Huval W V, Mathieson M A, Stemp L I, Dunham B M, Jones A G, Shepro D, Hechtman H B
Ann Surg. 1983 Feb;197(2):220-5. doi: 10.1097/00000658-198302000-00016.
The smooth muscle-constricting, platelet amine, serotonin (5-hydroxytryptamine; 5-HT) is theorized to play an important role in the cardiopulmonary dysfunction that accompanies embolization. The present study was designed to examine this hypothesis. Autologous clot, 0.75 g/kg, was injected IV into 14 dogs. After 30 minutes, one half of the animals were randomly assigned to the treatment group and received a bolus infusion of 0.15 mg/kg ketanserin, a quinazoline derivative known to be a selective 5-HT receptor antagonist. Five minutes after embolization there were increases in mean pulmonary arterial pressure (MPAP) from 12 mm to 48 mmHg (p less than 0.001); pulmonary vascular resistance (PVR) from 2.2 mm to 12.2 mmHg X min/L (p less than 0.001); physiologic shunt (QS/QT) from 12% to 44% (p less than 0.01); and physiologic dead space (VD/VT), calculated from end tidal and arterial PCO2, from 8% to 39% (p less than 0.001). Within 15 minutes platelet counts decreased from 186,000/mm3 to 134,800/mm3 (p less than 0.05); 5-HT contained in circulating platelets fell from 1.71 micrograms/ to 1.44 micrograms/10(9) platelets (p less than 0.05). Five minutes after ketanserin, MPAP declined to 27 mmHg and was lower than the control value of 41 mmHg (p less than 0.05); PVR decreased to 6.2 mmHg X min/L, lower than 12 mmHg X min/L in controls (p less than 0.01); QS/QT fell to 26% in contrast to 47% in controls (p less than 0.05); and VD/VT declined moderately to 32% (p less than 0.05), although this value was not different from 38% in control animals. Cardiopulmonary function continued to improve in treated animals until termination of the experiment at four hours when pulmonary angiograms and perfusion scans demonstrated vascular recruitment compared with untreated embolized control dogs. These data demonstrate that the cardiopulmonary consequences of experimental embolization are primarily determined by the vasoconstrictive and bronchoconstrictive actions of 5-HT.
平滑肌收缩性血小板胺5-羟色胺（5-羟色胺；5-HT）被认为在栓塞伴随的心肺功能障碍中起重要作用。本研究旨在验证这一假说。将0.75 g/kg的自体血凝块静脉注射到14只狗体内。30分钟后，将一半动物随机分配到治疗组，给予0.15 mg/kg酮色林静脉推注，酮色林是一种喹唑啉衍生物，已知为选择性5-HT受体拮抗剂。栓塞后5分钟，平均肺动脉压（MPAP）从12 mmHg升高至48 mmHg（p<0.001）；肺血管阻力（PVR）从2.2 mmHg·min/L升高至12.2 mmHg·min/L（p<0.001）；生理分流（QS/QT）从12%升高至44%（p<0.01）；根据潮气末和动脉血二氧化碳分压计算的生理死腔（VD/VT）从8%升高至39%（p<0.001）。15分钟内血小板计数从186,000/mm³降至134,800/mm³（p<0.05）；循环血小板中的5-HT从1.71 μg/10⁹血小板降至1.44 μg/10⁹血小板（p<0.05）。给予酮色林5分钟后，MPAP降至27 mmHg，低于对照组的41 mmHg（p<0.05）；PVR降至6.2 mmHg·min/L，低于对照组的12 mmHg·min/L（p<0.01）；QS/QT降至26%，而对照组为47%（p<0.05）；VD/VT适度降至32%（p<0.05），尽管该值与对照动物的38%无差异。治疗组动物的心肺功能持续改善，直至4小时实验结束，此时与未治疗的栓塞对照犬相比，肺血管造影和灌注扫描显示血管再通。这些数据表明，实验性栓塞的心肺后果主要由5-HT的血管收缩和支气管收缩作用决定。
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