HYPOMAGNESEMIA INHIBITS NITRIC-OXIDE RELEASE FROM CORONARY ENDOTHELIUM - PROTECTIVE ROLE OF MAGNESIUM INFUSION AFTER CARDIAC OPERATIONS

Citation
Pj. Pearson et al., HYPOMAGNESEMIA INHIBITS NITRIC-OXIDE RELEASE FROM CORONARY ENDOTHELIUM - PROTECTIVE ROLE OF MAGNESIUM INFUSION AFTER CARDIAC OPERATIONS, The Annals of thoracic surgery, 65(4), 1998, pp. 967-972
Citations number
24
Categorie Soggetti
Surgery,"Cardiac & Cardiovascular System","Respiratory System
ISSN journal
00034975
Volume
65
Issue
4
Year of publication
1998
Pages
967 - 972
Database
ISI
SICI code
0003-4975(1998)65:4<967:HINRFC>2.0.ZU;2-V
Abstract
Background. Postoperative hypomagnesemia is common in patients who hav e undergone cardiac operations and is associated with clinically signi ficant morbidity resulting from atrial and ventricular dysrhythmias. M agnesium supplementation may increase the cardiac index in the early p ostoperative period. Methods. The action of the magnesium cation on co ronary vascular reactivity was studied. Segments of canine epicardial coronary artery were suspended in organ chambers to measure isometric force (95% O-2/5% CO2, 37 degrees C). Results. In coronary segments co nstricted with prostaglandin F-2 alpha (2 x 10(-6) mol/L), acetylcholi ne and adenosine diphosphate (10(-9) to 10(-4) mol/L) induced vasodila tion in arteries with endothelium (n = 10, each group; p < 0.05). Acet ylcholine-mediated vasodilation was blocked by N-G-monomethyl-L-argini ne (10(-4) mol/L) and N-G-nitro-L-arginine (10(-4) mol/L), two inhibit ors of nitric oxide synthesis from L-arginine (n = 10, p < 0.05). The removal of magnesium from the organ chamber solution impaired vasodila tion in response to acetylcholine and adenosine diphosphate. However, normal endothelium-dependent vasodilation could be restored by return of magnesium to the bathing solution. Vascular relaxation in response to bradykinin (10(-9) to 10(-6) mol/L), which was found to induce endo thelium-dependent vasodilation independent of nitric oxide production, was unaffected by magnesium removal (n = 10). Conclusions. Hypomagnes emia selectively impaired the release of nitric oxide from the coronar y endothelium. Because nitric oxide is a potent endogenous nitrovasodi lator and inhibitor of platelet aggregation and adhesion, hypomagnesem ia could promote vasoconstriction and coronary thrombosis in the early postoperative period. (C) 1998 by The Society of Thoracic Surgeons.