百草枯中毒致肺损伤的64层螺旋CT表现

目的探讨百草枯中毒肺部64层螺旋CT表现及临床价值。方法对百草枯中毒患者的不同时期分别行胸部64层螺旋CT检查,并对74例胸部CT影像征象进行回顾性分析。结果 74例患者出现了肺纹理增多、肺实变和肺纤维化。结论百草枯中毒在肺部有明确的影像学征象,其影像学表现与病理密切相关,多层CT征象与中毒机制的对照研究对临床治疗有非常重要的指导意义。     

百草枯中毒肺损伤的影像学征象与病理基础对照分析

目的:探讨百草枯(Paraquat,PQ)中毒致肺损伤的影像学征象,并与病理学基础对照分析.方法:对8例PQ中毒患者的胸片及胸部CT资料进行回顾性分析.结果:病变早期(＜7 d)以肺纹理增多、模糊为主,部分出现磨玻璃样变；中期(7～14 d)主要表现为两肺弥漫磨玻璃样变和两下肺基底段肺实变；晚期(3周后)以肺间质纤维化及肺实质损害为主.结论:胸片、CT均能很好显示PQ中毒肺损伤的病理演变过程,对评估预后及指导临床治疗有重要意义.     

百草枯中毒早期胸部CT表现与临床预后的相关性分析

目的 探讨百草枯(PQ)中毒早期胸部CT表现与临床预后的关系,为临床病情评估提供依据。方法 选取宣城市人民医院2014年9月至2018年1月确诊为百草枯中毒的病人18例,分为存活组与死亡组,比较两组早期(＜1周)与中期(1~2周)胸部病变区域CT值、是否合并肺外征象及发病年龄的差异;采用Spearman等级相关分析中毒早期肺部病变范围与临床预后的相关性。结果 18例病人存活11例、死亡7例,病死率38.89%;两组年龄、中毒早期肺部病变CT均值、中毒中期肺部病变CT增加值、是否合并肺外征象比较,均差异无统计学意义(均P>0.05),两组中毒 后行多次CT复查的病人中,早期与中期CT均值(Uc=-2.701,P=0.007)和中毒中期胸部损伤范围变化(P=0.033)均差异有统计学意义。 病死率与中毒早期肺部损伤范围呈正相关(r_s=0.655,P=0.003)。结论 胸部CT对百草枯中毒病人肺部损伤的显示优势明显,在口服剂量不能获得的情况下,早期胸部CT检查有助于评估病人的中毒程度及预后。     

百草枯中毒的胸部CT表现

目的探讨百草枯中毒胸部CT表现及临床诊断价值。方法回顾性分析2009年1月至2012年11月该院收治的18例百草枯中毒患者的CT影像学资料及临床资料。结果 18例患者的胸部CT表现随着中毒时间的增加而发生不同的影像学改变,早期（〈7 d）主要表现为双肺纹理明显增粗增多,双肺胸膜下区分布为主的多发楔形实变影及磨玻璃密度增高影;中期（7～14 d）以双肺内广泛分布的磨玻璃密度影改变为主,同时伴肺纤维化、肺实变、双侧胸腔积液及心包积液;晚期（〉14 d）高分辨率X射线计算机体层摄影术（HRCT）影像表现主要为双肺胸膜下区的间质纤维化。另外,患者吸收中毒剂量少时胸部损害程度相对较轻,剂量多时胸部损害的程度相对严重。结论百草枯中毒时胸部CT有特定的影像学表现,特别是HRCT对肺损伤的早期轻微改变具有一定的特征性,其CT图像的变化对病情进展有十分重要意义。     

百草枯肺儿童肺部影像学改变和预后结局的临床分析

目的:总结百草枯肺儿童的肺部影像学改变和预后结局,提高随访诊治经验。方法:回顾性分析百草枯中毒合并肺部损害的52例患者的临床资料,统计分析肺部影响学改变情况,电话随访临床预后结局。结果:百草枯肺损害早期(7天)主要表现为双肺纹理增多、斑片影、条索影,可出现气肿表现,如纵膈积气等;中期(7~14天)主要表现为斑片影及磨玻璃密度影,伴不同程度的间质改变;晚期(14天)表现以肺间质纤维化为主。在明确预后结局的患儿中,病死率较高,为52.78%,平均死亡离服毒时间为8.84±7.81天。结论:百草枯肺是百草枯中毒的主要并发症和死亡原因,但儿童肺部发育与成人有差异,临床应加强对肺部影像学征象和临床预后结局的长期规范化的随访观察。     

百草枯中毒胸部CT表现

目的:分析探讨百草枯中毒致胸部损害的CT特征和诊断价值.方法:分析70例口服百草枯中毒致胸部损害的CT影像学资料.结果:早期(3 d内)主要表现为肺纹理增多、磨玻璃样改变、胸膜下线和心脏增大;早中期(4～7 d)主要表现为磨玻璃样改变、肺间质纤维化、胸膜下线、胸腔积液和心脏增大;中期(8～14 d)主要表现为肺纹理增多、磨玻璃样改变、肺间质纤维化、胸膜下线、胸膜增厚、心脏增大;中后期(15～28 d)主要表现为磨玻璃样改变、肺间质纤维化、胸膜下线、胸膜增厚;后期(＞28 d)则以肺间质纤维化、胸膜下线多见.结论:百草枯中毒的胸部CT表现具有一定特征性,其影像学变化对病情发展及指导临床治疗具有重要意义.     

百草枯中毒致胸部损害的CT分析

目的探讨CT在百草枯中毒胸部损害的应用价值。方法回顾性分析5例口服百草枯中毒致胸部损害的CT资料。结果 5例患者首次CT检查4例表现为肺内斑点状、斑片状、线条状密度增高影,伴少量胸腔积液;1例胸部未见明显异常。5例首次CT复查肺部病变和胸腔积液同时吸收1例,仅肺部病变吸收1例;1例首次CT检查胸部未见明显异常者出现肺部病变和胸腔积液;2例肺部病变范围增大;1例胸腔积液增多。4例第2次复查2例肺部病变和胸腔积液增多。3例第3次复查胸部病变基本吸收。结论 CT对百草枯中毒后胸部损害的评估、治疗和判断疗效有一定的指导价值。     

不同剂量盐酸氨溴索防治百草枯中毒肺损伤疗效观察

目的观察不同剂量盐酸氨溴索治疗百草枯中毒肺损伤的效果。方法将48例百草枯中毒患者分为常规剂量治疗组（24例）和大剂量治疗组（24例）常规治疗组给予盐酸氨溴索30mg静脉滴注,每12小时1次;大剂量治疗组给予盐酸氨溴索500mg静脉滴注,每12小时1次,观察2组治疗前、治疗后3、7、14d时动脉血气、胸部CT变化。结果盐酸氨溴索大剂量组与常规治疗组比较,血气改善更为显著,胸部CT表现有明显改善（P均〈0.05）,且治疗14d时的效果均优于治疗前及治疗3、7d,差异均有统计学意义（P〈0.05）。结论盐酸氨溴索大剂量组治疗可减轻肺组织损伤程度,对百草枯中毒急性肺损伤治疗有效。     

急性百草枯中毒的救治护理体会

百草枯又名一扫光,克无踪,作为高效除草剂之一,目前为各地广泛使用。对人、畜均有毒性,急性中毒的病死率极高,可达25％～76％,迄今为止仍无特效解毒剂。随着百草枯中毒（多为口服自杀）的逐年增多,血液进化技术作为清楚体内毒素的有效措施,被广泛应用于百草枯中毒的治疗。我科从2013年7月至今,收治急性百草枯中毒60例,现将治疗及护理体会报道如下。1百草枯中毒的机制及临床表现百草枯中毒的发病机制目前还不完全清楚,口服吸收率为5％～15％,2h血浆浓度达到高峰,并迅速分布到肺、肝、肾,因肺泡对百草枯的主动摄取和蓄积特点,所以肺含量最高也损害最大。百草枯在肺内产生氧自由基导致肺、肝、肾细胞膜膜脂质过度氧化破坏细胞结构。最终导致肺纤维化,甚至多脏器的功能损害。百草枯毒性大,接触后有明显的局部刺激症状,口服吸收迅速,口咽有灼烧感,并迅速出现口腔,舌咽溃烂疼痛并伴有恶心,呕吐,腹痛等。     

特发性肺纤维化薄层MSCT表现、肺功能检测及临床意义

目的探讨特发性肺纤维化（IPF）薄层多层螺旋CT（MSCT）表现特征、肺功能检测结果及其临床意义。方法经临床病理证实的30例IPF患者,其中男15例,女15例;年龄35～70岁。30例均行薄层MSCT扫描。所有病例均于薄层MSCT检查当日行肺功能检查。结果 30例IPF中,小叶间隔增厚出现频率最高为96.7%,胸膜下线出现频率最低为14.2%。小叶间隔增厚、小叶内间质增厚、蜂窝肺主要见于肺周边部,支气管血管束增粗主要见于肺中央部。30例IPF均表现为不同程度限制性通气功能障碍及弥散功能障碍。薄层MSCT各征象总半定量评分与限制性通气功能障碍分级（r=0.843,P〈0.01）、弥散功能障碍分级之间呈正相关（r=0.838,P〈0.01）。结论薄层MSCT能准确反应IPF的病理变化,肺功能检测可以了解患者肺功能受损害的程度,二者相结合有助于预测IPF的进展、预后及疗效反应。     

An antisense oligonucleotide to HSP47 inhibits paraquat-induced pulmonary fibrosis in rats

The most common cause of death from poisoning by the widely used, but highly toxic herbicide paraquat is respiratory failure from pulmonary fibrosis, which develops through pathological overproduction of extracellular matrix proteins such as the collagens. Heat shock protein (HSP47) is a collagen-specific molecular chaperone that assists in the posttranslational modifications of procollagens during collagen biosynthesis. We investigated whether treatment with an HSP47-antisense oligonucleotide would inhibit paraquat-induced pulmonary fibrosis in Wistar rats. Rats randomized into three groups (control, paraquat, and paraquat+antisense). Paraquat (20 mg/kg/day) (n=16) or a saline control (n=10) was administered to groups of Wistar rats. Intratracheal administration of the antisense oligonucleotide (100 nmol/kg in saline) was performed after the initial paraquat treatment (n=16). Treatment with paraquat alone induced pulmonary fibrosis in the entire group, while treatment with the antisense oligonucleotide alone did not produce any substantial change in lung histology. Administration of antisense oligonucleotides produced a substantial reduction in paraquat-induced pulmonary fibrosis. An immunoblot analysis confirmed that the HSP47-antisense oligonucleotide inhibited HSP47 production. These findings indicate that the HSP47-antisense oligonucleotide inhibited paraquat-induced pulmonary fibrosis and pneumopathy in rats.     

Effect of the inhalation of zinc and dietary zinc on paraquat toxicity in the rat.

A possible pharmacological effect of zinc against the pulmonary toxicant paraquat has been studied. Rats were treated with zinc either by inhalation of zinc oxide fume aerosol or consumption of zinc supplemented food. The animals were then injected with paraquat ip (30 mg/kg) and lethality monitored for 7 days. Neither zinc inhalation nor dietary zinc protected the animals against paraquat-induced lethality. In fact, exposure of rats to zinc oxide fume aerosol potentiated the lethal effects of paraquat. The mechanism of paraquat-induced lung toxicity at the cellular level does not appear to directly involve a zinc-dependent step. This distinguishes paraquat from other injurious agents which have been reported to respond to zinc.     

辅助性T细胞17活化在百草枯致小鼠肺纤维化模型中的作用

目的 观察辅助性T细胞17(Th17)活化在百草枯致小鼠肺纤维化模型中的作用.方法 将30只C57BL/6小鼠随机分为对照组(10只)和百草枯中毒组(20只).百草枯中毒组经腹腔注射百草枯35 mg/kg建立小鼠中毒模型;对照组经腹腔注入等体积生理盐水.观察2组小鼠肺脏组织病理变化情况及肺纤维化评分,检测外周血Th17细胞、肺组织中维甲酸相关核孤儿受体γt(RORγt)基因及蛋白的表达情况.结果 百草枯中毒组肺平均内衬间隔、肺泡腔与肺总面积比高于对照组,平均肺泡数低于对照组,外周血Th17细胞阳性率高于对照组,肺组织中ROR-γtmRNA和蛋白表达水平高于对照组(P＜0.01).结论 百草枯致小鼠肺纤维化模型外周血及肺组织中Th17细胞明显活化,提示Th17细胞活化在百草枯致肺纤维化过程中起着重要作用.     

Protective effect of liposome-associated alpha-tocopherol against paraquat-induced acute lung toxicity.

The present study was undertaken to investigate whether alpha-tocopherol, entrapped in liposomes and delivered directly to the lung, could protect against paraquat-induced lung damage in the rat. Plain liposomes (composed of dipalmitoylphosphatidylcholine, DPPC) or DPPC/alpha-tocopherol liposomes were administered intratracheally to animals 24 hr prior to an intraperitoneal injection of paraquat (20 mg/kg); rats were killed 24 or 48 hr after paraquat treatment. Results of this study showed that lungs of animals treated with paraquat were damaged extensively as evidenced by an increase in lung weight and a significant reduction in lung angiotensin-converting enzyme (ACE) activity and cytochrome P450 concentration. Furthermore, paraquat treatment resulted in a significant decrease in reduced glutathione (GSH) concentrations and a marked elevation in microsomal lipid peroxidation levels as measured by the formation of diene conjugates. Pretreatment of rats with DPPC liposomes alone did not alter significantly the paraquat-induced changes of all parameters examined. On the other hand, pretreatment of rats with DPPC/alpha-tocopherol liposomes 24 hr prior to paraquat challenge resulted in a significant increase in pulmonary alpha-tocopherol concentrations and antagonized paraquat-induced changes in lipid peroxidation, GSH/GSSG ratio, lung ACE activity and cytochrome P450 concentrations. Results of this study suggested that alpha-tocopherol, delivered directly to the lung in a liposomal formulation 24 hr prior to paraquat administration, confers protection against paraquat-induced lung damage.     

47例自服百草枯中毒患儿病例分析

目的:通过分析47 例儿童自服百草枯中毒病例的特征、治疗情况及预后,为防治儿童百草枯中毒措施的制定提供参考。 方法:回顾性分析某三甲儿童医院自2012年1月至2017年1月自服百草枯中毒患儿的临床资料,分析其人口学特征、临床特征、影响预后的因素以及随访生存情况。结果:自服患儿男29例,女18例,年龄(12.3±1.7)岁。所有患儿均来自农业种植地区,留守儿童占比42.6%(20/47)。百草枯均为浓度20%的水剂,服药量10(5,20)mL。34例患儿出现肺、肾、肝、心等两个以上器官损害。服药7 d后26例患者出现呼吸困难。病死率48.9%(23/47),死亡时间分布在中毒后30 d内,早期病死率高。将病例资料分为存活组、死亡组,与死亡组相比,存活组患儿服药量少、就医时间短(P<0.01)。结论:儿童自服百草枯以青少年为主,具有服药量大、致死率高的特点。急性百草枯中毒缺乏特效解毒药物,应采取综合治疗措施,中毒后早期的医疗干预尤为重要。     

百草枯中毒肺损伤的治疗前后CT表现特征与预后相关性分析

目的：探讨百草枯中毒所致肺损伤患者在不同剂量、治疗不同时期的CT影像学特征以及临床预后。方法选取我院2011～2013年收治的50例百草枯中毒患者,对患者不同剂量、不同治疗分期的CT表征与临床预后进行观察。结果患者早期治疗中的主要特征为肺纹理增多、纵隔气肿、磨玻璃征或无明显异常,而中期的主要特征为肺纹理增多、纵隔气肿、磨玻璃征、肺间质纤维化,治疗晚期阶段患者存活患者主要表现为肺间质纤维化。少量组22例患者均好转出院;中量组21例患者中15例好转出院,6例预后不良;大量组患者9例全部死亡。结论百草枯中毒患者肺损伤包括肺实质与间质同时受损,以纵隔气肿、磨玻璃征、实质病变、肺气肿与胸腔积液为主,晚期主要表现为间质纤维化,可以明确百草枯中毒肺损伤治疗具有明显的CT表征,且与预后存在明显相关性。     

Increased expression of endothelial iNOS accounts for hyporesponsiveness of pulmonary artery to vasoconstrictors after paraquat poisoning

Paraquat is a toxic herbicide that induces severe acute lung injury (ALI) and pulmonary hypertension in humans. Although vascular disorders are present and contribute to increased mortality in ALI patients, there is little data available on vascular responsiveness after toxic exposure to paraquat. We aimed to evaluate the vascular response of isolated pulmonary arteries from rats treated with a dose of paraquat that induces ALI. Paraquat treatment did not modify the relaxant response of pulmonary artery to acetylcholine, but greatly reduced phenylephrine-induced contraction. Removal of the endothelium, inhibition of nitric oxide synthase (NOS) with L-NAME or selective inhibition of inducible NOS (iNOS) with L-NIL, restored contraction of vessels from paraquat poisoned rats to the same level as those not exposed to paraquat. The basal production of NO and expression of iNOS were increased in endothelium-intact but not in endothelium-denuded vessels from paraquat-poisoned rats. Expression of endothelial NOS was not modified. Our findings suggest that paraquat poisoning increases endothelial iNOS expression and basal NO production decreasing responsiveness of pulmonary artery to vasoconstrictors. Thus, our results do not support the hypothesis that pulmonary hypertension in paraquat-induced ALI is mediated by a reduction in endothelial NO production or increased contractility of pulmonary artery.     

Kinetics of paraquat elimination in the dog

The elimination and distribution kinetics of paraquat and the effect of paraquat-induced renal damage on these parameters have been studied in the dog. After intravenous administration, low doses (30–50 μg/kg) of paraquat were rapidly excreted in the urine at a clearance rate in excess of glomerular filtration rate, indicating that paraquat was eliminated by active secretion. This secretion could be inhibited by competition with N′-methylnicotinamide, a quaternary ammonium compound. Large doses (20 mg/kg) of paraquat induced renal failure, the extent of renal function impairment depending on the dose. The plasma concentration-time curve showed a triexponential decline, so that the elimination of paraquat could be described by a three-compartment open model. Simulation of paraquat levels in the peripheral compartments indicated that with early renal failure, fivefold higher levels would be achieved in the slow uptake compartment than under conditions of normal renal function. Since the energy-dependent accumulation of paraquat by the lung is a slow process, it was assumed that the slow uptake compartment included the lung. The implications of this are discussed in relation to the rational treatment of paraquat poisoning in man.     

Toxicokinetics of paraquat in humans

1. The toxicokinetics of paraquat were studied in 18 cases of acute human poisoning using a specific radioimmunoassay. Plasma paraquat concentration exhibited a mean distribution half-life (t1/2 alpha) of 5 h and a mean elimination half-life (t1/2 beta) of 84 h. Cardiovascular collapse supervened early during the course of the intoxication and was associated with the distribution phase. Death related to pulmonary fibrosis occurred late and was associated with the elimination phase. 2. Pharmacokinetic analysis of urine paraquat excretion confirmed the biphasic decline of paraquat. Moreover, renal paraquat and creatinine clearances were not correlated but renal paraquat clearance was never higher than the renal creatinine clearance. 3. Tissue paraquat distribution was ubiquitous with an apparent volume of distribution ranging from 1.2 to 1.6 l/kg. Muscle could represent an important reservoir explaining the long persistence of paraquat in plasma and urine for several weeks or months after poisoning.     

Intravenous paraquat poisoning-induced multiple organ failure and fatality--a report of two cases

Paraquat poisoning is the most common cause of fatal herbicide intoxication, mostly through oral ingestion. This work reports two cases of death following intravenous paraquat injection. The clinical courses of the two cases were fulminated and fatal. Toxic symptoms and severe organ function impairment developed soon after paraquat injection. Timely treatment with activated charcoal hemoperfusion with pulse steroid and cyclophosphamide was attempted in both cases; however, both cases died within five days owing to multiple organ failure. In cases of intravenous paraquat intoxication, toxic signs develop more quicker than with oral ingestion. The prognosis of intravenous paraquat intoxication is extremely poor.