.4
Subject(s) - sepsis , oxidative stress , medicine , vascular permeability , nitric oxide , oncotic pressure , reactive nitrogen species , staphylococcus aureus , c reactive protein , anesthesia , pharmacology , immunology , inflammation , biology , bacteria , albumin , genetics
MRSA Sepsis remains a serious problem. Increased microvascular permeability is associated with high mortality in septic patients. Currently, we investigated the relationship between microvascular hyperpermeability and tissue expression of oxidative and reactive nitrogen species in MRSA sepsis. METHODS Sheep were surgically prepared and randomized to the groups: Control (non injured, n=6), and MRSA (injured, n=8). Injury consisted of smoke insufflation and instillation of 2‐5 x 10^11 CFU of live MRSA into the lungs. All animals were resuscitated with Lactated Ringer's solution. RESULTS Cardiovascular variables were stable in control animals. MRSA septic animals developed hypotensive and hyperdynamic sepsis, severe microvascular hyperpermeability (significantly increased flank lymph flow and permeability index, decreased plasma protein and oncotic pressure, and increased net fluid balance) compared to the control. The MRSA group also showed significantly higher plasma nitrate/nitrite levels, heart tissue inducible, endothelial, and neuronal nitric oxide synthase mRNA expressions, 3‐nitrothyrosine, and poly‐ADP ribose protein expressions compared to the control. CONCLUSION The data provides evidence that cardiovascular collapse in MRSA sepsis is mediated by excessive formation of reactive radicals and subsequent microvascular hyperpermeability to fluid and to protein.