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Inotropes inhibit endothelial cell surface adhesion molecules induced by interleukin-1beta
J D Fortenberry1, A R Huber, M L Owens
1Department of Pediatrics, Emory University School of Medicine, Atlanta, GA, USA.
Critical Care Medicine
|February 1, 1997
Summary
Amrinone and dopamine, inotropes that increase cyclic adenosine 3
Area of Science:
- Cellular biology
- Immunology
- Pharmacology
Background:
- Leukocyte-endothelial cell interactions are crucial in sepsis-induced organ failure.
- Increased cyclic adenosine 3',5'-monophosphate (cAMP) may inhibit endothelial adhesion molecules like E-selectin and VCAM-1.
Purpose of the Study:
- To investigate if clinically relevant concentrations of amrinone and dopamine inhibit cytokine-stimulated endothelial adhesion proteins.
- To test the hypothesis that inotropes increasing cAMP can reduce endothelial activation.
Main Methods:
- In vitro study using human umbilical vein endothelial cells and whole blood neutrophils.
- Cells were pretreated with amrinone or dopamine, stimulated with IL-1beta, and adhesion molecules (E-selectin, VCAM-1, ICAM-1) were measured via flow cytometry.
- Neutrophils were tested for CD11b upregulation after inotrope pretreatment and stimulation.
Main Results:
- IL-1beta significantly increased E-selectin, VCAM-1, and ICAM-1 on endothelial cells.
- Amrinone significantly reduced endothelial E-selectin, ICAM-1, and VCAM-1 at therapeutic concentrations.
- Dopamine inhibited E-selectin at relevant concentrations, but inotropes did not affect neutrophil CD11b upregulation.
Conclusions:
- Amrinone and dopamine, at clinically relevant concentrations, inhibit IL-1beta-induced increases in endothelial cell adhesion molecules in vitro.
- Further research is needed to explore the mechanisms and in vivo efficacy of inotropes as anti-inflammatory agents.