Effects of intravenously administered lidocaine on pulmonary vagal afferents and phrenic nerve activity in cats

The ability of lidocaine to suppress activity of single vagal afferent fiber and that of phrenic nerve was studied in 20 cats anesthetized with pentobarbital. Slowly adapting stretch receptors (SAR, n = 16) and rapidly adapting stretch receptors (RAR, n = 7) were identified by their discharge pattern to pulmonary inflation. Intravenous lidocaine (1mg·kg^–1 or 2mg·kg^–1) produced a suppression of SAR activity but not of RAR activity. Suppression of phrenic nerve activity lasted much longer than that of SAR. These findings indicate that iv lidocaine acts more dominantly on CNS than on peripherals. We conclude that iv lidocaine prevents cough and hemodynamic changes caused by airway manipulation mainly through its action on CNS and not on peripherals (peripheral nerves or their receptor).(Aoki M, Harada Y, Namiki A, et al.: Effects of intravenously administered lidocaine of pulmonary vagal afferents and phrenic nerve activity in cats. J Anesth 6: 395–400, 1992)     

Anesthetic management of a patient with Hallermann-Streiff syndrome

Key words  airway management - difficult intubation - Hallermann-Streiff syndrome     

赖诺普利与氯沙坦预防压力负荷性心肌肥厚的实验研究

目的 探讨大鼠心肌肥厚时心血管重构的结构、生化改变及赖诺普利与氯沙坦对心血管重构的预防作用。方法 膈下腹主动脉缩窄法建立大鼠心肌肥厚模型。假手术组、模型组、降压和非降压剂量赖诺普利与氯沙坦在术后第2天用药至30天后，检测平均动脉压(MAP)、心肌肥厚程度及局部心肌组织一氧化氮(N0)、一氧化氮合酶(NOS)和胶原蛋白含量。结果 (1)与假手术组相比，模型组MAP、左室重量(LVW)、左室重量指数(LVMI)、心肌细胞横径(TDM)、胶原蛋白分别提高28．6％、20．5％、26．9％、17．9％、54．4％(P＜0．01)；NO、NOS分别降低53．4％、51．2％(P＜0．01)。(2)降压剂量赖诺普利与氯沙坦和非降压剂量氯沙坦干预后，LVW、LVMI、TDM、NO、NOS、胶原蛋白含量与假手术组无明显差异。非降压剂量赖诺普利可使LVW、LVMI和TDM下降，但仍高于假手术组(P＜0．01)，NO、NOS改善不明显；(3)LVMI与MAP、胶原蛋白含量均呈正相关(分别为γ=0．7841，γ=0．8177，P＜0．01)，与NO显负相关(γ=-0．7730，P＜0．01)。结论 心血管重构与血压、心脏间质成分及NO有密切关系；赖诺普利预防心肌肥厚可能是血流动力学和非血流动力学因素共同作用的结果；氯沙坦可能主要依靠非血流动力学因素抗心肌肥厚。     

血管紧张素Ⅱ和氯沙坦对大鼠小动脉平滑肌细胞的基质金属蛋白酶2和9表达的影响

目的　为研究血管紧张素Ⅱ导致血管重构的机制是否与其影响平滑肌细胞的基质金属蛋白酶 2和 9的表达及活性有关。方法　应用RT PCR、Westernblot、明胶酶谱分析等方法观察不同浓度的血管紧张素Ⅱ对体外培养的大鼠肠系膜小动脉平滑肌细胞的金属蛋白酶 2和 9的表达及活性的影响。结果　高浓度的血管紧张素Ⅱ作用VSMC 48h时 ,可以诱导金属蛋白酶 2和 9的表达及活性增加。不同浓度影响程度不同 ,1× 10 - 8mol·L- 1和 1× 10 - 7mol·L- 1的血管紧张素Ⅱ影响最强。 1× 10 - 6 mol·L- 1氯沙坦可以部分阻断血管紧张素Ⅱ对金属蛋白酶 2和 9的诱导作用。结论　血管紧张素Ⅱ可以诱导小动脉VSMC的金属蛋白酶 2和 9的表达及活性增加 ;AT1受体参与介导此过程     

Effects of Nicotine on Bone and Calciotropic Hormones in Growing Female Rats

Limited research in young adults and immature animals suggests a detrimental effect of tobacco on bone during growth. This study investigated the effects of nicotine, the major alkaloid component of tobacco, on calciotropic hormone concentrations and bone status in growing female rats. One-month-old animals received either saline (n = 10), nicotine at 3.0 mg/kg/day (n = 10), or nicotine at 4.5 mg/kg/day (n = 10) administered subcutaneously via osmotic minipumps for either 2 or 3 months. Sera, femora, tibiae, and lumbar vertebrae (3–5) were collected at necropsy. The concentrations of serum calcium, phosphorus, 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D, parathyroid hormone, calcitonin, and insulin-like growth factor-I were determined. Bone variables evaluated included mineral content and density (vertebrae and femora), cancellous and cortical histomorphometry (tibiae), and bone strength (vertebrae and femora). Statistically significant differences in serum mineral and hormone concentrations were not associated with nicotine dose or exposure time. No significant nicotine treatment effects were detected for bone mineral content and density, bone histomorphometry, or bone strength. We conclude that nicotine treatment for 2 or 3 months at serum concentrations in the upper range of those found in smokers has no detrimental effect on bone mass, volume, or strength in the growing rat. Received: 20 May 1999 / Accepted: 21 January 2000     

骨重建过程"四环素活体标记"骨组织形态计量学指标在骨质疏松中的应用

扼要结合骨组织形态计量学指标与实验动物数据介绍影响骨质疏松中骨重建过程的动态指标变化及意义,讨论各指标间的关系及变化所代表的实验意义,还介绍了一系列骨计量学观测指标的标准名称,以及利用体视学和图像分析方法进行测量的公式、单位,并扼要介绍一组实验数据与骨计量学指标的相关分析意义,便于今后分析例样的应用查阅。     

Vascular compression of the airway: Indications for and results of surgical management

Vascular compression of the airway is a significant cause of respiratory compromise in children. While the indications for surgical repair are sometimes life threatening, they can also be subtle. This retrospective study examines 45 surgical cases of tracheobronchial compromise secondary to vascular compression at a large children's hospital between July 1983 and February 1996. A total of 34 were diagnosed with innominate artery compression, ten with a double aortic arch and one with an anomalous right subclavian artery. The 45 patients, 25 male and 20 female, ranged in age from 12 days to 11 years at surgery (average 13 months). A total of 21 (47%) presented with proven or suspected episodes of cyanosis or apnea. All 45 patients had evidence of vascular compression during microlaryngoscopy and bronchoscopy. The diagnosis was confirmed by magnetic resonance imaging (MRI) in 23/45 (51%), barium swallow in 22/45 (49%) and aortogram in 3/45 (7%). There was one death. One patient had a tracheotomy before surgery and continues to require it after surgery. Complete resolution of symptoms was achieved in 39/45 (87%) with five requiring more than one operation before their symptoms resolved completely. A total of four patients experienced a recurrence of symptoms within a variable length of time after surgery. Surgical indications and treatment alternatives will be discussed.     

Laryngotracheal stenosis in children

The diagnosis of laryngotracheal stenosis should be suspected in children with stridor, feeding difficulties, or atypical croup. Only half of the children with congenital laryngotracheal stenosis require tracheotomy, and many of these children can be decannulated following uncomplicated surgical therapy. In contrast, tracheotomy-dependent patients with acquired laryngotracheal stenosis require more extensive surgical intervention, which should be carried out as early as possible to provide the best opportunity for developing normal oral communication. Received: 8 March 1977 / Accepted: 31 July 1997     

胶质瘤血管发生发展机制研究

恶性胶质瘤是人体血管化程度最高的肿瘤,血管生成和增长在胶质瘤生长和侵袭过程中起重要作用,并与其恶性进展相关.内皮细胞在血管生成中起重要作用,内皮细胞与肿瘤细胞的相互作用是肿瘤血管生成的关键因素.血管生成因子以及微环境的改变主要调控胶质瘤的血管生成.组织重构的研究方法有助于对正常和病理性的血管生成分子机制进一步了解,胶质瘤血管生成机制将得以明确.     

后基因组时代的胶质瘤分子生物学研究

在后基因组时代,对胶质瘤组织重构过程中的组织病理学、细胞遗传学及其相应分子改变的深入研究,为胶质瘤的分子病因、恶性进展、分子分型、基因治疗靶点筛选及预后评估研究提供有价值的参考依据.全文介绍了在该领域的相关研究进展.