Abstract | BACKGROUND: METHODS: RESULTS: Without exposure to hyperkalemia, indomethacin (with or without glybenclamide) did not alter but L-NNA significantly reduced the relaxation (39.7% +/- 3.7%, p < 0.001). After exposure to K+, the indomethacin- and L-NNA-resistant relaxation was further reduced (7.4% +/- 3.2% for 20 mmol/L K+, p < 0.0001; or 13.5% +/- 8.4% for 50 mmol/L K+, p < 0.05, compared with rings without exposure), whereas the indomethacin- and glybenclamide-resistant relaxation was not altered. Incubation with hyperkalemia (50 mmol/L) also significantly reduced the sensitivity (increased EC50) of the indomethacin- and L-NNA-resistant relaxation (-9.75 +/- 0.06 versus -9.33 +/- 0.04 log M, p < 0.01). CONCLUSIONS: Exposure to hyperkalemia reduces the indomethacin- and L-NNA-resistant, endothelium-dependent (endothelium-derived hyperpolarizing factor-related) relaxation. Our study may suggest a new mechanism of coronary dysfunction after exposure to hyperkalemia and open a new area for protection of coronary endothelium in cardiac surgery and for organ preservation in transplantation surgery.
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Authors | G W He, C Q Yang |
Journal | The Annals of thoracic surgery
(Ann Thorac Surg)
Vol. 61
Issue 5
Pg. 1394-9
(May 1996)
ISSN: 0003-4975 [Print] Netherlands |
PMID | 8633948
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Cardioplegic Solutions
- Cyclooxygenase Inhibitors
- Nitric Oxide
- Indomethacin
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Topics |
- Animals
- Cardioplegic Solutions
(pharmacology)
- Coronary Vessels
(drug effects, physiology)
- Cyclooxygenase Inhibitors
(pharmacology)
- Endothelium, Vascular
(drug effects, metabolism, physiology)
- Heart Arrest, Induced
(adverse effects)
- Heart Diseases
(etiology, physiopathology)
- In Vitro Techniques
- Indomethacin
(pharmacology)
- Nitric Oxide
(pharmacology, physiology)
- Swine
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