| Nitrosoglutathione modulation of platelet activation and nitric oxide synthase expression in promotion of flap survival after ischemia/reperfusion injury. | |
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MedLine Citation:
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PMID: 15126088 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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BACKGROUND: Recent studies have shown that platelets play an important role in the pathogenesis of reperfusion injury. Using an inferior epigastric artery skin flap as a flap ischemia/reperfusion (I/R) injury model, we investigated whether the administration of a nitric oxide (NO) donor, nitrosoglutathione (GSNO), could decrease platelet activation and modulate the NO synthase (NOS) activity of platelets and promote flap survival. METHODS: Thirty minutes before flap reperfusion, normal saline (1 mL), nitrosoglutathione (GSNO 0.2, 0.6, 3 mg/kg), or N(G)-nitro-L-arginine-methyl ester (450 mg/kg) was injected intravenously in 10 rats, respectively. The p-selectin (CD62P) expression of platelet activation was detected by a flow cytometry. Immunohistochemical staining was performed to investigate the CD62P deposition on the microvasculature of the flap vessels. NOS isoform expression in the platelets was evaluated by Western blot. Tissue perfusion was monitored by using laser-Doppler flowmetry. Survival areas were assessed at 7 days postoperatively RESULTS: An optimal dose of GSNO (0.6 mg/kg), significantly decreased in CD62P expression on platelets (P < 0.001) and its deposition on the flap vessels, selectively suppressed iNOS induction of platelet, and significantly improved blood perfusion and the flap survival rate (59.8 +/- 4.9% versus 22.1 +/- 6.1%, P < 0.001). In contrast, the NO synthase inhibitor, N(G)-nitro-l-arginine methyl ester, although inhibiting iNOS expression of platelets, compromised platelet activation, tissue perfusion, and flap survival. CONCLUSION: This study suggests that GSNO can appropriately donate NO to suppress platelet activation and platelet iNOS induction, resulting in less platelet activation, better blood perfusion, and flap survival after I/R injury. |
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Authors:
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Yur-Ren Kuo; Feng-Sheng Wang; Seng-Feng Jeng; Hui-Chen Huang; Fu-Chan Wei; Kuender D Yang |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: The Journal of surgical research Volume: 119 ISSN: 0022-4804 ISO Abbreviation: J. Surg. Res. Publication Date: 2004 Jun |
Date Detail:
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Created Date: 2004-05-05 Completed Date: 2004-06-07 Revised Date: 2007-11-15 |
Medline Journal Info:
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Nlm Unique ID: 0376340 Medline TA: J Surg Res Country: United States |
Other Details:
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Languages: eng Pagination: 92-9 Citation Subset: IM |
Affiliation:
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Department of Plastic and Reconstructive Surgery, Chang Gung Memorial Hospital, Kaohsiung, Taiwan. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Arteries / surgery Blood Platelets / metabolism Blood Vessels / metabolism Dose-Response Relationship, Drug Down-Regulation Hemodynamics / drug effects Male Nitric Oxide Synthase / blood, metabolism* Nitric Oxide Synthase Type II P-Selectin / blood, drug effects, metabolism Platelet Activation / drug effects* Rats Rats, Inbred Lew Regional Blood Flow / drug effects Reperfusion Injury / blood, enzymology, physiopathology* S-Nitrosoglutathione / administration & dosage, pharmacology* Skin / blood supply*, enzymology* Surgical Flaps* Tissue Survival / drug effects |
| Chemical | |
Reg. No./Substance:
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0/P-Selectin; 57564-91-7/S-Nitrosoglutathione; EC 1.14.13.39/Nitric Oxide Synthase; EC 1.14.13.39/Nitric Oxide Synthase Type II; EC 1.14.13.39/Nos2 protein, rat |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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