| Autor: |
McKenna R; Upjohn Company, Kalamazoo, Michigan 49001, USA., Laskey RE, Wang Y, Jaeschke H, Mathews WR |
| Jazyk: |
angličtina |
| Zdroj: |
Shock (Augusta, Ga.) [Shock] 1996 Aug; Vol. 6 (2), pp. 106-11. |
| DOI: |
10.1097/00024382-199608000-00005 |
| Abstrakt: |
We have investigated endothelial function in a two-hit model of multiple organ failure. Male Fischer rats were subjected to 20 min of partial hepatic ischemia followed by reperfusion and administration of .5 mg/kg Salmonella enteritidis endotoxin at 30 min of reperfusion. After either 4 or 24 h of reperfusion, rings of aorta were prepared and suspended in bioassay baths, contracted with phenylephrine, and examined for endothelium-dependent relaxation in response to acetylcholine and endothelium-independent relaxation using nitroglycerin. Endothelium-dependent relaxation to acetylcholine was impaired in rings from animals exposed to endotoxin-enhanced reperfusion injury at both 4 h and 24 h. At 24 h of reperfusion the EC50 for acetylcholine relaxation was significantly increased from 45 +/- 8 nM to 258 +/- 105 nM. Endothelium-independent relaxation to nitroglycerin was not affected. The 21-aminosteroid Tirilazad mesylate (U-74006F) prevented endothelial dysfunction; at 24 h of reperfusion the EC50 for acetylcholine relaxation in U-74006F-treated animals was 55 +/- 8 nM. Thus, endothelial function is impaired in this model of multiple organ failure and this impairment is prevented by Tirilazad mesylate. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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