针刺“百会”、“大椎”对血管性痴呆大鼠脑内NO及NOS的影响

目的建立拟血管性痴呆（VD）的动物模型，探讨针刺百会及大椎对VD大鼠的认知行为及脑内一氧化氮（NO）及一氧化氮合酶（NOS）的影响。方法选用纯系Wistar老年大鼠36只，随机分为假手术组、模型组、针刺组和西药组，采用2-血管阻断法（2-VO）制作VD大鼠模型，之后进行百会、大椎针刺治疗。检测大鼠穿梭箱实验成绩及脑内NO的含量及NOS的活力。结果数据经统计学分析表明，针刺VD大鼠的百会、大椎穴，可明显减少VD大鼠在穿梭箱实验中的电击次数和电击时间，降低脑组织内NO的含量及NOS活性。结论针刺百会、大椎能提高VD大鼠的学习记忆能力．改善自南甚代谢．但讲VD大鼠的智能恢复．     

针刺百会、大椎对血管性痴呆大鼠认知行为及血液流变学的影响

目的 建立拟血管性痴呆（VD）的动物模型，探讨 针刺百会及大椎对VD大鼠的认知行为及脑内血液流变学的影响。方法 选用纯系Wistar老年大鼠36只，随机分为假手术组、模型组、针刺组和西药组，采用2-血管阻断法（2-VO）制作VD大鼠模型，之后进行百会、大椎针刺治疗。检测大鼠穿梭箱实验成绩及脑内的全血黏度、血浆黏度、红细胞压积及纤维蛋白原浓度的改变。结果 经统计学处理数据表明，针刺VD大鼠的百会、大椎，可明显减少VD大鼠在穿梭箱实验中的电击次数和电击时间，可使VD大鼠的全血黏度、血浆黏度、红细胞压积及纤维蛋白原浓度降低。结论 针刺百会、大椎能提高VD大鼠的学习记忆能力．改善VD大鼠的血漓流峦学状杰．从而改善大脑的血液供府．促进智能的恢复。     

针刺百会、大椎对老年性痴呆大鼠脑内SOD及AChE的影响

目的探讨针刺百会、大椎对老年性痴呆大鼠的脑内超氧化物歧化酶(SOD)及乙酰胆碱酯酶(AChE)含量的影响。方法选用纯系Wistar老年大鼠52只,随机分为假手术组、模型组、针刺组和西药组,采用β-淀粉样蛋白向海马CA1区定向注射制作老年性痴呆模型,进行百会、大椎针刺治疗。检测大鼠脑内SOD及AChE的含量。结果针刺老年性痴呆大鼠的百会、大椎穴,可明显提高脑组织内SOD的含量,降低脑组织内AChE的含量,与模型组比较有统计学意义(P<0.05)。结论针刺能提高老年性痴呆大鼠的学习记忆能力,改善自由基代谢,促进老年性痴呆大鼠的智能恢复。     

“益气调血、扶本培元”药线灸对多发梗死性痴呆大鼠海马乙酰胆碱、乙酰胆碱酯酶、胆碱乙酰转移酶含量的影响

目的观察"益气调血、扶本培元"药线灸对多发梗死性痴呆(MID)大鼠海马乙酰胆碱(ACh)、乙酰胆碱酯酶(AChE)、胆碱乙酰转移酶(ChAT)含量的影响。方法 100只雄性大鼠经MID造模、痴呆筛选后,随机分为正常组、模型组、假手术组、药线灸组、药物组和药线非穴组6组,各组10只;药线灸组予壮医药线点灸治疗,药物组给予多奈哌齐口服治疗,药线非穴组给予针刺两肋下非穴点治疗,余3组未给予特别治疗。经4 w干预后处死动物,分离海马,匀浆、分离上清,检测ACh、AChE与ChAT含量。结果模型组ACh、ChAT含量较正常组显著降低,AChE含量显著升高(P<0.05);药线穴组与模型组ACh、AChE无统计学差异(P>0.05),药线灸组能显著升高ACh、ChAT和降低AChE含量,而药物组只显著升高ACh和降低AChE含量(P<0.05);药物组与药线灸组比较无差异(P>0.05)。结论 "益气调血、扶本培元"药线灸可以全面改善MID大鼠海马ACh代谢障碍,且较多奈哌齐有疗效优势。     

针刺对帕金森模型大鼠纹状体多巴胺及代谢产物含量的影响

目的探讨针刺治疗帕金森病（PD）模型大鼠的疗效及作用机制.方法应用偏侧纹状体立体定向注射6-羟基多巴胺的方法制备PD模型大鼠,针刺百会、风府和双侧阳陵泉治疗,观察针刺前后PD模型大鼠阿朴吗啡诱导的行为学及纹状体多巴胺（DA）及代谢产物含量的变化.结果与模型组比较,针刺后PD大鼠行为学明显改善（P〈0.01）,同时针刺组大鼠纹状体DA及代谢产物的含量均显著增加（P〈0.01）.结论针刺可明显改善PD模型大鼠的行为学,并且可以提高纹状体DA及其代谢产物的含量.     

电针对脑卒中后抑郁大鼠脑神经细胞γ-氨基丁酸、血管内皮生长因子表达的影响

目的观察电针对脑卒中后抑郁(PSD)大鼠脑神经细胞γ-氨基丁酸(GABA)、血管内皮生长因子(VEGF)表达的影响,探讨电针治疗作用的分子机制。方法 Wistar大鼠随机分为正常组,假手术组,模型组,电针组。在建立PSD大鼠模型后,电针"百会"、"大椎"穴,旷场实验观察大鼠的穿线次数和抬壁次数,免疫组织化学染色技术观察脑组织GABA及VEGF表达含量。结果与模型组比较,电针组旷场实验中大鼠的抬壁次数和穿线次数明显增加(P0. 05),脑神经细胞的GABA免疫阳性细胞积分光密度显著减少,VEGF免疫阳性细胞积分光密度显著增加(P0. 05)。结论电针大鼠"百会"、"大椎"穴能改善PSD大鼠抑郁状态,其机制可能与减少脑GABA表达、增加VEGF表达有关。     

电针改善血管性痴呆大鼠学习记忆及其与海马神经细胞谷氨酸、NMDAR表达的关系

目的 观察电针对血管性痴呆(VD)大鼠学习记忆功能和海马谷氨酸及其NMDA受体表达的影响,探讨电针的治疗作用机制.方法SD大鼠,随机分为正常对照组、假手术组、模型组、电针组.在建立VD大鼠模型后,电针“百会”、“大椎”穴,水迷宫观察大鼠学习记忆能力,免疫组织化学染色技术观察脑组织海马谷氨酸及其NMDA受体染色结果.结果 与模型组比较,经电针治疗后水迷宫潜伏期明显缩短(P＜0.01),相同时间内在原平台象限跨越相应平台次数明显增多(P＜0.01);谷氨酸及其NMDA受体免疫阳性细胞积分光密度显著增加(P＜0.01).结论 电针大鼠“白会”、“大椎”穴能改善大鼠学习记忆能力,其机制可能与提高海马谷氨酸及其NMDA受体表达有关.     

电针与氢化麦角碱对血管性痴呆大鼠脑乙酰胆碱酯酶的作用

目的　探讨电针对血管性痴呆(VD)大鼠的学习记忆行为及乙酰胆碱酯酶(AChE)的影响。方法　将制成肾性高血压(RHR)后再造脑反复缺血拟VD的大鼠30只,随机分为模型组、电针组和药物组(用氢化麦角碱,DHET)各10只,共治疗28d。治疗后均以水迷宫检测学习记忆行为情况,并检测脑AchE含量。结果　电针组、药物组水迷宫潜伏期明显短于模型组(P＜0.05～P＜0.005),电针组短于药物组(P＜0.05～P＜0.005)。在海马、纹状体,电针组和药物组的AchE含量显著高于模型组,而电针组又高于药物组(P＜0.05)。结论　电针能改善VD大鼠学习记忆能力,提高脑AchE含量并使之重新分布,其作用优于DHET。     

壳聚糖磷脂胆碱对老年性痴呆大鼠模型脑细胞的修复作用

目的探讨壳聚糖磷脂胆碱对老年性痴呆（AD）大鼠模型脑细胞修复作用。方法选择健康SD大鼠50只,随机分为空白对照组（10只）、痴呆模型组（20只）、壳聚糖磷脂胆碱治疗组（20只）,采用脑内双侧Meynert基底核毁损术制备大鼠AD模型,各组大鼠应用不同药物灌胃,利用免疫组化等手段,观察壳聚糖磷脂胆碱对AD大鼠的海马和基底核脑组织乙酰胆碱酯酶（AchE）和神经生长因子（NGF）的影响。结果壳聚糖磷脂胆碱能提高脑组织AchE含量,对NGF含量无明显作用。结论壳聚糖磷脂胆碱可提高AD大鼠脑内AchE含量,改善脑功能。     

电针对血管性痴呆模型大鼠学习记忆功能及海马神经细胞凋亡和突触素表达的影响

目的观察电针对血管性痴呆(VD)大鼠学习记忆功能和海马神经细胞凋亡和神经突触素(Syp)表达的影响。方法 SD大鼠,随机分为假手术组、模型组、电针组,每组10只。在建立VD大鼠模型后,电针"百会"、"大椎"穴,每天1次,留针20 min,连续治疗10 d,水迷宫观察大鼠学习记忆能力,TUNEL染色技术观察脑组织海马神经细胞凋亡结果,免疫组织化学染色技术观察脑组织海马神经细胞Syp表达。结果与模型组比较,经电针治疗后水迷宫潜伏期明显缩短(P0.01),相同时间内在原平台象限跨越相应平台次数明显增多(P0.01);海马TUNEL免疫阳性细胞积分光密度显著减少(P0.05),海马Syp免疫阳性细胞积分光密度显著增加(P0.05)。结论电针大鼠"百会"、"大椎"穴能改善大鼠学习记忆能力,其机制可能与其抑制海马神经细胞凋亡和促进海马Syp表达有关。     

锌、铜对染砷小鼠肝及肾毒作用的干预研究

为观察补充锌、铜对染砷小鼠的肝、肾脏组织超氧化物歧化酶 (SOD)水平、丙二醛 (MDA)含量并初步探讨其作用机制 ,对染砷小鼠同步进行锌、铜干预试验 ,同时作肝脏、肾脏组织SOD活性及MDA含量测定和病理学观察。干预后 ,与阳性对照组相比 ,锌干预组肝脏、肾脏SOD活性升高 ,MDA含量下降 (P <0 .0 1) ,锌加铜组仅肾脏SOD活性升高 (P <0 .0 1) ,铜组肝、肾脏SOD活性及MDA含量均无显著性差异 (P >0 .0 5 )。病理学观察可见 ,锌干预组效果最好 ,其次为锌加铜组 ,而铜组无干预效果。提示补充一定剂量锌对染砷小鼠的脂质过氧化程度、抗氧化能力以及组织病理改变均有一定的干预效应。铜在该剂量下与锌起拮抗作用。     

Effects of therapeutic paracentesis on systemic and hepatic hemodynamics and on renal and hormonal function

Thirteen patients with cirrhosis and tense ascites (six with and seven without peripheral edema) underwent 4- to 15-liter paracentesis without intravenous "colloid" replacement. Cardiac output increased from 6.6 +/- 0.7 liters per min at baseline to 8.2 +/- 0.7 liters per min (p less than 0.003) 1 hr after large-volume paracentesis completion and fell to 7.5 +/- 0.69 liters per min (p less than 0.05 vs. baseline, p less than 0.02 vs. 1 hr) 24 hr after large-volume paracentesis completion. There was no change in mean arterial pressure or mean pulmonary artery pressure. Central venous pressure fell from 9.1 +/- 0.8 mm Hg at baseline to 8.6 +/- 1.4 mm Hg 1 hr post-large-volume paracentesis to 6.8 +/- 1.0 mm Hg (p less than 0.005 vs. baseline, p less than 0.02 vs. 1 hr value) at 24 hr, and pulmonary capillary wedge pressure fell from 13.1 +/- 0.9 to 11.1 +/- 1.3 mm Hg 1 hr after large-volume paracentesis and to 9.89 +/- 1.2 (p less than 0.01 vs. baseline, p less than 0.03 vs. 1 hr after large-volume paracentesis) at 24 hr. Heart rate fell from 90 +/- 3.0 to 85 +/- 2.9 beats per min (p less than 0.01) 1 hr after large-volume paracentesis completion, but increased to 89 +/- 2.5 beats per min (p less than 0.02 vs. 1 hr after large-volume paracentesis) at 24 hr.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of particle size on quartz-induced hemolysis and on lung inflammation and fibrosis

To assess the role of crystal size in biologic responses, we quantitated red blood cell lysis and lung inflammation and fibrosis in the mouse using 4 alpha-quartz preparations with average diameters of 1, 5, 7.8, and 11.2 microns. When compared on the basis of identical crystal surface areas, the 1-micron fraction was more hemolytic than the other 3 fractions. The three larger fractions had equivalent membranolytic activities. After 6 weeks of postintratracheal instillation of the crystals into mice, the 1-micron-diameter crystal fraction increased wet lung weights by 1.25 x that of saline controls, while a 1.75 x increase was found for the three larger crystal fractions. A similar response was found when evaluating fibrosis development by determining lung hydroxyproline levels. Measurement of the percentage of the crystal dose remaining in the lungs revealed that the biologic differences observed were not due to a difference in the clearance of the smaller crystal fraction. Thus, larger crystals of alpha-quartz produce a greater degree of inflammation and fibrosis when instilled into the lung than those of 1 micron diameter, even though the smaller crystals are more membranolytic in vitro and appear to be cleared from the lung at the same rate as the larger crystals.     

Effects of trenbolone acetate and testosterone on growth and on plasma concentrations of corticosterone and ACTH in rats

The effects of trenbolone acetate (TBA) on growth and on plasma concentrations of corticosterone were examined in male and female rats. At 5 weeks of age, rats were injected with TBA (0.8 mg/kg) dissolved in peanut oil, or with oil alone, daily for 10 days. In female rats, TBA caused an increase in weight gain (20-38%), a reduction in adrenal weight (19%) and a reduction in plasma concentrations of corticosterone (55%). In contrast, TBA-treated male rats showed no significant increase in weight gain, no significant change in adrenal weight and no reduction in plasma concentrations of corticosterone. The mechanism by which adrenal activity was suppressed in TBA-treated female rats was examined and the response compared with that to testosterone. Female rats (8 weeks old) were injected daily either with oil vehicle, TBA (0.8 mg/kg) or testosterone propionate (0.8 mg/kg). Testosterone increased weight gain (24%), but the growth response to TBA treatment was significantly greater (97%). A reduction in plasma concentrations of corticosterone (45%) was again observed in response to TBA. However, testosterone increased plasma concentrations of corticosterone (52%) above those of control values. Neither androgen affected plasma concentrations of ACTH. Finally, the effects of TBA were examined in 6-week-old female rats, to characterize further the apparent age-related increase in responsiveness. The growth response of 6-week-old rats (60-74%) was intermediate between that seen in 5- and 8-week-old animals. It is concluded that part of the anabolic activity of TBA may be related to a reduction in circulating concentrations of corticosterone.(ABSTRACT TRUNCATED AT 250 WORDS)     

Impact of adiponectin and ghrelin on incident glucose intolerance and on weight change

Objectives Adiponectin and ghrelin are associated with adiposity and type 2 diabetes in several studies. We sought to prospectively determine the interaction of adiponectin and ghrelin in the development of adiposity and hyperglycaemia. Design Prospective observational study. Participants 393 community‐dwelling Afro‐Jamaicans (mean age 47 ± 13 years; BMI 27·3 ± 6·3 kg/m²; 63% women) without glucose intolerance at baseline. Measurements Anthropometry, fasting plasma glucose, 2‐h plasma glucose, insulin resistance (HOMA‐IR), adiponectin and ghrelin concentrations were measured at baseline and 4·1 ± 0·9 years later. Multivariate analyses were used to explore the associations of HOMA‐IR, adiponectin and ghrelin with weight change and glycaemia. Results The mean weight change was 2·6 ± 5·5 kg. There were 114 incident cases of impaired glucose tolerance (IGT) and 35 cases of diabetes mellitus. Adiponectin was positively correlated with age and female sex (P‐values < 0·01). After adjusting for age and sex, adiponectin and ghrelin were significantly correlated with weight at baseline and follow‐up. However, they were not associated with weight change even after further adjustment for baseline weight. Adiponectin, but not ghrelin, was associated with 2‐h glucose concentrations at follow‐up even after adjusting for age, sex, HOMA‐IR and BMI (P = 0·04). In the fully adjusted logistic regression model, adiponectin predicted incident IGT (OR 0·93; 95% CI: 0·87–0·99) and attenuated the effect of BMI on incident IGT. Conclusions These longitudinal data show that adiponectin and ghrelin may not be causally involved in the development of obesity. However, adiponectin is independently associated with decreased risk of incident IGT.