慢性低浓度二硫化碳接触作业工人血脂的变化

对某化纤厂99名长期接触低浓度二硫化碳（CS2）作业工人和28名同厂非CS2作业工人的血脂进行流行病学横断面调查。结果发现：除接触组脂蛋白（a）［Lp（a）］浓度明显高于对照组外,其它血脂指标差别均无统计学意义;进一步通过多元逐步回归分析发现,长期低浓度CS2接触对Lp（a）的影响最大,二者呈正相关（r＝0．43,P＜0．01）。提示Lp（a）可能在CS2致脂质代谢障碍毒作用机制中起着重要作用。     

Effect of CCK-4 on a 35% carbon dioxide challenge in healthy volunteers

1. 1. The purpose of this study was to determine whether a subthreshold dose of CCK-4 would enhance the vulnerability of healthy subjects to a 35% carbon dioxide challenge.

2. 2. 27 subjects, with no prior or present psychiatric disorder and in good physical condition were challenged with a vital capacity breath of a 35% carbon dioxide mixture, immediately after an intravenous injection of 5 μg CCK-4 or placebo, according to a random order double blind crossover design.

3. 3. Subjects reported significantly less panic symptoms upon carbon dioxide after premedication with CCK-4 than after placebo.

4. 4. Both CCK-4 and carbon dioxide may act on the same neuronal pathways, but seem to inhibit rather than potentiate each other effects.

     

Metabolic base production and mucosal vulnerability during acid inhibition in a mammalian stomachin vitro

Acid inhibition increases gastric mucosal susceptibility to damage by luminal acid. This might be due to reduced metabolic CO₂ and bicarbonate whereas, during normal acid, secretion cytoprotective CO₂/HCO₃- production parallels acid production. Metabolic activity and mucosal damage caused by luminal acid perfusion was determined in anin vitro mouse stomach, with and without acid inhibition, and at 0%, 1%, or 5% serosal CO₂ supply. Without acid inhibition there was no mucosal damage at any level of serosal CO₂/HCO₃- supply. Acid inhibition reduced metabolic CO₂ production by 29% (P<0.004) and resulted in microscopic damage to 55% of the mucosal area and perforation in four of five stomachs (P<0.05). Although, 1% CO₂ supply completely replaced the reduction in metabolic CO₂, it did not protect against mucosal damage. Overreplacement by 5% serosal CO₂/HCO₃- was required to prevent damage. There was no correlation between luminal CO₂/HCO₃- output and mucosal damage. The protection by endogenous or exogenous CO₂/HCO₃- appears to act intracellularly rather than by intragastric or intercellular neutralization.This study was supported by Swiss National Foundation grants 32-26369.89 and 32-33626.92. The morphometry equipment was supported by a grant from the Osterreichische Nationalbank.     

Electroencephalographic effects of cigarette smoking

The effects of cigarette smoking on the electroencephalogram (EEG) of smokers were examined in a study involving both task and no-task conditions. Nonsmoking subjects were employed as controls. In light inhaling smokers, (depth of inhalation inferred from preto post-smoking changes in tidal breath carbon monoxide), smoking was found to attenuate EEG activity in the delta, theta, and alpha frequency bands, as well as facilitate behavioral performance. For theta, the attenuation was lateralized over the right frontal cerebral hemisphere. In deep inhaling smokers, smoking produced a symmetrical central midline increase in beta2 magnitude, an EEG effect that in the benzodiazepine literature is associated with anxiety relief.A preliminary version of these data was presented during the symposium Psychophysiology of Nicotine, held at the Thirtieth Annual Convention of the Society for Psychophysiological Research, Boston, October, 1990     

Pulse oximetry and capnography in anaesthetic practice: an epidemiological appraisal

In the evaluation of any medical technology the efficacy, effectiveness, and efficiency must each be considered before routine deployment is recommended. Since the widespread practice of patient monitoring by pulse oximetry and capnography has occurred before the performance of rigorously controlled trials, definitive proof of worth is lacking. The purpose of this review is to appraise critically the effectiveness of this technology. The assessment was performed using concepts developed in epidemiology and community medicine to establish a given factor to be causative to a given outcome. The current literature pertaining to anaesthetic adverse outcomes was reviewed, and the use of monitors evaluated against the criteria of a causal relationship. While the conclusions are based more on the absence of positive data (owing to low frequency of adverse anaesthetic occurrences) rather than negative results, it must be concluded that the effectiveness of such monitoring has yet to be demonstrated. Such a conclusion should not detract from their use, for the role of an individual factor in the complex chain of accident evolution will seldom be demonstrable. Rather, such an appraisal should encourage a clear perspective of the depth of our clinical science, and encourage more rigorous critical evaluation in the future.     

Stability of the intra-operative arterial to end-tidal carbon dioxide partial pressure difference in children with congenital heart disease

The purpose of this study was to evaluate the stability of the arterial PCO2 (PaCO2) to end-tidal PCO2 (PETCO2) partial pressure difference (Pa-ETCO2) during surgery using PETCO2 monitoring, in children with congenital heart disease (CHD). Forty children with CHD were studied: ten children with no interchamber communication and normal pulmonary blood flow (PBF) (normal group); ten acyanotic children with increased PBF (acyanotic-shunting group); ten cyanotic children with mixing type lesions and normal or increased PBF (mixing group), and ten cyanotic children with right-to-left intracardiac shunts demonstrating decreased and variable PBF (cyanotic-shunting group). Simultaneous PaCO2 recordings and PETCO2 measurements were obtained for each patient during five intraoperative events: (1) control time, arterial line placement under anaesthesia; (2) time 1, patient preparation; (3) time 2, immediately after sternotomy; (4) time 3, after heparin administration; and (5) time 4, immediately after aortic cannulation. Initially, cyanotic children demonstrated a greater Pa-ETCO2 compared with acyanotic children (P less than 0.05). There was no difference in the Pa-ETCO2 over time in the control, acyanotic-shunting, or mixing groups. The Pa-ETCO2 in the children with cyanotic-shunting lesions at times 2 and 3 was greater (P less than 0.05) than at their control times. We conclude that the Pa-ETCO2 of children with acyanotic-shunting and mixing congenital heart lesions is stable intraoperatively, although patients with mixing congenital heart lesions may demonstrate large individual variations. In children with cyanotic-shunting congenital heart lesions, the Pa-ETCO2 is not stable. The PETCO2 cannot be used during surgery to estimate reliably the PaCO2 in children with cyanotic CHD.     

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。     

超临界CO2萃取山茱萸成分研究

目的 :对山茱萸超临界CO2 流体萃取物进行研究。方法 :萃取条件为 :压力 15MPa,温度 4 0℃ ,时间2h ,液态CO2 流量 2 2 .0kg·h-1,,采用GC MS技术分析山茱萸CO2 超临界萃取物的化学组成。结果 :超临界CO2流体萃取法得率为 2 .4 2 %。鉴定了其中 31种成分 ,并用面积归一化法测定其相对含量。结论 :超临界CO2 流体萃取物主要成分有 1,2 苯二甲酸二 (1 丁基 2 异丁基 )酯 ,异丙基十四 [烷 ]酸酯等。     

玉米粉水解物作为红霉素发酵培养基的研究

研究了摇瓶试验中玉米粉水解物替代葡萄糖发酵红霉素的最佳培养基组成。用均匀设计法得到发酵基础培养基的最佳配比(wB，％)：玉米粉3．6，黄豆饼粉2．0，玉米浆0．23，碳酸钙0．5，淀粉0．6；用正交试验得到了优化的补混合料配比(％)：玉米粉4．5，黄豆饼粉2．0，硫酸铵1．0，酵母粉2．0；并得到了玉米粉的最适水解条件。30t发酵罐放大实验结果表明，用玉米粉水解物替代葡萄糖作碳源发酵红霉素，发酵单位提高5．8％，综合生产成本降低26．0％。     

Characterizing the influence of structure and route of exposure on the disposition of dithiocarbamates using toluene-3,4-dithiol analysis of blood and urinary carbon disulfide metabolites.

Differences in the toxicities observed for dithiocarbamates have been proposed to result from the influence of nitrogen substitution, oxidation state, and route of exposure. To better characterize the fate of dithiocarbmates in vivoas a function of structure and route of exposure, rats were administered equimolar doses of carbon disulfide (CS2), N-methyldithiocarbamate, pyrrolidine dithiocarbamate, N,N-diethyldithiocarbamate, or disulfiram daily for five days, either po or ip, and sequential blood samples obtained. Protein dithiocarbamates formed by the in vivo release of CS2, parent dithiocarbamate, and protein-bound mixed disulfides were assessed in plasma and hemolysate by measuring toluene trithiocarbonate generated upon treatment with toluene-3, 4-dithiol (TdT). To aid in determining the bioavailability of CS2 from the administered dithiocarbamates, the urinary CS2 metabolites, 2-thiothiazolidine-4-carboxylic acid (TTCA) and 2-thiothiazolidin-4-ylcarbonylglycine (TTCG), were also determined. The levels of TdT-reactive moieties detected depended upon both the compound administered and the route of exposure. Parent dithiocarbamates, with the exception of disulfiram, were eliminated from blood within 24 h; but protein associated TdT-reactive moieties persisted and accumulated with repeated exposure, regardless of the route of exposure. N-Methyldithiocarbamate demonstrated the greatest potential to produce intracellular globin modifications, presumably through its unique ability to generate a methylisothiocyanate metabolite. Urinary excretion of TTCA and TTCG was more sensitive than TdT analysis for detecting dithiocarbamate exposure, but TdT analysis appeared to be a better indicator of in vivo release of CS2 by dithiocarbamates than were urinary CS2 metabolites. These data suggest that CS2 is a more important metabolite, following oral exposure, than are other routes of exposure, e.g., inhalation or dermal. In addition, data also suggest that acid stability, nitrogen substitution, and route of exposure are important factors governing the toxicity observed for a particular dithiocarbamate.