Cable D G, Sorajja P, Oeltjen M R, Schaff H V
Section of Cardiovascular Surgery, Mayo Clinic, Rochester, MN 55905, USA.
Surgery. 1999 Nov;126(5):835-41.
Protamine administration may lead to systemic hypotension, perhaps because of vasodilatation produced by endothelial nitric oxide. This study compared release of vasoactive substances from canine coronary microvessels with that from paired conductance arteries.
Microvessels were mounted in a videoscopic no-flow system, and circumflex arteries were studied in organ chambers; both were induced to contract by endothelin-1.
Protamine (10 to 160 micrograms/mL) produced concentration-dependent relaxation in both microvessel and conductance arteries (46% +/- 14% maximal relaxations in microvessel and 82% +/- 15% in conductance arteries, n = 10 each). Removal of the endothelium abolished this relaxation (P < .05, n = 6). Indomethacin (10(-5) mol/L) did not alter the relaxation in either group (51% +/- 10% in microvessel and 103% +/- 7% in conductance arteries, n = 6 each). NG-monomethyl-L-arginine (L-NMMA, 10(-4) mol/L) attenuated relaxation in conductance arteries (38% +/- 12%, P = .04, n = 6) but had no effect on microvessel arteries (58% +/- 10%, n = 6). Tetraethylammonium chloride (10(-3) mol/L), an inhibitor of voltage-dependent potassium channels, had no effect on conductance arteries (103% +/- 9%, n = 6) but abolished relaxation in microvessels (-25% +/- 11%, P = .03, n = 6).
Protamine sulfate causes endothelium-dependent relaxation in microvessel and conductance arteries in the heart by different mechanisms--that is, by nitric oxide release in conductance arteries and by endothelium-derived hyperpolarizing factor (EDHF) release in microvessels. This is the first description of the release of EDHF in response to protamine administration.
使用鱼精蛋白可能导致全身性低血压，这可能是由于内皮一氧化氮产生的血管舒张作用。本研究比较了犬冠状动脉微血管与配对传导动脉中血管活性物质的释放情况。
将微血管安装在视频显微镜无血流系统中，在器官腔室中研究回旋支动脉；两者均用内皮素-1诱导收缩。
鱼精蛋白（10至160微克/毫升）在微血管和传导动脉中均产生浓度依赖性舒张（微血管中最大舒张率为46%±14%，传导动脉中为82%±15%，每组n = 10）。去除内皮可消除这种舒张作用（P <.05，n = 6）。吲哚美辛（10⁻⁵摩尔/升）对两组的舒张作用均无影响（微血管中为51%±10%，传导动脉中为103%±7%，每组n = 6）。N⁃单甲基⁃L⁃精氨酸（L⁃NMMA，10⁻⁴摩尔/升）减弱了传导动脉中的舒张作用（38%±12%，P =.04，n = 6），但对微血管动脉无影响（58%±10%，n = 6）。电压依赖性钾通道抑制剂四乙铵氯化物（10⁻³摩尔/升）对传导动脉无影响（103%±9%，n = 6），但消除了微血管中的舒张作用（-25%±11%，P =.03，n = 6）。
硫酸鱼精蛋白通过不同机制使心脏中的微血管和传导动脉产生内皮依赖性舒张，即在传导动脉中通过释放一氧化氮，在微血管中通过释放内皮衍生超极化因子（EDHF）。这是首次描述因使用鱼精蛋白而释放EDHF的情况。
