Pearson P J, Evora P R, Seccombe J F, Schaff H V
Section of Cardiovascular Surgery, Mayo Clinic and Mayo Foundation, Rochester, Minnesota 55905, USA.
Ann Thorac Surg. 1998 Apr;65(4):967-72. doi: 10.1016/s0003-4975(98)00020-4.
Postoperative hypomagnesemia is common in patients who have undergone cardiac operations and is associated with clinically significant morbidity resulting from atrial and ventricular dysrhythmias. Magnesium supplementation may increase the cardiac index in the early postoperative period.
The action of the magnesium cation on coronary vascular reactivity was studied. Segments of canine epicardial coronary artery were suspended in organ chambers to measure isometric force (95% O2/5% CO2, 37 degrees C).
In coronary segments constricted with prostaglandin F2alpha (2 x 10[-6] mol/L), acetylcholine and adenosine diphosphate (10[-9] to 10[-4] mol/L) induced vasodilation in arteries with endothelium (n=10, each group; p < 0.05). Acetylcholine-mediated vasodilation was blocked by NG-monomethyl-L-arginine (10[-4] mol/L) and NG-nitro-L-arginine (10[-4] mol/L), two inhibitors of nitric oxide synthesis from L-arginine (n=10, p < 0.05). The removal of magnesium from the organ chamber solution impaired vasodilation 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 endothelium-dependent vasodilation independent of nitric oxide production, was unaffected by magnesium removal (n=10).
Hypomagnesemia selectively impaired the release of nitric oxide from the coronary endothelium. Because nitric oxide is a potent endogenous nitro-vasodilator and inhibitor of platelet aggregation and adhesion, hypomagnesemia could promote vasoconstriction and coronary thrombosis in the early postoperative period.
术后低镁血症在接受心脏手术的患者中很常见，并且与房性和室性心律失常导致的具有临床意义的发病率相关。补充镁可能会在术后早期增加心脏指数。
研究了镁阳离子对冠状动脉血管反应性的作用。将犬心外膜冠状动脉段悬挂在器官腔室中以测量等长力（95% O₂/5% CO₂，37℃）。
在用前列腺素F₂α（2×10⁻⁶ mol/L）收缩的冠状动脉段中，乙酰胆碱和二磷酸腺苷（10⁻⁹至10⁻⁴ mol/L）在有内皮的动脉中诱导血管舒张（每组n = 10；p < 0.05）。乙酰胆碱介导的血管舒张被NG-单甲基-L-精氨酸（10⁻⁴ mol/L）和NG-硝基-L-精氨酸（10⁻⁴ mol/L）阻断，这两种是从L-精氨酸合成一氧化氮的抑制剂（n = 10，p < 0.05）。从器官腔室溶液中去除镁会损害对乙酰胆碱和二磷酸腺苷的血管舒张反应。然而，通过将镁重新加入浴液中可恢复正常的内皮依赖性血管舒张。对缓激肽（10⁻⁹至10⁻⁶ mol/L）的血管舒张反应不受镁去除的影响，缓激肽被发现可诱导不依赖一氧化氮产生的内皮依赖性血管舒张（n = 10）。
低镁血症选择性地损害冠状动脉内皮一氧化氮的释放。由于一氧化氮是一种强大的内源性硝基血管舒张剂以及血小板聚集和黏附的抑制剂，低镁血症可能在术后早期促进血管收缩和冠状动脉血栓形成。
