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Hemodynamic and hepatic microcirculational changes in endotoxemic rats treated with different NOS inhibitors.

机译:用不同NOS抑制剂治疗的内毒素血症大鼠的血流动力学和肝脏微循环变化。

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BACKGROUND/AIMS: Severe septic shock may produce hypotension, which is due to the vasodilatational effect of nitric oxide. The effects of different nitric oxide synthase inhibitors on the hemodynamic and hepatic microcirculation of the endotoxemic rats were studied. METHODOLOGY: A prospective controlled study was performed. Eighteen Sprague-Dawley male rats (250-300 g) were anesthetized and studied. The rats were divided into three groups. The rats in group A (n = 6) were injected with lipopolysaccharide (50 mg/kg BW) and L-NAME (5 mg/kg BW). The rats in group B (n = 6) were injected with the same dose of lipopolysaccharide and aminoguanidine (400 mumole/kg BW). The rats in group C rats (n = 6) were injected with same dose of lipopolysaccharide and normal saline as a control. The rats were cannulated with femoral arterial, venous, and jugular venous catheters. Cardiac output was measured using a thermodilutional method, and liver sinusoidal microcirculation was measured with Laser Doppler Flowmetry. The cardiac output, stroke volume, heart rate, blood pressure, and microcirculational flux of the liver in the three groups were measured and compared at 0, 20, 40, 60 and 80 minutes after injection. RESULTS: The rats of group A showed significant decrease of their cardiac output, stroke volume and hepatic microcirculation after the drugs were infused though their blood pressure increased. The rats of group B showed decrease of their blood pressure and stroke volume initially, but no significant change of their cardiac output and hepatic microcirculation. At the 80th min, the rats of group B had the significantly highest cardiac output, stroke volume and hepatic microcirculation among three groups. CONCLUSIONS: The aminoguanidine prevents the hypotensive effect as well as L-NAME during severe sepsis, but it can maintain cardiac output, stroke volume and hepatic microcirculation better than L-NAME.
机译:背景/目的:严重的脓毒性休克可能产生低血压,这是由于一氧化氮的血管舒张作用所致。研究了不同的一氧化氮合酶抑制剂对内毒素血症大鼠血液动力学和肝脏微循环的影响。方法:进行了一项前瞻性对照研究。麻醉和研究了18只Sprague-Dawley雄性大鼠(250-300 g)。将大鼠分为三组。 A组(n = 6)的大鼠注射脂多糖(50 mg / kg体重)和L-NAME(5 mg / kg体重)。 B组(n = 6)的大鼠注射相同剂量的脂多糖和氨基胍(400摩尔/千克体重)。 C组大鼠(n = 6)被注射相同剂量的脂多糖和生理盐水作为对照。用股动脉,静脉和颈静脉导管对大鼠进行插管。使用热稀释法测量心输出量,并使用激光多普勒血流仪测量肝脏正弦微循环。在注射后0、20、40、60和80分钟,测量并比较三组的心输出量,中风量,心率,血压和肝脏微循环通量。结果:A组大鼠在输注药物后尽管血压升高,但其心输出量,中风量和肝微循环明显降低。 B组大鼠最初显示血压和中风量下降,但心输出量和肝微循环无明显变化。在第80分钟时,B组大鼠在三组中的心输出量,中风量和肝微循环水平最高。结论:氨基胍可预防严重败血症时的降压作用和L-NAME,但与L-NAME相比,它可以更好地维持心输出量,中风量和肝微循环。

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