Remizova M I, Gerbut K A
Department of Blood Substitutes and Components, Russian Research Institute of Hematology and Transfusiology, Federal Medical and Biological Agency, St. Petersburg, Russia,
Bull Exp Biol Med. 2014 May;157(1):22-4. doi: 10.1007/s10517-014-2482-4. Epub 2014 Jun 8.
Effects of a NO donor L-arginine and a non-selective NO-synthase inhibitor N(G)-nitro-Larginine methyl ester on BP, microcirculation, acid-base balance, and gas content of blood were examined on rat model of hemorrhagic shock; the substances were administered without infusion media before blood loss. Bloodletting was stopped after manifestation of marked microcirculation disorders. Inhibition of NO synthesis in response to blood loss resulted in pronounced centralization of blood circulation with microcirculation disturbances, which was accompanied by metabolic changes aggravating hemorrhagic shock. Administration of NO donor reduced the degree of circulation centralization, maintained vasodilatatory vascular tone and perfusion of vital organs, improved animal resistance to blood loss, and prolonged their lifespan. Enhanced NO generation after administration of NO donor promoted longer microcirculation maintenance, which suggests that the so-called basal level of NO is essential at early stages of hemorrhagic shock.
在失血性休克大鼠模型上，研究了一氧化氮供体L-精氨酸和非选择性一氧化氮合酶抑制剂N（G）-硝基-L-精氨酸甲酯对血压、微循环、酸碱平衡及血液气体含量的影响；在失血前，不使用输注介质直接给予这些物质。在出现明显的微循环障碍后停止放血。失血后一氧化氮合成的抑制导致血液循环明显集中并伴有微循环障碍，同时伴有代谢变化，加重了失血性休克。给予一氧化氮供体可降低循环集中程度，维持血管舒张的血管张力和重要器官的灌注，提高动物对失血的耐受性，并延长其存活时间。给予一氧化氮供体后一氧化氮生成增加促进了微循环的较长时间维持，这表明在失血性休克早期，所谓的一氧化氮基础水平至关重要。
