外源性雄激素对幼年大鼠骨骼肌肌纤维及其运动终板形态的影响

目的：观察雄激素对骨骼肌肌纤维及其运动终板形态的影响。材料与方法：给５ ｄ 龄的Ｗｉｓｔａｒ 雄性大鼠持续５ 周肌内注射丙酸睾丸酮（每天４０ｍｇ／ｋｇ）,用肌球蛋白ＡＴＰ酶染色法（ｐＨ１０－４ 孵育液预处理） 和乙酰胆碱酯酶染色法分别对大鼠趾长伸肌的肌纤维和运动终板染色。结果：雄激素对幼年雄性大鼠趾长伸肌的肌纤维类型形态以及运动终板的结构均没有显著影响（Ｐ＞０－０５）。结论：从形态上可能说明雄激素对肢体骨骼肌的收缩速度没有显著影响。     

Vascular depression: a new view of late-onset depression

We have suggested that cerebrovascular disease may predispose, precipitate, or perpetuate some late-life depressive syndromes. The mechanisms of "vascular depression" include disruption of cortico-striato-pallido-thalamo-cortical (CSPTC) pathways or their modulating systems. This view is supported by the presentation of vascular depression, which consists of depressive symptoms, cognitive abnormalities, as well as neuroimaging findings that may result from CSPTC impairment. Moreover, clinical and electrophysiological evidence of CSPTC impairment, an abnormality frequently found in patients with vascular depression, appears to be associated with poor response to antidepressant treatment and early relapse and recurrence. The vascular depression hypothesis provides the conceptual background for studies that may have clinical and theoretical impact. Agents influencing dopamine, acetylcholine, and opioid neurotransmitters may be studied in vascular depression, since these are essential neurotransmitters of the frontostriatal circuitry. Drugs used for prevention and treatment of cerebrovascular disease may be shown to reduce the risk for vascular depression or improve its outcomes. The choice of antidepressants in vascular depression may depend on their effect on neurological recovery from ischemic lesions. Finally, identification of specific relationships between specific symptoms, cognitive deficits, and disability may lead to interventions that target the patients' deficits as well as their interactions with psychosocial factors known to contribute to depression. Research can clarify the pathways to vascular depression by focusing on the site of lesion, the resultant brain dysfunction, the presentation of depression and time of onset, and the contribution of nonbiological factors.     

Purinoceptor-mediated modulation by endogenous and exogenous agonists of stimulation-evoked [3H]noradrenaline release on rat iris

Summary To investigate whether endogenous purinoceptor agonists affect the sympathetic neurotransmission in the rat isolated iris, and to classify the purinoceptors modulating exocytotic [³H]-noradrenaline release, we have determined the effect of adenosine receptor antagonists on, and the relative potency of selected agonists in modulating, the field stimulation-evoked (3 Hz, 2 min) [³H]-noradrenaline overflow. In addition, the apparent affinity constants of 8-phenyltheophylline (8-PT) and 1,3-dipropyl-8-cyclopentylxanthine (DPCPX) in antagonizing the prejunctional effects of purinoceptor agonists were estimated.The relatively A₁-selective DPCPX 10 and 100 nmol/l increased the evoked [³H]-noradrenaline overflow by about 25%–35%a indicating a minor inhibition of evoked release by endogenous purinoceptor agonists probably via an A₁ adenosine receptor. Whereas the A₁/A₂-antagonist 8-PT failed to increase the evoked [³H]-noradrenaline overflow in the absence of exogenous agonists (without or with dipyridamole 1 pmol/l present), the relatively A₂-selective antagonist CP-66,713 (4-amino-8-chloro -1-phenyl(1,2,4)triazolo(4,3-a)quinoxaline) 100 nmol/l decreased it by 20%–30% in the absence and continuous presence of DPCPX. This may be compatible with a minor A₂-mediated facilitation by an endogenous purinoceptor agonist.All exogenous agonists tested (except UTP 100 mol/l) inhibited the evoked [³H]-noradrenaline overflow. The relative order of agonist potency (IC4o, concentration in mol/l for inhibition of evoked release by 40%) was CPA (N⁶-(cyclopentyl)adenosine, 0.004) > R-PIA (R(–)N6-(2phenylisopropyl)adenosine, 0.066) = CHA (N⁶-(cyclohexyl)adenosine, 0.082) > NECA (N⁵-(ethyl-carboxamido)adenosine 0.44) > ADO (adenosine, 4.1). ATP was n early equipotent with ADO. Maximum inhibition was 70%–80% and similar for all agonists. Adenosine deaminase 1 u/ml failed to affect the ATP-induced, but abolished the adenosine-induced prejunctional inhibition. The adenosine uptake inhibitor S-p-nitrobenzyl-6-thioguanosine (NBTG) failed to enhance the potency of ADO and ATP. The A₁-selective antagonist DPCPX 10 nmol/l did not reduce the ATP potency indicating an effect of ATP per se not mediated via an A₁ purinoceptor.Prejunctional affinity constants of 8-PT were 6.07 when tested against adenosine (in the presence of dipyridamole), and 6.60 against CHA. The apparent -log K_B of DPCPX tested against CPA was 9.71. The high DPCPX affinity is compatible with an A₁ adenosine receptor mediating inhibition of sympathetic neurotransmission in rat iris. This receptor may not be the only prejunctional purinoceptor on rat iris sympathetic nerves. The receptor by which ATP acts prejunctionally in this tissue remains to be determined.This study was supported by the Deutsche Forschungsgemeinschaft (Fu 163/2 and 163/3) Send offprint requests to H. Fuder at the above address     

Plasma catecholamines and oxygen consumption during weaning from mechanical ventilation

Previous studies on oxygen consumption ( ) during weaning from mechanical ventilation assumed that an increase in ( ) reflected oxygen consumption by respiratory muscles ( ), and proposed as a weaning predictor. We measured CO₂ production ( ) and plasma catecholamines in 20 short-term ventilated patients during weaning by SIMV and CPAP. as a percentage of during spontaneous ventilation ( %) ranged from 4.8% to 41.5%. also increased and correlated with . Plasma adrenaline and noradrenaline increased significantly to levels known to produce considerable increases in metabolic rate. Mean arterial pressure and heart rate concomitantly increased, but spontaneous minute ventilation decreased. Thus, since the increased plasma catecholamines are calorigenic, the assumption that represents is incorrect. Although mean % of successfully weaned patients was significantly less than that of failure-to-wean patients, the wide scatter of individual values in the latter group excludes % as an accurate weaning predictor.     

茵陈提取液对实验性动物肝损伤的作用

目的　研究茵陈提取液对实验性肝损伤的作用。 方法　 用茵陈提取液连续给小鼠灌胃 7d后 ,采用四氯化碳 (CCL4 )腹腔内注射造成小鼠急性肝损伤 ,造型 2 0h后摘除眼球取血 ,测ALT、AST、ALP、TP、G、A等指标 :给大鼠每周二次皮下注射 10 %CCL4油液 0 .5ml/ 10 0g ,造成慢性肝损伤 ,于中毒第三个月初起开始 ,每日用茵陈提取液连续给大鼠灌胃一个月 ,于末次给药 2 4h眶静脉取血 ,分离血清 ,AT、AST、总蛋白、白蛋白、白蛋白 /球蛋白 (A/G)等指示。 结果　CCL4造成小鼠急性肝脏损伤 ,出现明显肝功能异常 ,茵陈提取液治疗组小鼠各项指标较CCL4模型组均有所降低 ,但差异无显著性意义 (P >0 .0 5 ) ;在CCL4所致大鼠慢性肝损伤模型中 ,茵陈提取液治疗组可显著地降低大鼠由CCL4造成的AST活性升高 ,与模型组比较 ,P <0 .0 1。 结论　 茵陈提取液对CCL4所致大鼠慢性肝损伤有较好的治疗作用 ,但对CCL4造成小鼠急性肝伤模型没有保护作用。     

积雪草总苷对小鼠抑郁行为和脑内氨基酸含量的影响

目的：采用小鼠强迫游泳抑郁症模型，观察积雪草总苷的抗抑作用。方法：昆明种小鼠随机分为空白对照组、模型组、阳性对照丙咪嗪组和积雪草总苷组，分析药物对小鼠强迫游泳不动时间及脑内氨基酸含量的影响。结果：丙咪嗪组和积雪草总苷低、中、高3个剂量能够显著缩短小鼠强迫游泳不动时间，改善强迫游泳所致小鼠脑内氨基酸含量的失调。结论：积雪草总苷具有抗抑郁活性。     

枝管藻多糖对实验性高脂血大鼠血脂和过氧化水平的影响

目的:观察枝管藻多糖对实验性高脂血大鼠血脂和过氧化水平的影响。方法:以Wistar大鼠为研究对象,用高脂饲料建立高脂血症大鼠模型,分别ig枝管藻多糖和烟酸肌醇酯(枝管藻多糖的剂量为150mg·kg~(-1)·d~(-1),300mg·kg~(-1)·d~(-1),烟酸肌醇酯的剂量为 100mg·kg~(-1)·d~(-1)),连续40d。于实验的第 30天和第40天,各采血一次,分别测定血清 TC,TG,LDL-C,HDL-C,MDA,ROS含量和 SOD活性。结果:枝管藻多糖能显著抑制们喂高脂饲料大鼠的 TG(P<0.05)水平的升高,显著降低高脂血症大鼠的血清 TC(P<0.05)和TG(P<0.05)含量,但对血清LDL-C和HDL-C含量的变化几乎无影响;明显降低高脂血大鼠血清ROS,MDA含量,提高血清 SOD活性(P<0.01或 P<0.05)。结论:枝管藻多糖能够显著改善高脂血大鼠体内过氧化状态,但其抗高脂血效果低于烟酸肌醇酯。     

土鳖虫水提物对实验性高脂血症大鼠血管内皮和内皮素的影响

目的研究土鳖虫水提物对高脂血症大鼠血管内皮和内皮素 (ET)的影响。方法建立高脂血症大鼠模型 ,测定血浆ET的浓度 ,并应用内皮细胞铺片和免疫组化相结合的方法 ,在大鼠主动脉内皮细胞铺片上 ,计数内皮细胞和ET阳性细胞并定量分析ET的合成。结果实验第 80d ,与正常组比较 ,高脂组血浆ET显著增高 (P <0 .0 1) ;内皮铺片显示内皮细胞数量增多 ,排列紊乱 ,胞核大小和染色深浅不一 ,ET阳性细胞率显著升高 (P <0 .0 1)。土鳖虫中、高剂量组血浆ET水平和ET阳性细胞率显著降低 (P <0 .0 5～ 0 .0 1)。结论土鳖虫水提物能保护血管内皮 ,减少ET的合成与释放     

三种蝮蛇抗栓酶的毒性及性质的实验研究

目的:对三种蝮蛇抗栓梅的毒性及其性质进行实验研究。方法:小白鼠尾静脉注射急性毒性实验法和家兔亚急性毒性实验法。结果:三种蝮蛇抗栓酶的毒性强度用LD_50表示,分别是,蛇岛蝮蛇抗栓酶为1.68±0.35u/kg,东北陆生白眉蝮蛇抗栓酶为5.223±0.61u/kg,浙江蝮蛇抗栓酶为1.94±0.15u/kg。对家兔亚急性毒性实验表明,对血细胞、肝及肾功能、脏器等无明显影响。     

阵发性睡眠性血红蛋白尿辨治探讨

阵发性睡眠性血红蛋白尿是一种慢性血管内溶血 ,以与睡眠有关的、间隙发作的血红蛋白尿为特征。临床论治分为虚实两型 ,并提出其治则为实者凉血利水 ,虚者扶正利水 ,同时不可偏废活血化瘀。