Department of Anesthesiology and Critical Care Medicine, Lariboisière University Hospital, Paris, France.
Anesth Analg. 2010 Mar 1;110(3):845-51. doi: 10.1213/ANE.0b013e3181ca3c6f. Epub 2009 Dec 15.
Hypercapnia has been reported to modify liver circulation. The vascular regulations implicated in this response remain partly unknown.
Using anesthetized and ventilated rabbits, we designed this study to evaluate the hepatic artery and portal vein blood flow velocity adjustments (20 MHz pulsed Doppler) after changes in PaCO2 (by varying the inspiratory fraction of CO2 and to assess the proper role of pH, independent of PaCO2 changes, the role of portal vein CO2, and the effect of nitric oxide synthase inhibition on CO2-induced modifications of hepatic hemodynamics.
Increasing PaCO2 from 30.9 +/- 5 mm Hg to 77 +/- 11 mm Hg increased arterial blood pressure by 20% (P < 0.01) and hepatic artery blood flow velocity by 90% (P < 0.05) and decreased aortic blood flow velocity by 15% and portal vein blood flow velocity by 40% (both P < 0.05). Changes in pH (1 mL of 0.1 N hydrochloric acid infusion) or isolated changes in portal vein CO2 at constant PaCO2 induced by CO2 insufflation in an open abdomen had no effect on hepatic hemodynamics. Pretreatment with a nitric oxide synthase inhibitor, N(omega)-nitro-L-arginine (2.5 mg/kg), blunted the systemic response to hypercapnia, whereas the portal modifications persisted, with a largely attenuated hepatic artery blood flow increase.
CO2 per se acts on hepatic blood flow by its systemic effect, probably via chemoreflexes. Nitric oxide does not mediate hepatosplanchnic hemodynamic modifications to acute changes in PaCO2 but may play a permissive role by regulating the amplitude of hepatic vascular response.
高碳酸血症已被报道可改变肝脏循环。这种反应所涉及的血管调节机制在一定程度上尚不清楚。
我们使用麻醉和通气的兔子设计了本研究，以评估 PaCO2 变化后肝动脉和门静脉血流速度的调整（20MHz 脉冲多普勒），并评估 pH 对肝血流动力学的影响（通过改变 CO2 的吸气分数，以独立于 PaCO2 变化评估 pH 的作用）、门静脉 CO2 的作用以及一氧化氮合酶抑制对 CO2 诱导的肝血液动力学改变的影响。
将 PaCO2 从 30.9±5mmHg 增加到 77±11mmHg 使动脉血压升高 20%（P<0.01），肝动脉血流速度升高 90%（P<0.05），而主动脉血流速度降低 15%，门静脉血流速度降低 40%（均 P<0.05）。在腹部开放状态下通过 CO2 吹入引起的 pH 变化（1mL0.1N 盐酸输注）或门静脉 CO2 的单独变化对肝血流动力学没有影响。预先给予一氧化氮合酶抑制剂 N（ω）-硝基-L-精氨酸（2.5mg/kg），减弱了高碳酸血症的全身反应，而门静脉的改变仍然存在，肝动脉血流增加幅度大大减弱。
CO2 本身通过其全身效应作用于肝血流，可能通过化学感受器。一氧化氮不介导肝血流动力学对急性 PaCO2 变化的改变，但可能通过调节肝血管反应的幅度起允许作用。
