Hasebe N, Yamashita H
Hokkaido Igaku Zasshi. 1984 Mar;59(2):148-65.
It is generally accepted that a vasoconstrictive mechanism participates in transient pulmonary hypertension observed in miliary embolism, in addition to the mechanical blockade of pulmonary vascular tree. For the explanation, some neural and humoral factors, especially those released from adhesion-aggregation process of platelets, have been emphasized. In our previous reports, we have stressed the importance of some local vascular factors in this vasoconstrictive mechanism. Present study was undertaken to elucidate those local factors extensively. Miliary pulmonary embolism in the isolated perfused canine lung lobe was produced by injecting lycopodium spore suspension in saline, in which hepalinized autologous blood and three different artificial solutions were employed as the perfusate. Although each perfusate made a slight difference in perfusing condition, probably owing to its viscosity and oncotic pressure, all preparations showed definite response to embolization. After each embolization, pulmonary inflow pressure was raised rapidly and reached to a maximal level after 30-60 sec., then fell gradually. Repeated embolization at an interval of 6 min., before pulmonary inflow pressure returned to the control level, produced a cumulative effect. There was no significant difference between perfusations with autologous blood and artificial perfusates at the first and the second embolizations, but it was more distinct in those with autologous blood at the third and the fourth embolizations. The results have showed that the initial pulmonary pressure elevation in miliary embolism is observed apparently even under the bloodless and denervated conditions. It was concluded that "Myogenic Factor" (existing locally in the pulmonary arterial and arteriolar endothelium-smooth muscle) must play a very important role as to initial elevation in pulmonary arterial pressure induced by miliary embolizations. Further advanced studies on the myogenic factor is expected.
人们普遍认为,除了肺血管树的机械性阻塞外,血管收缩机制也参与了粟粒性栓塞中观察到的短暂性肺动脉高压。对于这种现象的解释,一些神经和体液因素,特别是那些从血小板黏附聚集过程中释放的因素,受到了重视。在我们之前的报告中,我们强调了一些局部血管因素在这种血管收缩机制中的重要性。本研究旨在广泛阐明这些局部因素。通过在盐水中注射石松子孢子悬浮液,在离体灌注的犬肺叶中制造粟粒性肺栓塞,其中使用肝素化自体血和三种不同的人工溶液作为灌注液。尽管每种灌注液在灌注条件上有轻微差异,可能是由于其粘度和胶体渗透压,但所有制剂对栓塞都表现出明确的反应。每次栓塞后,肺流入压迅速升高,在30 - 60秒后达到最高水平,然后逐渐下降。在肺流入压恢复到对照水平之前,以6分钟的间隔重复栓塞产生累积效应。在第一次和第二次栓塞时,自体血灌注和人工灌注液之间没有显著差异,但在第三次和第四次栓塞时,自体血灌注的差异更明显。结果表明,即使在无血和去神经条件下,粟粒性栓塞中最初的肺动脉压升高也明显可见。得出的结论是,“肌源性因子”(局部存在于肺动脉和小动脉内皮 - 平滑肌中)对于粟粒性栓塞引起的肺动脉压初始升高必定起着非常重要的作用。预计对肌源性因子将进行进一步深入的研究。