Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2011-6-14
pubmed:abstractText
Ex vivo circuits are commonly used to evaluate biomaterials or devices used for extracorporeal blood purification. However, various aspects of the ex vivo circuit, apart from the circuit materials, may affect inflammation and coagulation. One such aspect is temperature. The aim of this study was to evaluate the influence of different blood temperature conditions on inflammation parameters in an ex vivo circuit. Blood was collected from 20 healthy volunteers and run through three different experimental conditions for 4 h: a miniaturized ex vivo extracorporeal circuit equipped with a blood warmer set to 37°C, the same circuit without the warmer (23°C), and a tube placed in an incubator at 37°C (no circuit). We measured the granulocyte macrophage colony-stimulating factor, the tumor necrosis factor, and the interleukin (IL)-1?, IL-6, IL-8, and IL-10 concentrations at baseline, 15, 60, 120, and 240 min. Human leukocyte antigen (HLA)-DR, CD11b, CD11a, CD62L, tumor necrosis factor alpha converting enzyme, annexin V expression, and NFkB DNA binding were measured in monocytes and polymorphonuclear neutrophils (PMNs) using flow cytometry at baseline, 120 min, and 240 min. While cytokine production over time was very slight at room temperature, levels increased by more than 100-fold in the two heated conditions. Differences in the expression of some surface markers were also observed between the room temperature circuit and the two heated conditions (CD11b PMN, P < 0.0001; HLA-DR Mono, P=0.0019; and CD11a PMN, P<0.0001). Evolution of annexin V expression was also different over time between the three groups (P=0.0178 for monocytes and P=0.0011 for PMNs). A trend for a greater NFkB DNA binding was observed in the heated conditions. Thus, for ex vivo studies using extracorporeal circuits, heating blood to maintain body temperature results in significant activation of inflammatory cells while hypothermia (room temperature) seems to suppress the leukocyte response. Both strategies may lead to erroneous conclusions, possibly masking some specific effects of the device being studied. Investigators in this field must be aware of the fact that blood temperature is a crucial confounding parameter and the type of "background noise" they will face depending on the strategy adopted.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
1525-1594
pubmed:author
pubmed:copyrightInfo
© 2011, Copyright the Authors. Artificial Organs © 2011, International Center for Artificial Organs and Transplantation and Wiley Periodicals, Inc.
pubmed:issnType
Electronic
pubmed:volume
35
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
593-601
pubmed:dateRevised
2011-10-26
pubmed:meshHeading
pubmed:year
2011
pubmed:articleTitle
What blood temperature for an ex vivo extracorporeal circuit?
pubmed:affiliation
The CRISMA (Clinical Research, Investigation, and Systems Modeling of Acute Illness) Laboratory, Department of Critical Care Medicine, University of Pittsburgh Medical Center, Pittsburgh, PA, USA.
pubmed:publicationType
Journal Article, Research Support, N.I.H., Extramural