Abstract | OBJECTIVES: METHODS: RESULTS: After normothermic ischemia both strains had a similar mortality (wild-type, 22.9%; knock-out, 15.4%), which was completely abolished by hypothermia. Endothelial barrier function was disturbed after normothermic ischemia in both wild-type and knock-out mice. Mild hypothermia significantly reduced pulmonary Evans blue extravasation in wild-type mice, but not in knock-out mice. Myeloperoxidase activity increased after normothermic ischemia to the same degree in both strains. This response was significantly attenuated by hypothermia in wild-type mice, but not in knock-out mice. In wild-type mice, endothelial nitric oxide synthase expression and phosphorylation were higher after hypothermic ischemia than after normothermic ischemia. No effect of ischemia on expression of inducible nitric oxide synthase was found in wild-type or knock-out mice. CONCLUSION:
|
Authors | Li Zhang, Sanjeev Kumar, Alexander Kaminski, Cornelius Kasch, Christoph Sponholz, Christof Stamm, Yury Ladilov, Gustav Steinhoff |
Journal | The Journal of thoracic and cardiovascular surgery
(J Thorac Cardiovasc Surg)
Vol. 131
Issue 5
Pg. 969-74
(May 2006)
ISSN: 1097-685X [Electronic] United States |
PMID | 16678577
(Publication Type: Evaluation Study, Journal Article)
|
Chemical References |
- Peroxidase
- Nitric Oxide Synthase Type II
- Nitric Oxide Synthase Type III
|
Topics |
- Animals
- Capillary Permeability
(physiology)
- Disease Models, Animal
- Female
- Hypothermia, Induced
- Lung Diseases
(metabolism, prevention & control)
- Mice
- Mice, Knockout
- Nitric Oxide Synthase Type II
(biosynthesis)
- Nitric Oxide Synthase Type III
(biosynthesis, genetics)
- Peroxidase
(biosynthesis)
- Phosphorylation
- Reperfusion Injury
(metabolism, prevention & control)
|