SP/W-5186, A cysteine-containing nitric oxide donor, attenuates postischemic myocardial injury
Liu, Gao-Lin, Christopher, Theodore A., Lopez, Bernard L., Gao, Feng, Guo, Yaping, Gao, Erhe, Knuettel, Karlheinz, Feelisch, Martin and Ma, Xin L. (1998) SP/W-5186, A cysteine-containing nitric oxide donor, attenuates postischemic myocardial injury. The Journal of Pharmacology and Experimental Therapeutics, 287, (2), 527-537. (PMID:9808677).
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Description/Abstract
The effects of SP/W-5186, a cysteine-containing nitric oxide (.NO) donor, on myocardial reperfusion injury were studied in a rabbit ischemia (45 min) and reperfusion (180 min) model. Five min before reperfusion, either low-dose (0.3 micromol/kg) or high-dose (1 micromol/kg) SP/W-5186 was given intravenously as a bolus. Administration of 0.3 micromol/kg SP/W-5186 did not change mean arterial blood pressure, heart rate or pressure-rate index. However, administration of low-dose SP/W-5186 exerted marked cardioprotective effects as evidenced by improved cardiac functional recovery (P <.05 vs. vehicle), decreased plasma creatine kinase concentration (P <. 01) and reduced infarct size (P <.01). Moreover, administration of SP/W-5186 significantly decreased platelet aggregation (P <.01 vs. vehicle), attenuated polymorphonuclear leukocyte (PMN) accumulation in myocardial tissue, inhibited PMN adhesion to endothelial cells and preserved endothelial function. Administration of high-dose SP/W-5186 resulted in a transient but significant decrease in mean arterial blood pressure and exerted more cardiac protection compared with low-dose treatment. However, the effects on platelet aggregation, PMN accumulation and PMN adhesion did not differ significantly between the two SP/W-5186 groups. Furthermore, administration of SP/W-6373, an analogue of SP/W-5186 that lacks the NO moiety, failed to exert any protective effects. These results demonstrate that NO released from SP/W-5186 significantly protected myocardial tissue from reperfusion injury. The primary mechanisms of the observed cardioprotection by SP/W-5186 involve inhibition of platelet aggregation, attenuation of PMN-endothelium interaction and preservation of endothelial function.
| Item Type: | Article |
|---|---|
| ISSNs: | 1521-0103 (electronic) |
| Related URLs: | |
| Subjects: | Q Science > QP Physiology Q Science > QR Microbiology > QR180 Immunology |
| Divisions: | Faculty of Medicine > Infection, Inflammation and Immunity |
| Item ID: | 337885 |
| Date Deposited: | 29 Jun 2012 11:41 |
| Last Modified: | 29 Jun 2012 11:41 |
| Contributors: | Liu, Gao-Lin (Author) Christopher, Theodore A. (Author) Lopez, Bernard L. (Author) Gao, Feng (Author) Guo, Yaping (Author) Gao, Erhe (Author) Knuettel, Karlheinz (Author) Feelisch, Martin (Author) Ma, Xin L. (Author) |
| Date: | 1 November 1998 |
| Status: | Published |
| URI: | http://eprints.soton.ac.uk/id/eprint/337885 |
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