超顺磁氧化铁标记神经干细胞移植治疗帕金森病大鼠脑MRI改变的研究

目的研究应用超顺磁氧化铁（SPIO）标记神经干细胞（NSCs）移植治疗帕金森病（PD）大鼠脑部MRI的改变。方法从大鼠胚胎脑中分离培养中脑NSCs,用脂质体转染法将SPIO标记NSCs;同时制作大鼠PD模型,SPIO标记的NSCs移植到PD大鼠右侧纹状体区,分别在移植后1周、2周、4周、6周、8周和10周给大鼠行MRI检查,2周、4周、6周、8周、10周时进行旋转行为评分,并与NSCs组和对照组比较。结果脑内移植SPIO标记NSCs的PD大鼠1周后MRI检查显示在移植区呈低信号改变;移植后10周,在T2和T2梯度回波仍可观察到移植区的低信号,同时移植区有混杂信号。NSCs移植大鼠的旋转行为评分在移植后2-10周明显少于对照组（均P〈0.05）。结论SPIO标记的NSCs可以在MRI上显示其在移植大鼠脑部的分布和存活情况,有利于NSCs移植治疗PD后的疗效观察。     

尼莫地平对阿尔茨海默病大鼠脑组织NO、NOS含量及行为学的影响

目的：探讨尼莫地平对阿尔茨海默病（AD）大鼠脑组织一氧化氮(NO)、一氧化氮合酶（NOS）浓度及行为学改变的影响。方法：SD大鼠30只，随机分为空白对照组,AD模型组和尼莫地平组，采用大鼠脑组织立体定位微量注射技术，尼莫地平组和AD模型组用鹅膏蕈氨酸（IBO）1μl(5μg)损毁大鼠双侧迈内特基底核（nbM）建立AD动物模型，空白对照组以0.1mol/L pH7.4PB液代替IBO。尼莫地平组给予尼莫地平0.5mg/kg，空白对照组和AD模型组以生理盐水代替尼莫地平，连续灌胃60d，每d2次，每次2ml。做迷宫试验及跳台试验测学习记忆能力，然后将大鼠断头处死，分离海马及大脑皮质，分别检测NO,NOS含量。结果：AD模型组较空白对照组学习记忆能力显著降低，海马及大脑皮质NO,NOS含量显著升高，尼莫地平较AD模型组学习记忆能力显著升高，海马及大脑皮质NO、NOS含量显著降低。结论：用IBO损毁大鼠双侧nbM可建立AD动物模型，尼莫地平可显著改变AD模型大鼠的学习记忆能力，降低海马及大脑皮质NO、NOS含量。     

一氧化氮及一氧化氮合酶在遗传性癫痫易感大鼠惊厥发作中的作用

目的：探讨一氧化氮、一氧化氮合酶在遗传癫痫易感大鼠惊厥发作中的变化及作用。方法：选择惊厥评分在30－40的P77PMC大鼠35只，均分A－G7组，A组为对照组、G组预先30min腹腔注射一氧化氮合酶抑制剂L－NAME，分别于铃声刺激致惊后0．5、1、2、4,12h断头处死，取出脑组织分离双侧大脑皮层、海马等组织匀浆，测定一氧化氮及一氧化氮合酶，分别统计并进行t检验。结果：惊厥后0．5－1h皮层、海马一氧化氮、一氧化氮合酶逐渐升高，2h达峰值，4－12h恢复正常，应用L－NAME后，一氧化氮、一氧化氮合酶升高被抑制，但大鼠惊厥评分增高并致1例惊厥后死亡和明显延长惊厥持续时间。结论：惊厥后大鼠体内一氧化氮、一氧化氮合酶合成增加，给予合成酶抑制后能明显下降，但能加重惊厥程度和延长持续时间，提示一氧化氮于惊厥后升高，可能作为内源性抑制性性质，在惊厥发作自行终止机制中具有重要作用。     

Effects of Nitric Oxide on Proliferation and Apoptosis of Cultured Bovine Trabecular Meshwork Cell

Nitric Oxide (NO) shows a dualism in thepathogenesis of glaucoma:in one side,NO can im-prove outflow facility of aqueous humor and dropintraocular pressure (IOP) ;on the other side,ithas direct toxic effect on retinal ganglion cell[1] .Our preveious studies demonstrated,in some ex-tent,pressure could induce inducible nitric oxidesynthase(i NOS) m RNA expression,so to increase NOS synthesis and NO level[2 ] .In this experimentwe discussed the effects of NO on the proliferationand apopto…     

An in vitro study of nonadrenergic-noncholinergic activity on the cavernous tissue of mouse

The relaxant effects of electrical field stimulation (EFS) and exogenously applied acetylcholine (ACh) or acidified NaNO₂ (a-NaNO₂) were investigated in the isolated mouse corpus cavernosum precontracted with phenylephrine hydrochloride (PE). Tetrodotoxin (TTX) blocked the relaxant effects of EFS completely, whereas it had no effect on the responses to ACh or a-NaNO₂. Guanethidine and indomethacin failed to affect the electrically or ACh-induced relaxations. Atropine completely blocked the effect of ACh; however, it caused a slight reduction in the relaxation evoked by EFS.N ^G- Nitro-l-arginine (l-NOARG) reduced the effects of EFS and ACh significantly, but it was ineffective on the relaxations induced by a-NaNO₂. The inhibitory action ofl-NOARG was partly restored byl-arginine, but not byd-arginine. Methylene blue (MB) and hydroxocobalamin (HC) exhibited significant inhibition on the relaxations evoked by EFS, ACh and a-NaNO₂. Hydroquinone (HQ) reduced relaxation due to a-NaNO₂, but did not affect that of EFS and ACh. Our findings suggest that EFS-induced relaxations of mouse cavernosal tissue are mediated by a transmitter which probably resembles an organic nitrate.     

Nitric oxide is not involved in the initiation of insulin secretion from rat islets of Langerhans

Summary The involvement of nitric oxide as an intracellular messenger in the control of insulin secretion from pancreatic Beta cells was studied in rat islets of Langerhans by measuring: (i) nitric oxide generation in response to physiological insulin secretagogues; (ii) the effects of inhibitors of nitric oxide synthesis on insulin secretory responses to physiological secretagogues, and on insulin synthesis; (iii) changes in islet cyclic guanosine monophosphate in response to secretagogues; (iv) the effects of exogenous cyclic guanosine monophosphate and dibutyryl cyclic guanosine monophosphate on insulin secretion from electrically permeabilised islets and from intact islets, respectively. These studies produced no evidence that nitric oxide generation is required for the initiation of insulin secretion by common secretagogues. However, the results of our experiments suggest that the generation of nitric oxide may be involved in long-term, glucose-dependent increases in cyclic guanosine monophosphate content of islet cells, although the physiological relevance of these changes requires further investigation.     

Successful weaning from cardiopulmonary bypass after cardiac surgery using inhaled nitric oxide

Two cases of very difficult weaning from cardiopulmonary bypass after cardiac surgery in children with pulmonary hypertension and ventricular dysfunction are reported. Children fail to respond to conventional therapy combining nitrovasodilators and inotropic support and react successfully to combined inhaled nitric oxide (NO) and epinephrine or left atrial infused norepinephrine. Postoperative NO inhalation must be prolonged and no toxicity appears. Pulmonary endothelial function recovers only after several days.     

Should nitrous oxide be discontinued before desflurane after anaesthesia with desflurane/N2O?

Background : The appearance of hypoxaemia immediately after anaesthesia with nitrous oxide may be partially explained by diffusion hypoxia. This study was undertaken to evaluate circulatory and respiratory variables during emergence after desflurane/nitrous oxide anaesthesia, and whether there are any differences depending on which gas is discontinued first. Methods : 20 patients were studied after gynaecological laparoscopic surgery. The depth of anaesthesia was reduced 10 min prior to the emergence by stopping the administration of one of the two inhalational agents. Desflurane was discontinued first in Group 1, nitrous oxide in Group 2. Ventilation was controlled with E'C0₂ maintained at 5% until the administration of the second anaesthetic gas was discontinued. Thereafter, the patients breathed spontaneously. Results : The PaC0₂ at which the respiratory drive reappeared after controlled normoventilation was similar in both groups, 6.1–6.5 kPa, and extubation was performed after 10–11 min. At extubarion, the end–tidal C0₂ and total MAC were similar in the groups, about 6.2 vol% and 0.16, respectively. Mean arterial blood pressure was significantly higher in Group 1. The cardiac output increased in both groups from about 6 1/min at the conclusion of anaesthesia to 9.0 and 7.6 1/min at 15 min in the recovery period. End–tidal O₂ decreased and CO₂ increased in both groups during the first 10 min in the recovery period. pH was reduced at 15 and 30 min in both groups. Conclusion : Irrespective of which agent was discontinued first, there was an increase in cardiac output, decrease in oxygenation and a modest acidosis in the first 30–min recovery period. The only significant difference between the groups was in mean arterial blood pressure in the early emergence phase with a greater MAP when N₂O had been used until the conclusion of anaesthesia.     

一氧化氮在氯胺酮麻醉机制中的作用

目的：了解一氧化氮（ＮＯ）与氯胺酮麻醉作用间的关系。方法：６０只雄性昆明鼠分成４组，Ⅰ组氯胺酮１００ｍｇ／ｋｇ腹腔内注射，Ⅱ组连续３天腹腔内注射Ｎ－硝基左旋精氨酸甲酯（Ｌ－ＮＡＭＥ）５０ｍｇ／ｋｇ后，腹腔内注射氯胺酮１００ｍｇ／ｋｇ，Ⅲ组连续３天腹腔内注射左旋精氨酸３００ｍｇ／ｋｇ后，腹腔内注射氯胺酮１００ｍｇ／ｋｇ，Ⅳ组腹腔内注射氯胺酮１００ｍｇ／ｋｇ后，腹腔１小时内持续给予Ｓ－亚硝酰－Ｎ－乙酰青霉胺（ＳＮＡＰ）３０ｍｇ／ｋｇ。观察各组动物翻正反射丧失和抑制持续时间。结果：各组翻正反射丧失时间无明显差异，为１．３９～２．３０分钟。翻正反射丧失持续时间Ⅰ组４７．７１±５．１７分，Ⅱ组４７．８４±７．９９分，Ⅲ组和Ⅳ组明显比Ⅰ、Ⅱ组短，分别为３１．１４±２．４４和３２．７５±８．１４分（Ｐ＜０．０１）。结论：改变ＮＯ的生成量将影响着氯胺酮引起的小鼠翻正反射抑制的持续时间，ＮＯ在氯胺酮麻醉分子机制中起作用。