A role for nitric oxide in endotoxin-induced depletion of the peripheral catecholamine stores
| Autor: | Odd S. Steinsland, Yu Wang, Sharon H. Nelson |
|---|---|
| Rok vydání: | 2000 |
| Předmět: |
Lipopolysaccharides
Tail medicine.medical_specialty Epinephrine Nitric Oxide Synthase Type II Critical Care and Intensive Care Medicine Nitric Oxide Guanidines Nitric oxide Rats Sprague-Dawley Norepinephrine chemistry.chemical_compound Internal medicine Sepsis Adrenal Glands medicine Neurotoxin Animals Enzyme Inhibitors Lung Aorta biology Adrenal gland business.industry Myocardium Arteries Rats Nitric oxide synthase Endocrinology medicine.anatomical_structure NG-Nitroarginine Methyl Ester chemistry Emergency Medicine biology.protein Catecholamine Female Nitric Oxide Synthase business Spleen medicine.drug Blood vessel |
| Zdroj: | Shock (Augusta, Ga.). 13(2) |
| ISSN: | 1073-2322 |
| Popis: | Endotoxemia is associated with increased sympathetic nerve activity and depletion of norepinephrine (NE) and epinephrine (EPI) contents in the adrenal gland and in sympathetically innervated tissues. Endotoxin (bacterial lipopolysacchride [LPS]) causes an increased production of nitric oxide (NO) by inducing nitric oxide synthase (iNOS) expression in various tissues. This increased production of NO contributes significantly to the hypotension associated with endotoxemia. At high concentrations, NO also can act as a neurotoxin. In this study we tested the hypothesis that increased production of NO is involved in depletion of catecholamine content in various tissues from rats treated with a nonlethal dose of LPS. Catecholamine content was measured by high-performance liquid chromatography with electrochemical detection (HPLC-EC) and NOS activity was measured by the 3 H-1-arginine to 3 H-1-citrulline conversion method. The NE content was decreased in rat adrenal gland, lung, spleen, tail artery, and aorta after LPS. The maximal decrease was at 24 h and returned to control levels at 6 days (144 h). There was no depletion of the NE content in the heart. The EPI content in the adrenal gland was greatly depleted (91%) from 12 to 72 h after LPS. LPS increased the NOS activity in all tissues examined. The time course for NOS activity showed an increase at 3 h, a further increase at 6 h, and a return to control level at 48 h after LPS. The increase in NOS activity occurred before maximal catecholamine depletion. Aminoguanidine, a relatively selective iNOS inhibitor, completely prevented NE depletion in all tissues and partially prevented adrenal EPI depletion induced by LPS. These results are consistent with the hypothesis that LPS-induced production of NO plays a role in depletion of tissue NE and EPI. |
| Databáze: | OpenAIRE |
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