O'Shaughnessy M, Anderson G L, Acland R D, Barker J H
Division of Plastic and Reconstructive Surgery, Cork University Hospital, Ireland.
Plast Reconstr Surg. 1997 Mar;99(3):834-41. doi: 10.1097/00006534-199703000-00033.
Previous work suggests that cod liver oil helps to protect the microcirculation from the consequence of thromboembolic events. The possibility that altered synthesis of thromboxane A2 accounts for the protective effects seen with cod liver oil was investigated in the present study. This was done using the combined thromboxane A2 synthetase inhibitor and thromboxane A2-prostaglandin H2 receptor blocker R68070 (Ridogrel). A standardized microvascular injury was inflicted on the right iliac artery of the rat to generate emboli. The downstream cremaster muscle was used to visualize the passage of the ensuing emboli and to assess the effects of this arterial injury on capillary perfusion and arteriole diameters. The number of visible emboli was not changed by either cod liver oil diet or Ridogrel administration. However, capillary perfusion was preserved by using cod liver oil (n = 7) and was significantly increased by using Ridogrel (n = 7) in comparison with untreated controls (n = 7) in which capillary perfusion was decreased because of the emboli. The administration of Ridogrel to cod liver oil-treated animals (n = 7) provided no additive benefit. The percentage change in A-2 vessel diameters in cod liver oil-treated (n = 7) animals was no different from the control group (n = 7). Ridogrel (n = 7), on the other hand, produced a significant increase in A-3 vessel (n = 21) diameters, but its effects were comparatively less in the cod liver oil-treated animals (n = 7). The formation of platelet aggregates (emboli) appears relatively independent of thromboxane A2 in the rat. Ridogrel is very effective in protecting the microcirculation, and these effects appear to be mediated by A-3 vasodilatation, which, therefore, is at least partially thromboxane A2-dependent. The positive effects of cod liver oil may be mediated by a mechanism that reduces thromboxane A2 synthesis, but further studies are necessary.
先前的研究表明，鱼肝油有助于保护微循环免受血栓栓塞事件后果的影响。本研究调查了血栓素A2合成改变是否是鱼肝油产生保护作用的原因。这是通过联合使用血栓素A2合成酶抑制剂和血栓素A2 - 前列腺素H2受体阻滞剂R68070（利度罗）来实现的。对大鼠右髂动脉造成标准化的微血管损伤以形成栓子。利用下游的提睾肌来观察随后形成的栓子的通过情况，并评估这种动脉损伤对毛细血管灌注和小动脉直径的影响。鱼肝油饮食或给予利度罗均未改变可见栓子的数量。然而，与未治疗的对照组（n = 7）相比，使用鱼肝油（n = 7）可保留毛细血管灌注，使用利度罗（n = 7）可使毛细血管灌注显著增加，未治疗的对照组因栓子导致毛细血管灌注减少。对用鱼肝油治疗的动物（n = 7）给予利度罗未产生额外益处。用鱼肝油治疗的动物（n = 7）中A - 2血管直径的百分比变化与对照组（n = 7）无差异。另一方面，利度罗（n = 7）使A - 3血管（n = 21）直径显著增加，但其在鱼肝油治疗的动物（n = 7）中的作用相对较小。在大鼠中，血小板聚集体（栓子）的形成似乎相对独立于血栓素A2。利度罗在保护微循环方面非常有效，这些作用似乎是由A - 3血管舒张介导的，因此至少部分依赖于血栓素A2。鱼肝油的积极作用可能是通过减少血栓素A2合成的机制介导的，但还需要进一步研究。
