摘要
用小剂量ＣＣＩ＿４皮下注射与脂肪饲料及乙醇喂饲复制肝硬变门脉高压性瘀证大鼠模型，以探索中医舌脉变化与舌深静脉压、门脉压、门脉血流量之间的关系。实验结果表明，实验组大鼠均已形成肝硬变，并以假小叶形成的三期病变为主，肝窦不清晰，间隙变窄乃至闭塞；舌腹面粘膜下乃至肌间、食管及胃肠粘膜下均有微小血管淤血，脾脏淤血更为明显；舌深静脉压力升高，与门脉压升高呈正相关；门脉血流量明显减少，与正常对照组大鼠比较Ｐ＜０．０１．认为肝硬变门脉高压性瘀症的舌脉粗张与细络瘀血主要是因门脉血经门一腔侧支循环回流入上腔静脉，引起上腔静脉阻力增大，压力增高，导致舌的静脉系统回流受阻，使舌深静脉血流量增多，压力升高所致。
The model of rats cirrhosis with portal hypertensive stasis was reprodued bysubcutaneous injection of small dose of carbon tetrachloride and feeding with fatty foodsand alcohol.The model is used to explore the change of lingual vessels in relation to thepressure of deep lingual vein;portal vein and portal blood flow in view of traditionalChinese medicine,The experimental results indicated that in rats of the experimental grouphepatocirrhosis.were formed,mainly manifested with pseudolobules of the third stage lesion.Hepatic sinusoids were unclear and interspace became narrow and even occluded.Microvascular stasis were showed in submucous and intramuscular laver of the ventralsufaee of tongue,submucous of esophagus and gastrointestinal tract.Splenic vessels stasis weremuch more markedly.Elevation of venopressure in deep linguae appeared which was cor-related wiht that of portal pressure. Portal blood flow decreased predominantly,as comparedwith the control group(P<0.01)It was believed that its engorgement of lingual vessels andtheir branches in cirrhosis with portal hypertensive stasis were due to the portal blood passthrough portacaval collateral circulation inflow to superior venaecava causing increased re-sistance and pressure elevation that lead to obstruct its lingual venous system inflow andalso elevation of deep lingual venous pressure.
出处
《中国病理生理杂志》
CSCD
北大核心
1996年第4期422-424,共3页
Chinese Journal of Pathophysiology
基金
国家自然科学基金
