补肾中药对雄激素致不孕大鼠卵巢核仁组成区蛋白的影响

观察补肾中药对雄激素致不孕大鼠卵巢核仁组成区蛋白的影响。用ＳＤ雌性大鼠幼仔，出生９ｄ龄注射丙酸睾丸酮，制成雄激素致不孕大鼠（ＡＳＲ）模型。８０ｄ龄灌服补肾中药水溶液两周。１００ｄ龄心脏灌注处死。以核仁组成区蛋白嗜银染色（ＡｇＮＯＲ）和增殖细胞核杭原（ＰｃＮＡ）为指标，观察卵巢颗粒细胞、间质腺细胞的形态学变化。结果：补肾中药能够使ＡＳＲ卵巢颗粒细胞增殖、卵泡发育。治疗组的ＡｇＮＯＲ和ＰｃＮＡ计数明显高于模型组，而与对照组之间无显著差异。结论：补肾中药的这种作用可能是通过调节了下丘脑－垂体－卵巢性腺功能的结果，从而促使卵巢颗粒细胞发育、卵泡成熟。     

DIFFERENCES IN ENDOTHELIUM-DEPENDENT RELAXATION IN VARIOUS ARTERIES FROM WATANABE HERITABLE HYPERLIPIDAEMIC RABBITS WITH INCREASING AGE

1. Endothelium-dependent relaxation in response to acetylcholine (ACh) and the calcium ionophore A 23187 was examined in aorta, coronary, basilar and renal arteries isolated from Watanabe heritable hyperlipidaemic (WHHL) rabbits of 2, 6 and 12 months of age, with normolipidaemic heterozygous WHHL rabbits as controls. 2. In the rings of WHHL rabbit aortae and coronary arteries preconstricted with vasoconstrictors, endothelium-dependent relaxation in response to ACh was attenuated with age compared to the heterozygous WHHL rabbits. A significant negative correlation was found between the total cholesterol content and the relaxation response to ACh in the aortae or coronary arteries from 6 and 12 month old WHHL rabbits. 3. In the rings of basilar arteries, endothelium-dependent relaxations to ACh were not modified with age. Similarly, in the rings of renal arteries, the relaxation response to ACh was not changed with age, but in the 6 and 12 month preparations, after the age of 6 months, a contraction following the relaxation appeared at higher concentrations of ACh (10^?7 to 10^?6 mol/L). The contraction was endothelium-dependent and inhibited by indomethacin. 4. A 23187-induced endothelium-dependent relaxations were also markedly attenuated in the aorta and significantly in the coronary artery with age. 5. Endothelium-independent relaxation to sodium nitroprusside was not changed in all arteries from WHHL rabbits of different ages. 6. These findings indicate that in the aorta and coronary artery of the WHHL rabbit, the endothelium-dependent relaxation to ACh and A 23187 becomes impaired with increasing age (i.e., with the progression of cholesterol deposition in the arterial wall) but is preserved in the basilar and renal artery.     

Steroidal spirooxetanes. I. Synthesis and antiandrogenic properties of some 17-spirooxetanoandrostanes

Pharmaceutical Chemistry Journal -     

复治矽肺结核化疗效果观察

我们自１９８０～１９８８年对７９例复治矽肺结核进行化疗。其中绝大多数为慢性纤维化空洞性病例，均经细菌学证实，并由尘肺诊断组认定为矽肺合并结核。本组病例分别以ＫＭ、ＩＮＨ、ＲＦＰ、ＰＺＡ，或ＳＭ、ＩＮＨ、ＲＦＰ、ＥＢ联合，分两阶段治疗１８个月，获痰菌阴转７９．２％，其中ＫＨＲＺ与ＳＨＲＥ组分别为９３．９％与６８．２％（Ｐ＜０．０５）。自疗程结束追踪２～８年，其细菌复阳率分别为６．４５％和１０．０％（Ｐ＞０．１）。并对影响其过去治疗失败的原因及对策进行了讨论。     

健康人血清叶酸和维生素B_(12)水平的测定

本文对14岁以下健康小儿171名,成人30名及初生儿脐带血30份进行了血清叶酸和维生素B_(12)含量测定,171名小儿于采血前均经补足叶酸和维生素B_(12)。结果:血清叶酸(nmol/L)的正常值低限,<4岁者为6.1,4～14岁为8.4,成人为5.0;血清维生素B_(12)(pmol/L)的正常值低限,<1岁为459,1岁～成人为107。     

Biological activity of fluorinated 3,4-dihydroisoquinolines

Translated from Khimiko-farmatsevticheskii Zhurnal, Vol. 26, No. 1, pp. 44–45, January, 1992.     

过度训练的病理生理及康复 Ⅰ.大鼠过度训练模型的建立

实验表明,运用大鼠跑台运动,以心电图、体重、饮食量、精神状况、毛发脱落、尿蛋白、血清睾酮、皮质醇等为监测指标建立大鼠过度训练模型的方法是可行的。本文并首次模拟出大鼠运动性心律失常心电图。     

异叶梁王茶中三萜皂甙的研究

从异叶梁王茶树皮的醇提取物中分离得到两种新的三萜皂苷化学物，异叶梁王茶苷Ⅶ[1]和异叶梁王茶苷Ⅷ[2]；以及一种已知化合物梁王茶苷Ⅱ[3]。经光谱和化学分析，分别鉴定为3－0－β－（2′，4′-O-二乙酰基）－D－吡喃木糖－3β－羟齐墩果－12－烯－28，29双羧酸－28－O－[α－L－吡喃鼠李糖（1－4）－β－D－吡喃葡萄糖（1－6）－β－D－吡喃葡萄糖]酯苷[1]；3－O－β－（3′－O－乙酰基）－D－吡喃木糖－3β－羟齐墩果－12－烯－28，29－双羟酸－28－O－［α－L－吡喃鼠李糖（1－4）－β－D－吡喃葡萄糖（1－6）－β－D－吡喃葡萄糖］酯苷［2］。     

Inhibition of GABA-gated chloride channel function by arachidonic acid

The effects of arachidonic acid and its metabolites on gamma-aminobutyric acid (GABAA) receptor function were determined in rat cerebral cortical synaptoneurosomes. Incubation of synaptoneurosomes with phospholipase A2 decreased muscimol-induced 36Cl- uptake. Arachidonic acid, the major unsaturated fatty acid released by phospholipase A2, also inhibited muscimol-induced 36Cl uptake. Similar inhibition was obtained with other unsaturated fatty acids (docosahexaenoic, oleic) but not with saturated fatty acids (stearic, palmitic). The effect of arachidonic acid on muscimol responses was inhibited by bovine serum albumin (BSA), and BSA enhanced muscimol responses directly, indicating the generation of endogenous arachidonic acid in the synaptoneurosome preparation. The generation of endogenous arachidonic acid was also indicated by the ability of 2 inhibitors of arachidonic acid metabolism, indomethacin and nordihydroguaiaretic acid (NDGA), to inhibit muscimol-induced 36Cl uptake. We conclude that arachidonic acid probably has both direct and indirect actions on muscimol responses since both enzyme inhibitors inhibited muscimol responses but did not prevent the effect of exogenously added arachidonic acid. In additional experiments, arachidonic acid metabolites generated by cyclooxygenase, prostaglandins D2, E2 and F2 alpha, each decreased muscimol responses; prostaglandins F2 alpha was the most potent inhibitor. Since the unsaturated fatty acids and their metabolites are most susceptible to peroxidation, a generating system of superoxide radicals was tested on muscimol responses. A combination of xanthine and xanthine oxidase inhibited muscimol-induced 36Cl uptake in a concentration-dependent manner. We propose that the inhibition of GABAA neurotransmission by arachidonic acid and its metabolites can lead to increased neuronal excitability. This mechanism may play an important role in the development of neuronal damage following seizures or cerebral ischemia.