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The role of the L-arginine/nitric oxide pathway in myocardial ischaemic and reperfusion injury.
Acta Physiol Scand. 1999 Oct; 167(2):151-9.AP

Abstract

Myocardial ischaemia followed by reperfusion (I/R) is associated with impaired endothelial function including diminished release and/or effects of nitric oxide (NO) which may contribute to the development of I/R injury. The aim of the present study was to investigate the role of the L-arginine/NO pathway in myocardial I/R injury. In isolated rat hearts subjected to global ischaemia followed by reperfusion L-arginine and the NO donor S-nitroso-N-acetyl-D,L-penicillamine (SNAP), but not D-arginine, significantly enhanced the recoveries of mycardial performance and coronary flow, and reduced the area of no-reflow and creatine kinase outflow. The NO synthase inhibitor NG-nitro-L-arginine (L-NNA) abolished the protective effects of L-arginine. Endothelium-dependent vasodilatation after I/R was preserved in L-arginine treated but not in vehicle hearts. Following I/R Ca2+-dependent NO synthase activity was reduced by 90% in comparison with non-ischaemic hearts. L-arginine but not D-arginine significantly increased NO synthase activity. In anaesthetized pigs, L-arginine given by local coronary venous retroinfusion reduced myocardial infarct size induced by 45 min of coronary artery ligation and 4 h of reperfusion to 35% of the area at risk from 76% in controls. The protective effect of L-arginine was blocked by L-NNA. Acetylcholine-induced coronary vasodilatation following I/R was attenuated in controls but not in L-arginine treated pigs. It is concluded that L-arginine or the NO donor SNAP reduces I/R-induced myocardial and endothelial injury. The protective effect of L-arginine seems to be mediated through maintained production of NO by preserving the function of Ca2+-dependent NO synthase in the heart.

Authors+Show Affiliations

Department of Cardiology, Karolinska Hospital, Stockholm, Sweden.No affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

10571551

Citation

Pernow, J, and Q D. Wang. "The Role of the L-arginine/nitric Oxide Pathway in Myocardial Ischaemic and Reperfusion Injury." Acta Physiologica Scandinavica, vol. 167, no. 2, 1999, pp. 151-9.
Pernow J, Wang QD. The role of the L-arginine/nitric oxide pathway in myocardial ischaemic and reperfusion injury. Acta Physiol Scand. 1999;167(2):151-9.
Pernow, J., & Wang, Q. D. (1999). The role of the L-arginine/nitric oxide pathway in myocardial ischaemic and reperfusion injury. Acta Physiologica Scandinavica, 167(2), 151-9.
Pernow J, Wang QD. The Role of the L-arginine/nitric Oxide Pathway in Myocardial Ischaemic and Reperfusion Injury. Acta Physiol Scand. 1999;167(2):151-9. PubMed PMID: 10571551.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The role of the L-arginine/nitric oxide pathway in myocardial ischaemic and reperfusion injury. AU - Pernow,J, AU - Wang,Q D, PY - 1999/11/26/pubmed PY - 1999/11/26/medline PY - 1999/11/26/entrez SP - 151 EP - 9 JF - Acta physiologica Scandinavica JO - Acta Physiol. Scand. VL - 167 IS - 2 N2 - Myocardial ischaemia followed by reperfusion (I/R) is associated with impaired endothelial function including diminished release and/or effects of nitric oxide (NO) which may contribute to the development of I/R injury. The aim of the present study was to investigate the role of the L-arginine/NO pathway in myocardial I/R injury. In isolated rat hearts subjected to global ischaemia followed by reperfusion L-arginine and the NO donor S-nitroso-N-acetyl-D,L-penicillamine (SNAP), but not D-arginine, significantly enhanced the recoveries of mycardial performance and coronary flow, and reduced the area of no-reflow and creatine kinase outflow. The NO synthase inhibitor NG-nitro-L-arginine (L-NNA) abolished the protective effects of L-arginine. Endothelium-dependent vasodilatation after I/R was preserved in L-arginine treated but not in vehicle hearts. Following I/R Ca2+-dependent NO synthase activity was reduced by 90% in comparison with non-ischaemic hearts. L-arginine but not D-arginine significantly increased NO synthase activity. In anaesthetized pigs, L-arginine given by local coronary venous retroinfusion reduced myocardial infarct size induced by 45 min of coronary artery ligation and 4 h of reperfusion to 35% of the area at risk from 76% in controls. The protective effect of L-arginine was blocked by L-NNA. Acetylcholine-induced coronary vasodilatation following I/R was attenuated in controls but not in L-arginine treated pigs. It is concluded that L-arginine or the NO donor SNAP reduces I/R-induced myocardial and endothelial injury. The protective effect of L-arginine seems to be mediated through maintained production of NO by preserving the function of Ca2+-dependent NO synthase in the heart. SN - 0001-6772 UR - https://www.unboundmedicine.com/medline/citation/10571551/The_role_of_the_L_arginine/nitric_oxide_pathway_in_myocardial_ischaemic_and_reperfusion_injury_ L2 - https://doi.org/10.1046/j.1365-201x.1999.00588.x DB - PRIME DP - Unbound Medicine ER -