小儿疳疾临床治验

小儿疳疾是指多种原因导致小儿脾胃损伤，运化失常，以致气液耗伤、全身虚弱赢瘦的疾患，疳证若得不到及时合理治疗，常影响小儿正常生长发育，重的出现体质衰竭，继发多种疾病，甚至危及生命。笔者十多年来在临床上观察治疗小儿疳疾200余例，根据临床小儿疳疾多脾虚肝旺的病症特征，采用扶土抑木的治法，结果收到较好疗效。笔者在本文中将十余年治疳经验做了总结分析。     

光动力疗法与微波对正常大鼠胃损伤的研究

目前，光动力疗法（PDT）治疗胃肠道肿瘤报道较多，但有关PDT对组织损伤机制的研究尚少。本文从显微及超微水平比较PDT与微波对大鼠胃损伤的差异，探讨其损伤机制，旨在为胃肠道肿瘤治疗方法的选择和联合应用，提供理论依据。材料和方法光敏剂：血时财衍生物（Hematoporphyinderivative，HPD）由北京制药工业中心提供。光源：美国产氩离子泵染料激光，氩离子输出波长514．5um，DCM染料经滤光片输出波长630um。石英光导纤维直径为30μm。JK-1型多路温度自动测量仪：军事医学科学院放射医学研究所研制。微波内镜治疗仪：合肥产WNZ-B…     

环氧合酶-2抑制剂对盐酸诱导大鼠胃粘膜损伤后上皮细胞增殖和愈合的影响

目的:探讨特异性和非特异性环氧合酶-2(COX-2)抑制剂,对盐酸诱导胃粘膜损伤后上皮细胞增殖和损伤愈合的影响。方法:大鼠胃内给予06mol/LHCl1mL后,胃内给予NS-398或吲哚美辛,Westernblot和免疫组化法分析盐酸灌胃前、后胃粘膜COX-2表达,免疫组化检测增殖细胞核抗原(PCNA)评价上皮细胞的增殖状态,小格图纸法计算胃损伤指数(LI)。结果:盐酸灌胃后,COX-2在胃粘膜表层上皮细胞和腺颈部成体干细胞高表达。盐酸灌胃后24h,NS-39840mg/kg组及吲哚美辛组PCNA标记指数(PCNA-LI)分别为(22.72±4.33)%和(21.98±5.18)%,明显低于对照组(34.46±3.61)%(P<0.05);NS-3984mg/kg组和40mg/kg组LI分别为(1.28±0.58)%和(1.16±0.56)%,显著高于对照组(0.58±0.24)%(P<0.05)。结论:COX-2抑制剂抑制胃粘膜上皮细胞增殖,延迟大鼠胃粘膜损伤的愈合,提示COX-2表达在胃粘膜再生过程中起重要作用。     

脾胃湿热证病因病机及疾病分布规律浅探

脾胃湿热证是中医脾胃证候中一个常见的实性证候，在气候潮湿、高温多雨的地区容易发生，尤其在岭南地区多见。随着人民生活水平的日益提高，由于纵恣口腹、偏嗜肥甘或嗜食辛辣等导致脾胃损伤、蕴湿生热者也逐渐增多。因此深入系统地研究脾胃湿热证的病因与发病，探讨其疾病分布规律，有助于推动中医脾胃学说理论的发展．提高脾胃湿热证的辨证论治水平。     

胸腔胃在食管癌术后辅助放疗中的剂量分析及胃镜下胃黏膜表现

目的:分析食管癌术后辅助放疗对胸腔胃的照射剂量及胃镜下胃黏膜变化。方法:收集食管癌术后辅助放疗的患者45例,利用治疗计划系统制作放疗计划,并给予50Gy/25f的处方剂量。根据术后胸腔胃位置不同,分为左侧、右侧及纵隔3组,每组15例。利用体积-剂量直方图分析比较各组胸腔胃接受的平均剂量（Dmean）、接受5Gy、25Gy、40Gy、50Gy照射的靶体积百分比（V5、V25、V40、V50）。观察患者放疗中上消化道不良反应情况,放疗后定期复查胃镜,观察胃黏膜变化。结果:纵隔胸腔胃受到照射的Dmean、V5、V25、V40、V50明显高于左侧及右侧胸腔胃（P＜0.05）,左侧及右侧胸腔胃受照剂量无明显差异（P＞0.05）。通过胃镜检查发现大部分患者出现黏膜充血水肿的表现,少部分患者有黏膜糜烂出血的表现。结论:纵隔胸腔胃较左侧及右侧胸腔胃受照剂量较大,放射性胃损伤发生几率可能高。     

Gastric mucosal injury due to hemorrhagic reperfusion and efficacy of Salvia miltiorrhizae extract F and cimetidine

AIM: To observe the gastric mucosal injury caused by hemorrhagic shock and reperfusion and to compare the effect between Salvia miltiorrhizae extract F (SEF) and cimetidine (CI) on it. METHODS: A model of hemorrhage/reperfusion injury was produced by Itoh method. Wistar rats were randomly divided into three groups: 0.9% sodium chloride treatment group (NS group), SEF treatment group (SEF group), and CI treatment group (CI group). Saline, SEF and CI were injected respectively. The index of gastric mucosal lesions (IGML) was expressed as the percentage of lesion area in the gastric mucosa. The degree of gastric mucosal lesions was categorized into grades 0, 1, 2, 3. Atom absorption method was used to measure the intracellular calcium content. Radioimmunoassay was used to measure the concentrations of prostaglandins. RESULTS: IGML (%) and grade 3 (%) were 23.18±6.82, 58.44±9.07 in NS group, 4.42±1.39, 20.32±6.95 in SEF group and 3.74±1.56, 23.12±5.09 in CI group, and the above parameters in SEF group and CI group decreased significantly (IGML: SEF vs NS, t=6.712, P=0.000<0.01; CI vs NS, t=6.943, P=0.000<0.01; grade 3: SEF vs HS, t=8.386, P=0.000; CI vs HS, t=8.411, P= 0.000), but the grade 0 and grade 1 damage in SEF group (22.05±5.96, 34.12±8.12) and CI group (18.54±4.82, 30.15±7.12) were markedly higher than those in NS group (3.01±1.01, 8.35±1.95; grade 0: SEF vs HS, t=8.434, P=0.000<0.01; CI vs NS, t=7.950, P=0.000<0.01; grade 1: SEF vs NS, t =8.422, P=0.000<0.01; CI vs NS, t=8.448, P=0.000<0.01). The intracellular calcium content (μg/mg) in SEF group (0.104±0.015) and CI group (0.102±0.010) was markedly lower than that in NS group (0.131±0.019, SEF vs NS, t=2.463, P=0.038<0.05; CI vs HS, t=3.056, P=0.017<0.05). The levels (pg/mg) of PGE_2, 6-keto-PGF_(1α) and 6-keto-PGF_(1α)/TXB_2 were 540±183, 714±124,17.38±5.93 in NS group and 581±168, 737±102, 19.04±8.03 in CI group, 760±192,1 248±158, 33.42±9.24 in SEF group, and the above parameters in SEF group markedly raised (PGE_2: SEF vs NS, t=2.282, P=0.046<0.05; SEF vs CI, t=2.265, P=0.047<0.05; 6-keto-PGF_(1α): SEF vs NS, t=6.583, P=0.000<0.000; SEF vs CI, t=6.708, P=0.000<0.01; 6-keto-PGF_(1α)/TXB_2: SEF vs NS, t=3.963, P=0.003<0.001; SEF vs Cl, t=3.243, P=0.009<0.01), whereas TXB_2 level in SEF group (45.37±7.54) was obviously lower than that in NS group (58.28±6.74, t=3.086, P=0.014<0.05) and CI group (54.32±6.89, t=2.265, P=0.047<0.05). No significant difference was shown between NS group and CI group (PGE_2: t=0.414, P=0.688>0.05; 6-keto-PGF_(1α): t=0.310, P=0.763>0.05; TXB_2: t=1.099, P=0.298>0.05; 6-keto-PGF_(1α)/TXB_2: t=0.372, P=0.718>0.05). CONCLUSION: Both SEF and CI could inhibit reperfusioninduced injury in gastric mucosa, but with different mechanisms. SEF could not only enhance the protective effect of gastric mucosa, but also abate the injury factors, while CI can only abate the injury factors.     

二甲基甲酰胺吸入致大鼠急性胃损伤的研究

目的通过动物实验探讨二甲基甲酰胺（DMF）对大鼠胃黏膜急性损伤的机制。方法大鼠静式吸入不同浓度（1446．2mg／m^3,3212．3mg／m^3,6524．0mg／m^3）的二甲基甲酰胺气体,观测胃黏膜大体损伤情况、胃黏膜的病理改变及胃黏膜血流（GMBF）、黏膜结合黏液量、谷胱甘肽（GSH）、丙二醛（MDA）、前列腺素E2（PGE2）、胃泌素（Gas）等指标。结果3个浓度组均见胃黏膜出血、糜烂等明显损伤,黏膜结合黏液量降低;低浓度组胃黏膜内谷胱甘肽降低,低、中浓度组胃泌素降低（P〈0．05）;光镜下各浓度组均可见黏液减少,黏膜出血、充血明显,黏膜紊乱。透射电镜可见颈黏液细胞与壁细胞核破裂,核内物质溢出核外。结论二甲基甲酰胺使胃黏膜出血糜烂,可能是损害了颈黏液细胞,使其分泌黏液的能力降低,影响胃的黏液一黏膜屏障系统,并且使胃泌素分泌减少使其营养胃黏膜的作用减弱。