氦—氖激光照射对小鼠脑细胞多巴胺含量的影响

目的：探讨氦－氖激光对小鼠脑组织多巴胺（ＤＡ）有无影响。方法：在麻醉状态下, 开小鼠头部皮肤,暴露颅骨及脑组织,用氦－氖激光仪垂直照射小鼠额叶皮质,采用高效液相色谱－电化学检测方法测定不同剂量氦－氖激光照射后小鼠脑组织ＤＡ含量的变化。结果：激光照射各组可明显增加小鼠脑组织ＤＡ含量,以剂量为５５．１ｊ／ｃｍ＾２和２７．６５／ｃｍ＾２组最明显,差异有高度统计学意义。结论：氦－氖激光脑局部照射可增加小鼠     

氦—氖激光对离体宫颈癌细胞增殖的影响

目的：全面认识氦－氖激光的生物效应。方法：分别用１７．２７Ｊ／ｃｍ＾２，３４．５４Ｊ／ｃｍ＾２，６９Ｊ／ｃｍ＾２剂量的氦－氖激光照射人宫颈癌ＨｅＬａ细胞，隔天１次，共６次。照射结束后４７，７２，９６小时对８组细胞进行增殖实验分析。结果：３组细胞增殖加快（Ｐ〈０．０５），１组降低（Ｐ〈０．０１），４组无差异（Ｐ〉０．１），所有数据经秩和检验表明，氦－氖激光照射对细胞增殖无明显影响（ｕ＝１．６１５８，     

氦—氖激光对真皮下血管网皮瓣的影响

目的：探讨氦－氖激光对真皮下血管网皮瓣成活的作用。方法：采用能量密度为２．３９Ｊ／ｃｍ＾２的氦－氖激光照射豚鼠背部随意型真皮下血管网皮瓣，对皮瓣的成活、微血管变化状况以及过氧化脂质含量的变化进行了观测。结果：氦－氖激光照射可扩张血管，促进血液供应，降低皮瓣内过氧化脂质的含量，减轻组织细胞损伤，增加皮瓣成活。最佳照射时间为５￣１０天。结论：氦－氖激光对真皮下血管网皮瓣成活有促进作用。     

氦—氖激光对大鼠皮瓣存活的影响

目的：观察氦－氖激光照射对大鼠皮瓣存活的影响。方法：采用氦－氖激光，波长６３２．８ｎｍ，能量密度０．６３Ｊ／ｃｍ＾２，对照大鼠背部超长随意型皮瓣，１５分种，每日２次，连续照射。进行９９ｍＴｃ清除率实验，皮瓣透明标本观察，皮瓣病理切片检查，皮瓣组织匀浆ＳＯＤ检测。结果：激光照射组术后第９日皮瓣存活面积明显大于对照组（Ｐ〈０．００１）。结论：氦－氖激光可以改善皮瓣血供，刺激毛细血管增生，促进皮肤成纤维     

氦—氖激光照射对脾T细胞转化及T细胞亚群的影响

以能量密度分别为３．９Ｊ／ｃｍ＾２、７．８Ｊ／ｃｍ＾２、１９．５Ｊ／ｃｍ＾２和Ｈｅ－Ｎｅ激光照射小鼠脾区，观察其脾Ｔ淋巴细胞转化率和Ｔ细胞亚群的变化。结果表明，Ｈｅ－Ｎｅ激光照射小鼠脾区后，脾Ｔ淋巴细胞转化率、辅助性Ｔ细胞（ＴＨ）均显著增加，抑制性Ｔ细胞（Ｔｓ）显著减少，尤以７．８Ｊ／ｃｍ＾２、１９．５Ｊ／ｃｍ＾２组最显著（Ｐ〈０．０５）。     

氦—氖激光对人大颗粒淋巴细胞内嗜天青颗粒影响的图像分？…

目的 探讨氦－氖（Ｈｅ－Ｎｅ）激光对人体的免疫刺激作用的机理。方法 用３．１Ｊ／ｃｍ＾２、９．４Ｊ／ｃｍ＾２、２５．０Ｊ／ｃｍ＾２和４９．９Ｊ／ｃｍ＾２剂量的Ｈｅ－Ｎｅ激光分别在体外辐射人外周血，细胞化学方法显示大鼠粒淋巴细胞内嗜天青颗粒，产用图像分析系统对嗜天青颗粒作定量分析。结果 ３．１Ｊ／ｃｍ＾２辐照组的嗜天青颗粒数目、颗粒面积、颗粒面积与细胞面积比值和颗粒积分光密度四项参数值与对照组比较无     

氦氖激光照射大鼠心前区对血液流变学指标的影响

目的 应用不同剂量的氦氖激光照射成年Ｗｉｓｔａｒ大鼠的心前区,研究低能量激光对血液流变的影响,为氦氖激光应用于临床提供依据。方法 就用１０．３Ｊ／ｃｍ＾２,２０．６Ｊ／ｃｍ＾２、６０．５Ｊ／ｃｍ＾２三种剂量照射成年和幼年大鼠心前区,检测其血液流变学指标。结果 能量密度为６０．５Ｊ／ｃｍ＾２的氦氖激光照射,能降低成年鼠的血细胞压积、全血粘度,增强其红细胞变形性,延长红细胞聚集时间。结论 氦氖激光照射     

氦—氖激光对人淋巴细胞中酸性α—醋酸萘酯酶影响的图象分析

用３．１Ｊ／ｃｍ＾２、９．４Ｊ／ｃｍ＾２、２５．０Ｊ／ｃｍ＾２和４９．９Ｊ／ｃｍ＾２剂量的Ｈｅ－Ｎｅ激光分别辐照人外周血。应用酶细胞化学方法显示淋巴细胞内酸性α－醋酸萘酯酶（ＡＮＡＥ）反应物，并用图像分析系统对ＡＮＡＥ反应物作定量分析。结果表明，３．１Ｊ／ｃｍ＾２辐照组的酶反应物颗粒数目、颗粒面积、颗粒面积与细胞面积比值和颗粒积分光密度４项参数值与对照组比较无明显变化；９．４Ｊ／ｃｍ＾２辐照组的四     

氦－氖激光照射对脾T细胞转化及T细胞亚群的影响

以能量密度分别为３．９Ｊ／ｃｍ２、７．８Ｊ／ｃｍ２、１９．５Ｊ／ｃｍ２的Ｈｅ－Ｎｅ激光照谢小鼠脾区，观察其脾Ｔ淋巴细胞转化率和Ｔ细胞亚群的变化。结果表明，Ｈｅ－Ｎｅ激光照射小鼠脾区后，脾Ｔ淋巴细胞转化率、辅助性Ｔ细胞（ＴＨ）均显著增加，抑制性Ｔ细胞（Ｔｓ）显著减少，尤以７．８Ｊ／ｃｍ２、１９．５Ｊ／ｃｍ２组最显著（Ｐ＜０．０５）。     

氦-氖激光对人大颗粒淋巴细胞内嗜天青颗粒影响的图像分析研究

目的探讨氦－氖（ＨｅＮｅ）激光对人体的免疫刺激作用的机理。方法用３．１Ｊ／ｃｍ２、９．４Ｊ／ｃｍ２、２５．０Ｊ／ｃｍ２和４９．９Ｊ／ｃｍ２剂量的ＨｅＮｅ激光分别在体外辐照人外周血，细胞化学方法显示大颗粒淋巴细胞内嗜天青颗粒，并用图像分析系统对嗜天青颗粒作定量分析。结果３．１Ｊ／ｃｍ２辐照组的嗜天青颗粒数目、颗粒面积、颗粒面积与细胞面积比值和颗粒积分光密度四项参数值与对照组比较无明显变化；９．４Ｊ／ｃｍ２辐照组的四项参数值明显增高；２５．０Ｊ／ｃｍ２辐照组的四项参数值进一步增高；４９．９Ｊ／ｃｍ２辐照组的四项参数值较２５．０Ｊ／ｃｍ２辐照组明显降低。结论适当剂量的ＨｅＮｅ激光能活化人大颗粒淋巴细胞内嗜天青颗粒，提高机体的免疫功能；最适激光剂量的选择是临床应用中应考虑的一个重要因素。     

常压高浓度氧环境对早产大鼠脑损伤的影响

目的 观察常压高浓度氧（NH）对早产大鼠脑组织病理学改变及脑组织中丙二醛（MDA）含量和超氧化物歧化酶（SOD）活性的影响,探讨NH对未成熟大鼠脑损伤的影响及其作用机制。方法 取21 d早产新生Wistar大鼠192只,于生后12 h随机分为对照组（空气吸入）、NH 1组（吸入体积分数0.30氧气）、NH 2组（吸入体积分数0.60氧气）和NH 3组,（吸入体积分数0.95氧气）,每组48只。NH 1组、NH 2组和NH 3组于NH环境养育72 h,各组分别于吸氧结束后第0、3、5和10天灌注取脑组织,在光镜下观察其病理改变,并分别测定脑组织匀浆中MDA含量和SOD活性的变化。结果 与对照组、NH 1组比较,NH 2组、NH 3组光镜下脑组织均可见神经元变性和脑组织水肿,NH 3组可见明显胶质细胞反应,且NH 3组脑损伤程度较NH 2组加重。对照组和NH1组各时间点的MDA含量和SOD活性比较差异无显著性（P〉0.05）。NH 2组、NH 3组吸入NH后脑组织MDA含量升高,SOD活性下降,吸氧结束后第0、3、5天的MDA含量、SOD活性与对照组和NH 1组比较差异均有显著性（F=93.91～786.97,q=4.82～53.50,P〈0.01）。第10天NH 3组与对照组和NH 1组、NH 2组比较MDA含量、SOD活性差异均有显著性（F=4.03～5.26,q=0.80～5.05,P〈0.05、0.01）。结论 持续吸入NH可能引起早产大鼠脑损伤,适当控制吸氧浓度和时间有助于减少脑损伤的发生,减轻脑损伤的程度。     

BRAIN TO BRAIN TRANSMISSION OF THE SUBMAXILLARY GLAND VIRUS IN YOUNG GUINEA PIGS

The submaxillary gland virus of guinea pigs was serially transmitted from brain to brain in young guinea pigs. The source of virus was the submaxillary glands of six groups of stock animals. Brain to brain transfer was effected in two series, in one to the second generation and in the other to the third. The transmission was evidenced by the presence of nervous symptoms and death and by a typical microscopic pathology of the brain. Only certain attempts were successful, ten of twenty-three brain to brain injections being fatal with the specific histopathology present in five. A few observations suggest that the virus may be present spontaneously in the gland and experimentally in the brain without cellular changes being demonstrable, or before they are evident. While we were able to transmit the virus from brain to brain with fatal results by single injections of small doses, this was not readily accomplished and the transmission failed after two or three passages. We were unable to show any perceptible increase in virulence or adaptation of the virus to the brain tissue of the natural host. The histopathology was that of a meningoencephalitis. The inflammatory reaction irregularly involved the meninges, the underlying brain substance, and the perivascular tissue of the meninges and upper cortical layer. These structures were infiltrated with mononuclear cells, many of which contained a typical acidophilic inclusion. Congestion of cerebral capillaries uniformly occurred and various degrees of recent hemorrhage were frequently found. Necrosis was noted only when associated with an occasional area of extensive hemorrhage. Similar changes were observed in sections of the spinal cord. When sufficient time (15 days or more) elapsed between cerebral inoculation and death, typical cellular inclusions were seen in the salivary glands, whereas none was found in animals that died earlier (7 to 9 days). Under the first mentioned conditions, inclusions were demonstrated in the parotid and mucous portion of the submaxillary glands, although in spontaneously infected animals, we failed to find the mucous portion involved and other workers report that the parotid is spared. About one-third of the stock guinea pigs examined showed cellular inclusions in both the nucleus and cytoplasm of epithelial duct cells of the serous part of the submaxillary gland. From an analysis of the results of brain to brain inoculations, it was evident that spontaneous infection and resistance to cerebral inoculation increased with age. The 3rd week of life is the period of choice for such experimentation.     

ANAEROBIC GLYCOLYSIS OF THE BRAIN IN EXPERIMENTAL POLIOMYELITIS

The rate of anaerobic glycolysis of brain tissue was compared for normal animals and animals with experimentally induced poliomyelitis, using two different strains of mice and two different procedures. The report of interference of poliomyelitis with anaerobic glycolysis of brain was not confirmed. In one series there was a small increase and in the other series a small decrease in the brain Q_COCO2 ^N₂ calculated for infected animals as compared to normal animals. When the calculations were made on the basis of wet weight of brain there was no difference in glycolysis. It is considered that the methods so far used for study of the enzymes may be inadequate, and that no decision is as yet possible on the effect of poliomyelitis on anaerobic glycolysis.     

窒息心脏骤停后脑的温度对于脑水肿和脑血流的作用

目的；探讨鼠6min窒息心脏骤停后，脑温度变化对脑水肿和脑血流的作用。方法：在浅麻醉和潘蔻罗宁麻痹下，心脏骤停前和后3h使用间歇正压通气。窒息6min后，给肾上腺素和碳酸氢钠并立即开始心肺复苏。激光－多谱勒血流计在皮质连续测定脑血流。在心脏骤停后3h，用碘125标记的白蛋白和湿重与干重的比例来测定脑水肿。自主循环恢复后15min，脑的温度，1组（n＝8）降低到30～31℃，2组（n＝8）保持在37～38℃，3组（n＝8）升高到39～40℃，保持3h，直肠的温度均保持在37～38℃，T检验比较组间资料的差异。结果：在自主循环恢复后1h和2h，1组完全防止了皮质低灌注，2组和3组的皮质脑血流明显低于心脏骤停前。血脑屏障渗透指数，1组（8．9±1．8）明显低于2组（17．1±2．4，P＜0．05）。结论：心脏骤停后，选择性脑低温能增加脑血流和预防脑水肿。     

颅脑MRI在无神经功能异常的慢性头痛中的诊断价值

目的:评价颅脑MRI在慢性头痛而无神经功能异常的成年患者中发现异常的作用。方法:回顾性调查338例无神经功能异常的慢性头痛患者的临床资料和颅脑MRI检查结果,并根据MRI发现分成三组:颅脑MRI无异常组、次要异常组和重要异常组。结果:无异常组患者218例(64.5%),次要异常组113例(33.4%),重要异常组7例(2.1%,95%可信区间上限为4.2%)。其中,在55例不明原因头痛(无法明确分类的头痛)患者中MRI提示重要异常的有5例(9.1%,95%可信区间上限为20.0%)。造影增强扫描(n=16)或重复MRI检查(n=35)均无其它异常发现。结论:神经功能正常的慢性头痛的诊断可能不必要行颅脑MRI检查,造影增强扫描或重复MRI检查也无助于诊断,而不明原因头痛的诊断则有必要进行该检查。     

脑外伤病人血液流变学改变的初步探讨

本文对脑外伤病人的血液流变学变化进行初步分析，并指出血液粘滞性对脑血流的影响。     

甘露醇灌洗脑创面对兔创伤性脑水肿的疗效研究

目的　观察局部应用甘露醇治疗兔创伤性脑水肿的疗效。方法　应用骨窗成形硬膜打击法制备脑挫裂伤动物模型 ,实验组用甘露醇冲洗脑创面 ,对照组不用。按预定时间处死动物 ,测定脑组织含水量及血清髓鞘碱性蛋白。结果　实验组血清碱性蛋白及脑组织含水量较对照组低。结论　局部应用甘露醇可减轻继发性脑水肿。