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向胆道加压至 4kPa ,可同时引起血压降低和Oddi括约肌 (SO)肌电活动减弱或消失 ,这总称为胆道加压反射 ,其中前者称为胆道 血压反射 ,后者称为胆道 SO反射。本实验应用 3 2只家兔观察一氧化氮 (NO)对胆道加压反射活动的影响。在静脉滴注去甲肾上腺素 4 μg/(kg·min)引起血压升高和SO肌电振幅增大的基础上 ,再行胆道加压至 4kPa ,仍同时引起血压降低和Oddi括约肌 (SO)肌电活动减弱 ;而在静脉注射NO合酶抑制剂NG 硝基 L 精氨酸 (L NNA) 10mg/kg引起血压升高和SO肌电振幅增大的基础上 ,再行胆道加压至 4kPa,全部动物胆道 血压反射受到完全抑制 ,即未出现血压降低反应 ;少数 ( 3 /8)动物胆道 SO反射受到完全抑制 ,多数 ( 5 /8)动物该反射受到明显抑制 (P <0 0 1)。向SO局部灌注L NNA ,只引起SO肌电振幅增大而不影响血压 ,在此基础上行胆道加压 ,对胆道 SO反射的影响与全身用药相似 ,对胆道 血压反射却无影响。这提示 ,这两种反射活动是相对独立的 ,是经不同传出途径和效应器实现的 ;且这两种反射都主要是通过NO介导的
Pressure to the biliary tract to 4kPa, both caused by hypotension and sphincter of Oddi (SO) myoelectrical activity decreased or disappeared, which is commonly referred to as biliary reflex, of which the former is called biliary pressure reflex, which is called biliary SO reflex. In this experiment, 32 rabbits were used to observe the effect of nitric oxide (NO) on biliary reflex activity. On the basis of intravenous drip of norepinephrine 4 μg / (kg · min) on the basis of increasing blood pressure and increasing amplitude of SO myoelectricity, biliary tract pressure was further increased to 4 kPa and blood pressure and Oddi sphincter (SO) Myoelectrical activity weakened; while intravenous injection of NO synthase inhibitor L-NNA 10 mg / kg caused by increased blood pressure and increased amplitude of SO myoelectricity, then biliary tract pressure to 4kPa , The biliary blood pressure reflex was completely inhibited in all animals, that is, there was no blood pressure lowering reaction. SO in biliary tract was completely inhibited in a few animals (3/8), and the reflex was significantly inhibited in most animals (P <0.01) . Partial perfusion of LN with SO resulted in only an increase in amplitude of myoelectricity of SO without affecting blood pressure. On the basis of this, biliary pressure was applied and the effect on biliary SO reflexes was similar to that of systemic medication with no effect on biliary pressure reflex. This suggests that these two reflexes are relatively independent and are delivered via different efferent pathways and effectors; and both of these reflections are predominantly mediated by NO