The effect of different duration of exercise preconditioning (EP) on protecting from exhaustive exercise-induced cardiac injury (EECI) has been optimized in rats. Male Sprague-Dawley rats were divided into six groups: the control group, exhaustive exercise (EE) group, EP 20-min + EE group, EP 40-min + EE group, EP 60-min + EE group and EP 80-min + EE group. The EP groups were subjected to treadmill running at the intensity of 74.0% V̇O2 max. Changes of exercise capacity, cardiac pathology, myocardial enzymology, electrocardiogram (ECG), cardiac function, and mitochondrial respiratory function were compared. Compared to the C group, the EE group has shown significant decrease of exercise capacity, elevation of serum N-terminal pro B-type natriuretic peptide (NT-proBNP) and cardiac troponin-I (cTn-I) levels, cardiac morphology change, ECG disturbance, cardiac dysfunction and reduction of myocardial mitochondrial respiration function. Compared to the EE group, the EP groups have shown significant elevation of exercise capacity, decrease of serum NT-proBNP and cTn-I, improvement of cardiac function and myocardial mitochondrial electron transfer pathway complex I, II and IV activity. The correlation analyses showed protection of EP was proportional to EP duration from 20-min to 60-min. EE caused cardiac injury. EP could protect from EECI by alleviating myocardial damage, improving cardiac function and mitochondrial ETP complex I, II and IV activity. EP protection was positively correlated to EP duration from 20-min to 60-min with EP intensity fixed at 74.0% V̇O2 max.
To investigate the persistence time and the effectiveness of exercise preconditioning (EP) on myocardial protection in exhausted rats from myocardial enzymes, electrocardiogram (ECG), cardiac function, and mitochondrial respiratory function after cessation of exercise training. One hundred and twelve healthy male Sprague–Dawley rats were randomly divided into seven groups (n = 16): control group (CON), exhaustive exercise (EE) group, EP group, and EE after EP (EP + EE); furthermore, EP + EE group was randomly divided into 1D, 3D, 9D, and 18D groups (1D, 3D, 9D, and 18D) and performed exhaustive treadmill exercise at a speed of 30 m/min on the 1st, 3rd, 9th, and 18th days separately after EP exercise stopped. We detected the serum contents of N-terminal pro B type natriuretic peptide (NT-proBNP) and cardiac troponin I (cTnI) by the enzyme-linked immunosorbent assays method, recorded ECG, detected heart function by pressure volume catheter, measured the respiratory rates of rat myocardial mitochondria state 3 and 4 of complex I, complex II, and IV by high-resolution breathing apparatus. EP could decrease the serum content of NT-proBNP and cTnI, improved the electrical derangement and the left ventricular function in exhausted rats. Moreover, the protective effect was more obvious in the 9th day after EP stopped, whereas it would disappear when EP stopped for more than 18 days. Compared with EE group, the respiratory rate value of myocardial mitochondrial complex increased in 1D, 3D, and 9D groups. Therefore, the protective effect of EP on the heart of exhausted rats decreased with the prolongation of stopping training time, and the effect was significant within 3 days of discontinuing training, then decreased gradually, and completely disappeared in the 18th day. EP enhanced the cardiac function in exhausted rats through raising the nicotinamide adenine diphosphate hydride (NADH) electron transport chain and increased the respiration rates of mitochondrial respiratory complex I and IV state 3, thereby improved myocardial mitochondrial respiratory function and energy metabolism.
Abstract Background There are no reports on the incidence of chronic mercury poisoning in a large population in China. This study investigated the epidemiology, clinical manifestations, treatment, and follow-up of Chinese patients with chronic mercury poisoning. Methods Data for 288 mercury poisoning patients were collected at our hospital from July 2014 to September 2019, including sex, age, admission time, blood mercury content, urine mercury content, creatinine, urinary mercury/creatinine ratio, 24-h urinary protein levels, electromyography (EMG) findings, renal biopsy, and follow-up. Patient characteristics were evaluated by statistical and correlation analyses. Results First, mercury poisoning in China mainly occurred through occupational exposure and the inappropriate use of mercury-containing cosmetics and Chinese folk remedies (CFRs). Second, the most common symptoms were nervous system (50.3 %), kidney (16.4 %) and breathing (8.0 %). Mercury poisoning-induced Nephrotic syndrome (NS) and peripheral neuropathy are common long-term complications. The complications of occupational and cosmetics-induced mercury poisoning are consistent with international belief. However, the NS caused by CFRs is mainly membranous nephropathy and the probability of peripheral neuropathy caused by CFRs is higher than other pathogens. Third, follow-up data shows that 13 patients with EMG-confirmed neurological injury, 10 showed full recovery after 38.50 ± 8.03 months. Furthermore, among 18 patients with NS, 15 had normal urine protein and serum albumin levels after 22.67 ± 10.26 months. Conclusions Regulation of skin-lightening cosmetic products, safety surveillance of CFRs, and prevention and control of occupational exposure must be improved to decrease the incidence of mercury poisoning in China.
OBJECTIVES:Carbon monoxide (CO) poisoning is one of the most frequent causes of fatal poisoning worldwide. Few studies have explored the mortality trends of CO poisoning grouped by age and gender, at the regional, national and global levels. We therefore aimed to determine the pattern of CO poisoning mortality, as well as temporal trends at all levels.DESIGN:A cross-sectional survey design was used in this study.SETTING:CO poisoning data collected from the Global Burden of Diseases (GBDs), from 1990 to 2017, was arranged by sex, age, region and country. In addition, we used human development index data at the national level from the World Bank.PARTICIPANTS:We collected over 100 000 information on CO poisoning mortality between 1990 and 2017, derived from the GBD study in 2017.MAIN OUTCOMES AND MEASURES:We have calculated the estimated annual percentage changes in CO poisoning age-standardised mortality rate (ASR), by sex and age at different regions and countries to quantify the temporal trends in CO poisoning ASR.RESULTS:Globally, death cases of CO poisoning decreased 7.2% from 38 210 in 1990 to 35 480 in 2017. The overall ASR decreased by an average of 1.83% (95% CI 2.10% to 1.56%) per year in this period. This decreasing pattern was heterogeneous across ages, regions and countries. The most pronounced decreases were generally observed in countries with a high sociodemographic index, including Estonia, South Korea and Puerto Rico.CONCLUSIONS:Current prevention strategies should be reoriented, and much more targeted and specific strategies should be established in some countries to forestall CO poisoning.
运动作为一种应激源,是一把双刃剑,适度运动可以改善心脏功能,在心脏受到损伤性刺激时对心脏起到保护作用.而超负荷的大强度运动则对心脏产生损伤.既然运动与我们的生活息息相关,所以明确不同运动方式对心脏的不同影响以及不同作用的产生机制必要且重要.运动能通过多种途径对心脏产生影响,运动也会对心肌细胞离子通道产生影响.ATP敏感性钾通道[ATP-sensitive potassium channels,K(ATP)]广泛存在于心肌细胞,它将代谢与细胞膜的兴奋性联系起来,在心肌缺氧缺血过程中发挥重要作用,是完成运动对心肌细胞作用的必需结构.本文就不同运动方式对心肌K(ATP) 通道的表达及功能影响,以及运动通过影响K(ATP)发挥心脏保护效应做一总结.
目的 研究我国一氧化碳(CO)中毒死亡的变化趋势.方法 从2017年全球疾病负担研究中收集1990至2017年我国及全球CO中毒的详细信息,根据性别、年龄、社会人口指数(SDI)等计算CO中毒年龄标准化死亡率(ASMR)的估计年百分比变化(EAPC),以量化CO中毒ASMR的变化趋势,并将我国及全球趋势进行对比.结果 2017年全球CO中毒死亡人数较1990年有所下降,而我国死亡人数上升,从1990年的13779例增长至2017年的14255例,增长了3.45%;在此期间全球及我国的CO中毒ASMR均呈下降趋势,但我国ASMR下降趋势(EAPC=-0.46;95%CI-0.56~-0.36)明显低于全球水平(EAPC=-1.83;95%CI-2.10~-1.56);我国CO中毒ASMR的下降趋势在不同性别及年龄中是不同的,其中,男性呈下降趋势,女性呈上升趋势;最明显的下降为<5岁的人群,而≥50岁的人群呈明显的上升趋势.结论 CO中毒在我国仍是一个重要的公共卫生问题,尤其应针对老年人建立更有效的预防及治疗方案.
Acute mercury poisoning, involving a number of organs, leads to severe dysfunctions, such as acute renal failure (ARF), and even threatens patients' lives. A case of acute severe mercuric chloride (HgCl2) poisoning with multiple organ failure was reported in this study. A 38-year-old woman orally took about 50 g HgCl2 powder in 2015, and showed nausea, emesis, clouding of consciousness, lip and nail cyanosis, and dark red bloody fluid from bilateral nostrils. Based on chest and abdominal CT examinations, gastroscopy, and colonoscopy, the patient was found to suffer oral mucosal hyperemia and ulceration, gastrointestinal bleeding (haematemesis and hemafecia), ARF, metabolic acidosis, collapse and shock. Despite assisted respiration and relevant active treatments, the patient's condition deteriorated gradually and she was dead eventually. The study suggests that the best treatments for acute HgCl2 poisoning accompanied with ARF are early blood purification and mercury elimination on the basis of conventional therapy.
OBJECTIVE To investigate whether salidroside (Sal) protected the rat heart from exhaustive exercise-induced injury by inducing nuclear factor erythroid 2-related factor 2 (Nrf2) expression. METHODS Forty-eight male Sprague-Dawley rats were divided into four groups (n = 12 rats per group): the control, the exhaustive swimming (ES) group, the low-dose Sal plus acute exhaustive swimming (SLE) group, and the high-dose Sal plus acute exhaustive swimming (SHE) group. In the SLE and SHE groups, 15 and 30 mg/kg Sal were administered, respectively, once a day. The rats in the control and ES groups were administered the same amount of physiological saline, respectively, once a day. On the 14th day, the rats in the ES, SLE and SHE groups underwent exhaustive swimming training once. Then cardiac function parameters and electrocardiograms were recorded. Biomarkers of myocardial injury in the serum and oxidative stress factors in the myocardial tissue were evaluated using ELISA tests. The levels of Nrf2, nuclear Nrf2 and Kelch-like ECH-associated protein 1 (Keap1) messenger RNA and proteins were assessed in the myocardium using q-PCR and Western blotting, respectively. RESULTS Compared to the control group, the ES group showed remarkable increases in serum brain natriuretic peptide (BNP), cardiac troponin I (cTnI) and reactive oxygen species levels, but significant decreases in catalase and glutathione levels (p < 0.05). Compared to the ES group, the Sal treatment decreased serum BNP and cTnI levels and alleviated the changes in levels of oxidative stress-related factors. After treatment with Sal, nuclear and intracellular levels of Nrf2 protein were increased in the myocardial cells, while the level of Keap1 protein was decreased (p < 0.05). CONCLUSIONS Sal protected the heart from exhaustive exercise induced injury, and it may improve cardiac function and cardiac bioelectricity in exhausted rats by inducing Nrf2 expression.
双硫仑(disulfiran)样反应又称戒酒硫样反应,作用机制与双硫仑反应机制类似,主要是特定药物因分子结构中含特殊基团与乙醇相互作用而抑制乙醇的代谢,导致人体乙醛增多和儿茶酚胺类物质减少引起的临床症状[1].近年来,服用头孢类药物期间或前后饮酒而出现双硫仑样反应的报道较多,未见服用治疗肩周炎药物后饮酒引起双硫仑样反应的报道.解放军总医院第五医学中心南院区中毒救治中心于2019年1月31日成功救治1例口服肩周炎药物饮酒后引起酒精中毒伴双硫仑样反应的患者,现将救治与护理过程汇报如下.
力竭运动可引起运动性心脏损伤,而运动预适应产生运动性心脏保护作用.在运动预适应对心脏的保护机制中,磷脂酰肌醇3‐激酶/蛋白激酶B (PI3K‐Akt)信号通路的激活在抑制心肌细胞凋亡的过程中发挥重要作用.通过干预激活PI3K‐Akt信号通路,研究其对心肌细胞的影响,可为运动预适应的心脏保护作用提供理论依据.
Thallium ion (Tl+) and its neurotoxic products are widely known to cause severe neurological complications. However, the exact mechanism of action remains unknown, with limited therapeutic options available. This study aims to examine the toxic effects of Thallium (I) Nitrate (TlNO3) on primary hippocampal neurons of E17-E18 Wistar rat embryos, and the potential neuroprotective role of Nrf2- Keap1 signaling pathway against thallium-induced oxidative stress and mitochondrial dysfunction. TlNO3 induces a significant increase in reactive oxygen species levels and mitochondrial dysfunction in primary hippocampal neurons. Furthermore, the Nrf2-Keap1 signaling pathway played a protective role against TlNO3-induced hippocampal neuronal cytotoxicity. Moreover, mitochondrial fusion protein Mitofusin 2 (Mfn2) levels significantly decreased in hippocampal neurons when exposed to TlNO3, indicating that Mfn2 protein levels are linked to TlNO3-induced neurotoxicity. t-BHQ, a Nrf2 and phase II detoxification enzyme inducer, counteracted the oxidative damage in hippocampal neurons by activating the Nrf2-Keap1 signaling pathway after TlNO3 exposure; the activated Nrf2-Keap1 pathway could then maintain Mfn2 function by regulating Mfn2 protein expression. Thus, Nrf2-Keap1 pathway activation plays a protective role in Tl+-induced brain damage, and specific agonists have been identified to have great potential for treating thallium poisoning.
目的 总结39例汞中毒肾病综合征(NS)患者的临床资料及治疗特点,以提高该病的诊治水平.方法 收集2012年7月至2017年9月在解放军总医院第五医学中心治疗的汞中毒NS患者的临床资料,对其病因、临床表现、化验检查、治疗、预后及随访情况进行回顾性分析.结果 共收集39例患者,其中女性33例(84.6%),平均年龄(37.44±11.17)岁.表现除全部出现泌尿系统症状外,尚有6例出现神经系统症状、1例出现皮肤表现.汞中毒NS的病理类型主要为微小病变肾病(MCD)和膜性肾病(MN),其中MCD多因患者美容所致,MN多因美容及中药偏方使用不当所致.此外,MCD患者中8例应用激素治疗,显著多于MN中应用激素的患者(4例).39例患者经过以驱汞为主的综合治疗后,症状逐渐缓解,血汞浓度显著减少,随访发现无明显后遗症.结论 美容引起的汞中毒NS的病理类型主要为MN和MCD.中药偏方引起的汞中毒NS主要为MN.及时脱离汞源并行驱汞治疗,症状缓解,预后较好.
目的:探讨影响百草枯中毒患者预后的相关因素,为患者预后评估提供参考.方法:回顾分析2009-04-2013-10期间百草枯中毒住院患者272例,根据存活、死亡分为两组,分析服药剂量、就诊时间、住院天数、A-PACHE Ⅱ评分、生化指标(血清钾、钠、氯、钙、谷丙转氨酶、谷草转氨酶、总胆红素、肌酐、尿素氮、CK-MB、乳酸脱氢酶、二氧化碳结合力、超敏C反应蛋白)与患者预后的相关性,然后采用多因素logistic回归分析筛选出有效因素,并通过ROC曲线评价其相关因素在百草枯中毒预后的诊断价值.结果:272例百草枯中毒患者中,死亡133例,通过多因素logistic回归分析,得出服毒量、血清百草枯浓度、尿液百草枯浓度、血清Ca2+、Cl-、肌酐、尿素氮为影响患者预后的因素,差异有统计学意义(P<0.05),对相关因素进行ROC曲线分析,得出尿液中百草枯的浓度、血清钙、Cl-、BUN的OR值小于1,是保护因素;服毒量、血液中百草枯浓度、Cr的OR值大于1,是危险因素.对服毒量、血液中百草枯浓度、尿液中百草枯的浓度、血清钙、Cl-、肌酐、尿素氮进行ROC曲线下面积分析,其各自的曲线下面积依次为0.8425、0.7972、0.6959、0.6941、0.6636、0.5089、0.4829.结论:百草枯的服毒量及血浆中百草枯的浓度是影响预后的两个关键因素,尿液中百草枯的浓度、血清钙、Cl-、尿素氮是保护因素;服毒量、血液中百草枯浓度、肌酐是危险因素.
铊是一种无臭、无色、无味的重金属 , 铊及其化合物均为剧毒类毒物,具有很强的蓄积作用 [1].铊于 1920 年开始以杀虫剂运用于德国.铊中毒国内外均有报道,根据美国毒物数据中心报道,1995 年至 2005 年共有 830 例铊中毒患者,包括 1 例死亡报道,近年来每年有约 20 例铊中毒的新发病例 [2].国内铊中毒案例也时有报道 [3].
This study was conducted to analyze the clinical characteristics of and treatment strategies for botulism among patients receiving cosmetic injection of botulinum toxin (BoNT). A total of 86 botulism patients caused by cosmetic injection of BoNT were enrolled in our study. All of the patients were diagnosed according to their history of cosmetic BoNT injection, clinical symptoms and signs, and other auxiliary examinations (including those on renal and liver functions, blood index detection, and chest X-ray). All of the patients received comprehensive treatments and botulinum antitoxin serum injection. The main symptoms of botulism patients included headache, dizziness, insomnia, fatigue, blurred vision, eye opening difficulty, slurred speech, dysphagia, bucking, constipation, and anxiety. These clinical symptoms occurred 0∼36 days after BoNT injection, especially from 2nd to 6th day after the operation. Furthermore, the usage dose of BoNT was negatively related to latent period. Finally, patients all discharged from our hospital 1∼20 days after treatments, and their symptoms relieved or disappeared. Botulism is a severe side effect for BoNT injection. Injecting botulinum antitoxin serum may be an effective approach to improve clinical outcomes of botulism cases.
Objective To investigate the effect factors of Vitamin K1 maintenance dose in patients with anticoagulant rodenticide poisoning. Methods This retrospective study was analyzed 36 cases in our hospital from January 2013 to October 2014. The correlation between Vitamin K1 and types of anticoagulant rodenticide and toxic dose, prothrombin time activity (PTA), prothrombin time (PT), activated partial thromboplastin time (APTT), prehospital duration (from poisoning to hospitalization), and length of hospital stay (duration of Vitamin K1 treatment) were collected and analyzed by Spearman rank correlation analysis and multivariate regression analysis. Results The dose of Vitamin K1 was positively correlated with brodifacoum (r=0.356, P<0.05), negative correlated with PTA, prehospital duration and length of hospital stay (r=-0.325, -0.420, -0.407, all P<0.05). However, there were no significant correlation between dose of Vitamin K1 and PT, APTT, bromadiolone (r=0.295, -0.312, 0.192, all P > 0.05). The multivariate regression analysis also showed that prehospital duration [95% confidence interval: (-0.536, -0.103), P=0.002] and length of hospital stay [95% confidence interval: (-1.955, -0.248), P=0.013] had significant effect on the maintenance dose of vitamin K1 in the patients with coagulation function stable. Conclusion After stabilizing the coagulation function, the demanded maintenance dose of vitamin K1 can be gradually decreased with time prolonged, and have no relationship with type of anticoagulant rodenticide and toxic dose.