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目的通过观察急性坏死性胰腺炎(acute necrotizing pancreatitis,ANP)大鼠肺组织中诱导型一氧化氮合酶(inducible nitric oxide synthase,i NOS)mRNA和内皮型一氧化氮合酶(endothelial nitric oxide synthase,eNOS)mRNA的表达,探讨内源性NOS在ANP肺损伤中的作用。方法 40只Wistar大鼠随机分为ANP组(n=30)和假手术组(SO组,n=10),采用5%牛磺胆酸钠逆行胆胰管注射法建立大鼠ANP模型。光镜下观察ANP造模后3 h、6 h及12 h时大鼠肺组织病理变化,并应用RT-PCR法检测相应时相肺组织中i NOS及eNOS mRNA的表达水平。结果随着病程延长,ANP组肺组织可见不同程度的充血、水肿、炎性细胞浸润、出血、坏死等病理损害,各时间点其肺损伤评分均明显高于SO组(P<0.05),且呈逐渐升高趋势(P<0.05)。ANP组3 h、6 h及12 hi NOS和eNOS mRNA的表达水平较SO组均有明显升高(P<0.05)。结论肺组织中i NOS及eNOS mRNA的过度表达可能是大鼠ANP肺损伤发生的重要原因之一,这为采用抑制i NOS及eNOS mRNA的表达减轻ANP肺损伤的治疗手段提供了理论依据。
OBJECTIVE: To observe the expression of inducible nitric oxide synthase (iNOS) mRNA and the expression of endothelial nitric oxide synthase (iNOS) mRNA in lung tissue of rats with acute necrotizing pancreatitis (ANP) , eNOS) mRNA expression, to explore the role of endogenous NOS in ANP lung injury. Methods Forty Wistar rats were randomly divided into ANP group (n = 30) and sham operation group (n = 10). Rat ANP model was established by 5% sodium taurocholate retrograde cholangiopancreatography. The pathological changes of lung tissue were observed under light microscope at 3 h, 6 h and 12 h after ANP modeling. The expression of iNOS and eNOS mRNA in the corresponding phase and phase tissues were detected by RT-PCR. Results With the prolongation of duration, the lung tissues of ANP group showed pathological changes such as congestion, edema, infiltration of inflammatory cells, hemorrhage and necrosis. The lung injury scores of ANP group were significantly higher than those of SO group (P <0.05) Showed a gradual upward trend (P <0.05). The ANP group at 3 h, 6 h and 12 hi NOS and eNOS mRNA expression levels were significantly higher than the SO group (P <0.05). Conclusion Overexpression of iNOS and eNOS mRNA in lung tissue may be one of the important causes of lung injury in rats with ANP. This provides a theoretical basis for the treatment of ANP-induced lung injury by inhibiting the expression of iNOS and eNOS mRNA.