简介：本文研究了双波长差示一阶导数分光光度法运用于作为对照品的一氧化碳（ＣＯ）饱和水浓度标定及定性与定量测定微粒体代谢中生成的一氧化碳的方法。本法的优点在于能显著消除试样本底干扰，大大提高了定量准确性及灵敏度。在ＣＯ浓度２～１０μｍｏｌ·Ｌ１范围内与导数光谱峰（４１５ｎｍ）和谷（４２６ｎｍ）之间距离（Ｄ）呈良好线性关系，ｒ＝０．９９９９（ｎ＝５），回归方程Ｃ（ｍｍｏｌ·Ｌ１）＝１７．６Ｄ０．４。最低检测浓度低于０．１μｍｏｌ·Ｌ１ＣＯ。系统回收率和加样回收率（Ｘ±ＲＳＤ）分别为１０２．１±２．９％（ｎ＝７）和７９．７±６．８％（ｎ＝１２）；日内、日间精密度（ＲＳＤ）分别为４．４％（ｎ＝１８）和６．１％（ｎ＝１６）。将本法用于４个三卤苯胺和一个三卤苯的体外代谢测定，结果表明，仅２，４，５三氟苯胺在体外能被大鼠肝微粒体、ＮＡＤＰＨ和分子氧代谢生成一氧化碳。苯巴比妥和地塞米松等肝药酶诱导剂能显著提高一氧化碳的代谢转化速率，它们分别为空白对照组的３或８倍。

简介：摘要IntroductionDelayed encephalopathy due to carbon monoxide (CO) poisoning can even occur in patients with mild symptoms of acute CO poisoning. Some cases taking conventional hyperbaric oxygen (HBO) therapy or steroid-pulse therapy may be insufficient, and AchEI may be effective.Patient concerns and diagnosesWe report two cases of delayed encephalopathy after acute CO poisoning involving two women aged 69 (Case 1) and 60 years (Case 2) whose cognitive function improved with acetylcholinesterase inhibitor (AchEI) treatment. Delayed encephalopathy occurred 25 and 35 days after acute CO poisoning in Case 1 and Case 2, respectively. Both patients demonstrated cognitive impairment, apathy, and hypokinesia on admission.Interventions and outcomesAlthough hyperbaric oxygen therapy did not yield any significant improvements, cognitive dysfunction improved substantially. This was evidenced by an improved Mini-Mental State Examination score from 9 to 28 points in Case 1 and an improved Hasegawa′s dementia rating scale score from 4 to 25 points in Case 2 after administration of an AchEI. In Case 1, we administered galantamine hydrobromide, which was related with improved white matter lesions initially detected on brain magnetic resonance imaging. However, in Case 2 white matter lesions persisted despite AchEI treatment. AchEI treatment may result in improved cognitive and frontal lobe function by increasing low acetylcholine concentrations in the hippocampus and frontal lobe caused by decreased nicotinic acetylcholine receptor levels in delayed encephalopathy after CO poisoning.ConclusionPhysicians should consider AchEIs for patients demonstrating delayed encephalopathy due to CO poisoning.

简介：摘要BackgroundIt is important to prevent the development of delayed neuropsychiatric sequelae (DNS) in acute carbon monoxide (CO) intoxication, but no effective treatment has been clearly identified. Hyperbaric oxygen (HBO) therapy is one of the treatment options in acute CO poisoning; however, whether it can prevent the development of DNS is controversial.ObjectiveThe purpose of this study is to compare the effectiveness of normobaric oxygen (NBO) and HBO in preventing DNS.MethodsThis prospective observational study was conducted on all patients with CO poisoning admitted to the emergency department of a tertiary hospital from 2016 to 2019. We followed-up patients to determine whether symptoms of DNS occurred at ≤6 months. We matched the propensity score to an equivalent distribution of potential covariates.ResultsA total of 224 patients with CO poisoning were enrolled in this study. NBO was used for 26 patients and HBO for 198 patients. DNS occurred in 40 patients. There were significant differences between the NBO and HBO groups in terms of carboxyhemoglobin, loss of consciousness, dizziness, chest pain, hospitalization, and length of hospital stay. The incidence of DNS was 19.2% in the HBO group, which was higher than the 7.7% observed in the NBO group, but the difference was not significant (P＝0.18). After propensity score matching, the incidence of DNS did not differ between the NBO and HBO groups (8.3% vs. 10.4%, P>0.99)．ConclusionThere was no difference in the incidence of DNS between groups receiving HBO and NBO in acute CO intoxication.

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简介：摘要BackgroundDelayed encephalopathy (DE) is the most severe complication after acute carbon monoxide (CO) poisoning, which seriously affects the outcome of patients and leads to a high disability rate. Prior studies have shown that hyperbaric oxygen (HBO2) therapy is therapeutic for DE due to reducing immune-mediated neuropathology and thus improving cognitive performance.MethodsIn our present perspective study, five DE patients were treated regularly with HBO2 therapy. The mini-mental state examination (MMSE) and Barthel index (BI) were intermittently collected during their hospitalization for mental and physical status evaluation, the peripheral bloods were serially sampled to determine the concentration changes of circulating stem cells, as well as corresponding BDNF and neural markers.ResultsMMSE and BI showed series of improvements after multiple HBO2 therapies. The CD34+/CD90+ and CD34+/CD133+ dual positive cells, which were categorized as circulating stem cells, were observed an overall up-regulation since the beginning of the DE onset upon the application of HBO2 therapy. Characteristic neurotrophin BDNF, neural markers such as nestin and synaptophysin (SYP) were also up-regulated after exposure of HBO2. Conclusion The application of HBO2 therapy is of significance in improving the cognition of DE patients, along with mobilized circulating stem cells.ConclusionWe primarily infer that the CD34+/CD90+ and CD34+/CD133+ cells were mobilized by HBO2 exposure and have played a positive role in cognition improvement on DE patients by up-regulation of BDNF, nestin and SYP. The altering amount of circulating stem cells mobilized in peripheral blood could be a potential marker on predicting the outcome of DE.