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Endotoxemia-induced lymphocyte apoptosis is augmented by a hyperinsulinemic-euglycemic clamp.
Jeppe Sylvest Nielsen1, Anders Larsson, Vibeke Brix-Christensen
1Department of Anesthesiology and Intensive Care, Aarhus University Hospital, Nørrebrogade 44, DK-8000 Aarhus, Denmark.
Anesthesiology
|March 26, 2005
Summary
Sepsis and endotoxemia increase lymphocyte apoptosis, contrary to expectations. A hyperinsulinemic-euglycemic clamp (HEC) further augmented this apoptosis, worsening immune suppression in pigs.
Area of Science:
- Immunology
- Critical Care Medicine
Background:
- Sepsis and endotoxemia are linked to lymphocyte apoptosis, exacerbating immune suppression.
- Normalization of blood glucose is known to improve outcomes in critically ill patients.
Purpose of the Study:
- To investigate the effects of endotoxemia and a hyperinsulinemic-euglycemic clamp (HEC) on lymphocyte apoptosis in pigs.
- To determine if insulin and normoglycemia inhibit lymphocyte apoptosis during endotoxemia.
Main Methods:
- 38 pigs were divided into four groups: control, HEC, endotoxemia (lipopolysaccharide infusion), and combined HEC and endotoxemia.
- Lymphocyte apoptosis in spleen tissue was analyzed using stereologic methods and immunohistochemistry for active caspase-3, CD21 (B cells), and CD3epsilon (T cells).
- Statistical analysis involved two-way ANOVA to examine interactions between endotoxemia and the clamp.
Main Results:
- Endotoxemia significantly increased B and T lymphocyte apoptosis in the spleen, independent of the HEC.
- The hyperinsulinemic-euglycemic clamp (HEC) also independently increased B and T lymphocyte apoptosis.
- Contrary to the hypothesis, the HEC augmented lymphocyte apoptosis during acute endotoxemia.
Conclusions:
- Both endotoxemia and HEC increase lymphocyte apoptosis in the spleen.
- The study's hypothesis that insulin and normoglycemia would inhibit lymphocyte apoptosis was not supported; HEC augmented apoptosis during endotoxemia.