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Value of fever versus hypothermia in severe sepsis
Author(s) -
Liu Elaine,
Corrigan Joshua J,
Lewis Kevin,
AlSaffar Hiba,
Krall Catherine M,
Singh Anju,
Kulchitsky Vladimir A,
Simons Christopher T,
Petersen Scott R,
Musteata Florin M,
Bakshi Chandra S,
Romanovsky Andrej A,
Sellati Timothy J,
Steiner Alexandre A
Publication year - 2013
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.27.1_supplement.868.4
Subject(s) - hypothermia , medicine , sepsis , systemic inflammation , inflammation , pathophysiology , hypoxia (environmental) , shivering , anesthesia , immunology , pharmacology , chemistry , organic chemistry , oxygen
A switch from fever to hypothermia occurs in severe cases of systemic inflammation, but its impacts on the pathophysiology and outcome of this malady are unknown. This question was addressed in the present study. Following administration of LPS (5 or 18 mg/kg) or E. coli (5 × 10 9 or 1 × 10 10 CFU/kg), hypothermia developed in rats exposed to a mildly cool environment, but not in rats exposed to a warm environment; only fever was revealed in the warm environment. Development of hypothermia instead of fever suppressed endotoxemia and the lung infiltration by neutrophils in E. coli ‐infected rats, but not in LPS‐injected rats. These potentially beneficial effects came with costs, as hypothermia increased the liver bacterial burden. Furthermore, hypotensive responses to LPS or E. coli were exaggerated in hypothermic rats. This exaggeration, however, occurred independently of changes in inflammatory mediators and was not necessarily associated with tissue hypoxia. Despite possible costs, development of hypothermia lessened abdominal organ injury and reduced overall mortality rates in both the E. coli and LPS models. It is concluded that naturally occurring hypothermia may be more advantageous than fever in severe forms of aseptic (LPS‐induced) and septic ( E. coli ‐induced) systemic inflammation. Support: AHA, NIH, FAPESP.