Jett G K, Guyton R A, Hatcher C R, Abel P W
Department of Cardiothoracic Surgery, Carlyle Fraser Heart Center, Crawford W. Long Memorial Hospital, Emory University, Atlanta, Ga.
J Thorac Cardiovasc Surg. 1992 Oct;104(4):977-82.
The internal mammary artery is currently the preferred conduit for myocardial revascularization; however, perioperative vasospasm of the internal mammary artery may limit its use as a bypass graft. The ability of various vasodilators to inhibit internal mammary artery contraction was investigated with the use of discarded segments of human internal mammary artery not used in coronary artery bypass grafting. Ring segments of human internal mammary arteries were suspended on strain gauges in muscle baths containing 37 degrees C Krebs solution for measurement of isometric tension in vitro. Arterial contraction was stimulated by elevating the extracellular potassium concentration to 70 mmol/L or by exposure to a 10 mumol/L concentration of norepinephrine, and inhibition of contraction by vasodilators was measured. The order of potency to inhibit potassium-induced contraction was as follows: nifedipine > verapamil > nitroprusside > papaverine. At maximal effective doses, nifedipine, verapamil, and papaverine almost completely inhibited potassium-induced contraction, whereas nitroprusside inhibited contraction by only 55%. When norepinephrine was used to contract the arteries, a biphasic relaxation curve was seen with nifedipine, but not with other vasodilator drugs. The order of potency to inhibit norepinephrine-induced contraction was as follows: nifedipine > nitroprusside > verapamil > papaverine. Maximal inhibition of norepinephrine contraction by these vasodilators ranged from 68% to 95%. Nitroglycerin, isoproterenol, and adenosine produced little or no inhibition of internal mammary artery contraction caused by potassium or norepinephrine. Although nifedipine was the most potent vasodilator, papaverine produced the greatest maximal inhibition of both potassium- and norepinephrine-induced contraction of human internal mammary artery.
目前，乳内动脉是心肌血运重建的首选血管；然而，乳内动脉围手术期血管痉挛可能会限制其作为旁路移植血管的应用。利用冠状动脉旁路移植术中未使用的废弃人乳内动脉节段，研究了各种血管扩张剂抑制乳内动脉收缩的能力。将人乳内动脉的环形节段悬挂在含有37℃ Krebs溶液的肌肉浴中的应变片上，用于体外测量等长张力。通过将细胞外钾浓度提高到70 mmol/L或暴露于10 μmol/L去甲肾上腺素浓度来刺激动脉收缩，并测量血管扩张剂对收缩的抑制作用。抑制钾诱导收缩的效力顺序如下：硝苯地平＞维拉帕米＞硝普钠＞罂粟碱。在最大有效剂量下，硝苯地平、维拉帕米和罂粟碱几乎完全抑制钾诱导的收缩，而硝普钠仅抑制55%的收缩。当使用去甲肾上腺素使动脉收缩时，硝苯地平呈现双相舒张曲线，而其他血管扩张剂药物则未出现这种情况。抑制去甲肾上腺素诱导收缩的效力顺序如下：硝苯地平＞硝普钠＞维拉帕米＞罂粟碱。这些血管扩张剂对去甲肾上腺素收缩的最大抑制范围为68%至95%。硝酸甘油、异丙肾上腺素和腺苷对钾或去甲肾上腺素引起的乳内动脉收缩几乎没有抑制作用。尽管硝苯地平是最有效的血管扩张剂，但罂粟碱对人乳内动脉钾和去甲肾上腺素诱导的收缩均产生最大的抑制作用。
