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Diminished basal nitric oxide release after myocardial ischemia and reperfusion promotes neutrophil adherence to coronary endothelium.
Abstract
We measured changes in basal release of nitric oxide and its effect on polymorphonuclear leukocyte (PMN) adherence to endothelial cells (ECs) in a feline model of myocardial ischemia (90 minutes) and reperfusion. Basal release of nitric oxide from the left anterior descending coronary artery (LAD) after myocardial ischemia/reperfusion and from the control left circumflex coronary artery (LCX) was assessed by NG-nitro L-arginine methyl ester (L-NAME)-induced vasocontraction. L-NAME induced a significant EC-dependent vasocontraction in control LCX rings (0.28 +/- 0.04 g), which was fully reversed by L-arginine but not D-arginine. L-NAME-induced vasocontraction of LAD rings was not significantly changed after 90 minutes of myocardial ischemia without reperfusion. However, 10 minutes of reperfusion reduced the L-NAME-induced vasocontraction to 0.13 +/- 0.04 g (p < 0.05), and this was restored by addition of 3 mM L-arginine but not D-arginine. Longer periods of reperfusion progressively decreased L-NAME-induced vasocontraction. After 270 minutes of reperfusion, L-NAME-induced vasocontraction was virtually abolished. Myocardial ischemia without reperfusion did not increase PMN adherence to ECs. However, PMN adherence to LAD ECs was significantly increased after 20 minutes of reperfusion (39 +/- 6 to 105 +/- 9 PMNs/mm2, p < 0.01), and incubation of LAD segments with L-arginine significantly attenuated this increase in PMN adherence. After 270 minutes of reperfusion, PMN adherence to LAD ECs was further increased to 224 +/- 10 PMNs/mm2 (p < 0.001). This increase in PMN adherence was almost completely blocked by MAb R15.7, a monoclonal antibody against CD18 of PMNs, and was significantly attenuated by MAb RR1/1, a monoclonal antibody against intercellular adhesion molecule-1 of ECs (p < 0.01). These results indicate that decreased basal release of endothelium-derived relaxing factor after myocardial ischemia/reperfusion precedes enhanced PMN adherence to the coronary endothelium, which may lead to PMN-induced myocardial injury.
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Cites
Nitric oxide release accounts for the biological activity of endothelium-derived relaxing factor
Palmer, R. M. J., Ferrige, A. G., & Moncada, S. (1987) · Nature · doi:10.1038/327524a0 · Cited by 10,704
Cited by
The multifaceted roles of nitric oxide in cancer
Wink, D. (1998) · Carcinogenesis · doi:10.1093/carcin/19.5.711 · Cited by 682
Kin, H. (2004) · Cardiovascular Research · doi:10.1016/j.cardiores.2004.01.006 · Cited by 561
Nitric oxide in myocardial ischemia/reperfusion injury
Schulz, R. (2004) · Cardiovascular Research · doi:10.1016/j.cardiores.2003.09.019 · Cited by 462
Calvert, J. W., Gundewar, S., Jha, S., Greer, J. J. M., Bestermann, W. H., Tian, R., & Lefer, D. J. (2008) · Diabetes · doi:10.2337/db07-1098 · Cited by 422
Self-citationThe intriguing role of polymorphonuclear neutrophils in antitumor reactions
Di Carlo, E., Forni, G., Lollini, P., Colombo, M. P., Modesti, A., & Musiani, P. (2001) · Blood · doi:10.1182/blood.v97.2.339 · Cited by 419
Metadata
- Authors
- Ma, X. L., Weyrich, A. S., Lefer, D. J., & Lefer, A. M.
- Venue
- Circulation Research
- Published
- 1993-02
- Volume
- 72
- Issue
- 2
- Pages
- 403-412
- ISSN
- 0009-7330 (ISSN-L)
- 1524-4571
- OpenAlex
- W1973470186
- Cited by
- 491
- References
- 1
- FWCI
- 18.10
- Type
- journal article
- Language
- en
- Open access
- closed
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- Ma, X. L., Weyrich, A. S., Lefer, D. J., & Lefer, A. M. (1993). Diminished basal nitric oxide release after myocardial ischemia and reperfusion promotes neutrophil adherence to coronary endothelium. Circulation Research. https://doi.org/10.1161/01.res.72.2.403
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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