门脉高压大鼠胃粘膜损害的发生机制及其与断流术的关系

THE MECHANISM OF GASTRIC MUCOSAL LESIONS IN PORTAL HYPERTENSIVE RATS AND THE RELATION BETWEEN THE LESIONS AND DEVASCULARIZATION

对门脉高压大鼠胃粘膜的损伤因素和防御因素进行了观察研究,包括测定空腹胃酸分泌量,空腹胃液中胃蛋白酶的活性,胃壁结合粘液量及胃粘膜下层厚度等,并与正常大鼠作了对比。结果发现门脉高压大鼠与正常大鼠的胃酸排出量和胃液中胃蛋白酶活性无显著性差异[(156±48VS 126±54m—Eq/4h,P>0.05)(0.564±0.112VS 0.514±0.717mg/h·ml,P>0.05)]门脉高压大鼠胃壁结合粘液量却明显低于正常对照鼠(1.60±0.42VS 2.30±0.30mg,P<0.001);门脉高压大鼠的胃粘膜血流量也明显低于正常对照鼠(2.22±0.90VS 18.43± 3.88ml/h·kg P<0.001):而门脉高压大鼠胃粘膜下层厚度却远大于正常对照鼠(30.72±3.42VS 14.70±3.77um,P<0.001)断流术半月后门脉高压大鼠的胃酸排出量和胃蛋白酶活性与非手术门脉高压鼠和正常对照鼠比较无显著性差异;其胃壁结合粘液量较非手术门脉高压鼠为低(1.40±0.23VS 1.60±0.42mg,P>0.10)但更低于正常对照鼠(1.40±0.23VS 2.30±0.30mg,P<0.001)断流术后大鼠的胃粘膜血流量也较非手术门脉高压大鼠为低(1.078±1.009VS 2.220±0.901ml/h·kg,P<0.05),且更低于正常对照鼠(1.078±1.009VS 18.43±3.880m/h·kg,P<0.001)断流术后大鼠的胃粘膜下层厚度比非手术门脉高压鼠虽明显变小(25.4±4.08VS 30.

It has been known that portal hypertension ( PHT ) is often complicated by gastric mucosal lesions, but the mechanism of it remains unclear. The purpose of this study is to evaluate the changes of damaging factors and protective factors of gastric mucosa in PHT rats. Gastric acid, pepsin in gastric juice, gastric gel mucus (GGM) , gastric mucosal blood flow (G-MBF ) and gastric submucosal width(GSMW), were measured and compared with the normal. The results revealed that the output of fasting gastric acid and the activity of pepsin in fasting gastric juice did not differ significantly between PHT rats and normal rats(156 +48 vs 126+54 mEq/4h, p>0.05), ( 0.564+0.112 vs 0.514 +0,171 mg/h ml, p>0.10).The quantity of GGM in PHT rats decreased signifieantly(1.60+0.42 vs 2.30+0.30mg, p<0.001);GMBF decreased markedly(2.22+ 0,90 vs 18.43 +3.88ml/h kg,p< 0,001 ), GSMW in PHT rats was much bigger (30.72+3.49 vs 14.70 + 3.77um, p<0.001 ) . Comparison between post-devascularizative portal hy-pertensive(PDPH)and non-operative portal hypertensive(NOPH)rats showed the gastric acid,pepsin and GGM had no signficant changes; but the GMBF and GSMW decreased after operation ( 1.08+1.10 vs 2.22 +0.90 ml/h kg, p<0.05 ) , (25.43+4.08 vs 30.37+3.49um, p<0.05),although the GSMW in PDPH rats was still much bigger than the normal ( 25.43+4.08 vs 14.70 +3.77um, p<0.001 ) . These results indicate that the nain cause of the gastric mucosal lesions in PHT is the disturbance of the protective mechanisms of gastric mucosa, rather than ibe increase of damaging factors, such as gastric acid and pepsin. Since the popular devascularization surgery will result in further reduction of the protective capacity of gastric mucosa and a hith incidance of posoperative gastric mucosal lesions, improvement of this surgery is indicated.