縱隔、皮下氣腫及氣胸是百草枯中毒后的一種嚴(yán)重、預(yù)后極差的并發(fā)癥,臨床少見(jiàn)。本院收治1例,現(xiàn)報(bào)告如下。
目的 探討百草枯中毒致肺纖維化的機(jī)制。方法 SD 大鼠隨機(jī)分為對(duì)照組6 只、四氫吡咯二硫代氨基甲酸酯( PDTC) 對(duì)照組36 只、百草枯染毒組36 只、PDTC 干預(yù)組36 只。染毒組和PDTC 干預(yù)組給予百草枯80 mg/kg 一次性灌胃后2 h, 染毒組給予等量生理鹽水腹腔注射, PDTC 干預(yù)組給予PDTC 100 mg/kg 一次性腹腔注射; 對(duì)照組和PDTC 對(duì)照組予生理鹽水1 mL/kg 灌胃后2 h, 對(duì)照組給予等量生理鹽水腹腔注射, PDTC 對(duì)照組給予PDTC 100 mg/kg 一次性腹腔注射。于不同處理后1、3、7、14、28、56 d 觀察大鼠中毒表現(xiàn), 并分別處死6 只大鼠觀察肺組織病理改變, 測(cè)定肺組織羥脯氨酸含量, 測(cè)定血清胰島素樣生長(zhǎng)因子1( IGF-1) 、轉(zhuǎn)化生長(zhǎng)因子β1 ( TGF-β1 ) 、血小板源性生長(zhǎng)因子( PDGF) 水平及肺組織結(jié)締組織生長(zhǎng)因子( CTGF) 的表達(dá), 分析它們與肺組織羥脯氨酸含量的關(guān)系。結(jié)果 染毒早期( 1 ~7 d) 病理特征為急性肺泡炎, 表現(xiàn)為肺充血、肺水腫及炎性細(xì)胞浸潤(rùn)。后期( 14 ~56 d) 炎性病變減輕, 支氣管周圍、肺泡間隔及肺泡內(nèi)大量成纖維細(xì)胞增殖、膠原纖維增生。干預(yù)組的肺部炎性改變及膠原纖維增生程度均明顯減輕。與對(duì)照組比較, 染毒組IGF-1 含量3 ~56 d 明顯升高( P lt;0. 01) , TGF-β1 含量各時(shí)段均明顯升高( P lt; 0. 01) , PDGF 含量7 ~56 d 顯著升高( P lt;0. 01) 。經(jīng)PDTC 干預(yù)后, 上述細(xì)胞因子水平明顯降低, 相應(yīng)時(shí)點(diǎn)差異有統(tǒng)計(jì)學(xué)意義( P lt;0. 05 或P lt;0. 01) 。免疫組化顯示, 染毒組3 d 即有CTGF陽(yáng)性表達(dá), 表達(dá)強(qiáng)度較弱, 主要表達(dá)于炎癥細(xì)胞;7、14 d表達(dá)進(jìn)一步增強(qiáng), 28、56 d 表達(dá)持續(xù)增強(qiáng), 主要表達(dá)于巨噬細(xì)胞和成纖維細(xì)胞。干預(yù)組CTGF 陽(yáng)性表達(dá)細(xì)胞與染毒組相同, 但各時(shí)段表達(dá)強(qiáng)度均顯著降低( P lt; 0. 05 或P lt; 0. 01) 。結(jié)論 細(xì)胞因子IGF-1、TGF-β1 、PDGF及CTGF的過(guò)度表達(dá)是參與百草枯致肺纖維化的重要機(jī)制。PDTC 可能通過(guò)抑制NF-κB 活化進(jìn)而抑制上述細(xì)胞因子的表達(dá), 減輕百草枯中毒大鼠的肺損傷和肺纖維化。
目的 探討急性百草枯(PQ)中毒鼠肺組織病理?yè)p傷和肺組織血紅素氧合酶-1(HO-1)的表達(dá)及三七總皂甙(PNS)的保護(hù)作用。 方法 150只SD雄性鼠分為正常對(duì)照組(C組)30只、PQ中毒組(PQ組)60只及PNS組60只。PQ組和PNS組一次性灌胃PQ 25 mg/kg染毒,C組給予等體積生理鹽水灌胃。其中PNS組于染毒前15 min以PNS 50 mg/kg陰莖靜脈注射保護(hù),以后1次/d給藥直至處死前;PQ組、C組分別在同時(shí)間點(diǎn)給予等體積生理鹽水。觀察各組大鼠在中毒后6、12 h,1、3、5、7 d肺組織病理改變,采用蛋白質(zhì)印跡法分析肺組織HO-1蛋白表達(dá)和反轉(zhuǎn)錄-聚合酶鏈反應(yīng)方法測(cè)定鼠肺組織HO-1 mRNA的表達(dá)。 結(jié)果 C組HO-1蛋白和HO-1 mRNA絕大多數(shù)標(biāo)本有弱表達(dá),個(gè)別標(biāo)本不表達(dá);與C組相比PQ組及PNS組HO-1蛋白和HO-1 mRNA表達(dá)增強(qiáng),差異有統(tǒng)計(jì)學(xué)意義(P<0.05);PQ組HO-1蛋白和HO-1 mRNA的表達(dá)在1 d達(dá)高峰之后下降,第3天基本恢復(fù)到C組水平;PNS組與PQ組相似,但在6 h、12 h、1 d及3 d高于PQ組,差異有統(tǒng)計(jì)學(xué)意義(P<0.05),至第5天和第7天二者相比差異無(wú)統(tǒng)計(jì)學(xué)意義(P<0.05)。PQ組肺組織病理?yè)p傷評(píng)分在6、12 h,1、3 、5、7 d各亞組均高于PNS相應(yīng)組,差異有統(tǒng)計(jì)學(xué)意義(P<0.05),C組肺組織病理大致正常,與PQ組及PNS組相比,差異有統(tǒng)計(jì)學(xué)意義(P<0.001)。 結(jié)論 HO-1參與PQ中毒所致急性肺損傷,PNS對(duì)PQ中毒所致急性肺損傷有保護(hù)作用。
【摘要】 目的 探討口服百草枯中毒患者口腔護(hù)理的方法及早期護(hù)理的臨床意義?!》椒ā?009年1月-2010年3月,采用半隨機(jī)方法將62例白草枯中毒患者按中毒時(shí)間的長(zhǎng)短分A組(中毒時(shí)間lt;3 d,n=32)、B組(中毒時(shí)間gt;3 d,n=3),比較兩組患者口腔潰瘍的治愈率、并發(fā)癥發(fā)生狀況,分析早期口腔護(hù)理的必要性。 結(jié)果 A組患者百草枯所致的口腔黏膜損害明顯減輕,并發(fā)癥發(fā)生率降低,為改善預(yù)后提供了條件,顯示了早期加強(qiáng)口腔護(hù)理的成效?!〗Y(jié)論 重視百草枯早期口腔護(hù)理,能夠減輕口腔糜爛潰瘍痛苦,減少并發(fā)癥,提高患者生活質(zhì)量。【Abstract】 Objective To investigate the clinical significance of early oral care for paraquat-poisoned patients. Methods A quasi-randomized controlled trial was used. A total of 62 paraquat-poisoned patients (from January 2009 to March 2010) were divided into experimental group and control group in order to compare the healing rate of oral ulcer, complications and the necessity of early oral care between the two groups. Results The oral mucosa lesions in experimental group obviously alleviated and the complications decreased. The effective early oral care provided the very favorable conditions for better prognosis. Conclusion The early oral care for paraquat-poisoned patients could relieve the pain of oral ulcer, reduce the complications and improve patient′s life quality.
【摘要】 目的 觀察百草枯中毒大鼠腎組織中血紅素氧合酶1(HO1)的表達(dá),探討其病理生理機(jī)制。 方法 SD大鼠126只隨機(jī)分為空白對(duì)照組、中毒組和褪黑素組,各42只。中毒組、褪黑素組予以百草枯(25 mg/kg)腹腔注射染毒,對(duì)照組予以等量生理鹽水腹腔注射,15 min后褪黑素組予以褪黑素(10 mg/kg)腹腔注射,對(duì)照組、中毒組予以等量生理鹽水腹腔注射。于1、3、6、12 h,1、2、3、5 d時(shí)各組隨機(jī)取6只處死。蘇木精〖CD3/5〗伊紅(HE)染色觀察各組腎組織病理學(xué)變化,采用免疫組識(shí)化學(xué)和RTPCR觀察腎組織HO1蛋白和mRNA表達(dá)。 結(jié)果 ①與對(duì)照組相比,中毒組染毒后3 h即可見(jiàn)充血、水腫及空泡變性等病理變化,1 d達(dá)頂峰,病理?yè)p傷評(píng)分3.30±0.31(Plt;0.05),其后緩解趨勢(shì)不明顯;而褪黑素組病理變化明顯減輕且緩解趨勢(shì)明顯,1 d時(shí)病理?yè)p傷評(píng)分2.70±0.26,與中毒組相比差異有統(tǒng)計(jì)學(xué)意義(Plt;0.05)。②與對(duì)照組相比,中毒組染毒3 h在皮質(zhì)部腎小管上皮細(xì)胞的細(xì)胞膜及細(xì)胞漿HO1呈陽(yáng)性表達(dá),免疫組識(shí)化學(xué)評(píng)分(IHS)3.33±1.75,HO1 mRNA表達(dá)增強(qiáng),與對(duì)照組相比差異有統(tǒng)計(jì)學(xué)意義(Plt;0.05),1 d達(dá)頂峰,HIS為7.00±2.00,之后減弱,5 d仍有陽(yáng)性表達(dá),但與對(duì)照組相比差異無(wú)統(tǒng)計(jì)學(xué)意義(Pgt;0.05);褪黑素組HO1表達(dá)較中毒組明顯增強(qiáng),IHS評(píng)分6 h~3 d差異具有統(tǒng)計(jì)學(xué)意義(Plt;0.05),5 d不再有統(tǒng)計(jì)學(xué)意義(Pgt;005)。 結(jié)論 HO1在百草枯中毒大鼠腎組織中呈高表達(dá),褪黑素能明顯改善百草枯中毒腎臟病理?yè)p傷,增強(qiáng)HO1表達(dá)可能是其作用途徑之一,而氧化損傷可能是百草枯中毒腎損傷病理生理機(jī)制之一。【Abstract】 Objective To investigate the expression of heme oxygenase1 (HO1) in paraquartinduced renal injury in rats and the protective effects of melatonin, and explore possible mechanism of paraquartinduced renal injury. Methods One hundred and twentysix adult healthy SpragneDawley rats were randomly divided into three groups and 42 in each group: control group (A), paraquart group (B), and melatonin group (C). The rats in group B and group C were treated with paraquart (25 mg/kg) intraperitoneally, the rats in group A were treated with the same dose of normal saline. In 15 minutes, the rats in group C were given melatonin intraperitoneally at a dose of 10 mg/(kg·d) and the rats in group A and B were treated intraperitoneally with the same dose of normal saline. Six rats in each group were randomly sacrificed at one, three, 12 hours and one, tou, three, five days respectively. Renal histopathological changes were observed under light microscope by HE staining. The protein and mRNA expressions of HO1 were evaluated by immunohistochemical staining and RTPCR respectively. Results ①In group B, there were obvious lesions in the renal tubule of cortical part, including edema, congestion and vacuolar degeneration. These pathologic changes gradually reached the peak on the first day and did not relieved till the end of this study, the pathologic injury score was 3.30±0.31, and there was a statistical significance between group B and group A (Plt;0.05). The aforementioned pathological lesion was more palliative in group C, the pathologic injury score was 2.70±0.26 at the first day; Compared with group B, there was a statistical significance. ②In group A, there was no or weak expression of HO1 and HO1 mRNA. At the third hour, the expression of HO1 in group B was observed in the membrane and cytoplasm of renal tubular epithelial cell of cortical part. Immunohistochemistry score (IHS) was 3.33±1.75 and the expression of HO1 mRNA increased, there was a statistical significance between group B and group A (Plt;0.05). It reached the peak on the first day, IHS was 7.00±2.00, but there was no statistical difference between group B and group A on the fifth day (Pgt;0.05); Compared with group B, the expression in group C was enhanced obviously, IHS were higher obviously on the six hour till to the third day (Plt;0.05), but there were no statistical differences on the fifth day (Pgt;0.05). Conclusion The expression of HO1 in the paraquartdamaged kidney increases and melatonin surely has an protective effect by increasing the expression of HO1, which suggests that oxidative injury might be the main mechanism of paraquartinduced renal injury.
目的:探討貫葉連翹提取物對(duì)百草枯誘導(dǎo)的大鼠肺纖維化模型的干預(yù)作用及機(jī)制。方法:20只Sprague-dawly大鼠隨機(jī)等分為4組:百草枯組,貫葉連翹提取物組,百草枯+貫葉連翹提取物組和對(duì)照組。百草枯液按80mg/kg一次性灌胃,貫葉連翹提取物按400mg/kg灌胃,連用3d,對(duì)照組僅用生理鹽水。于21d處死后取肺臟行HE染色鑒定,并用堿水解法測(cè)羥脯氨酸含量,同時(shí)以八木國(guó)夫熒光法測(cè)定肺組織脂質(zhì)過(guò)氧化產(chǎn)物,鹽酸羥胺法測(cè)定組織總超氧化物歧化酶的酶活力。結(jié)果:百草枯染毒動(dòng)物可致肺纖維化,羥脯氨酸和丙二醛含量明顯增高。百草枯+貫葉連翹提取物組與百草枯組比較,第21天時(shí)肺纖維化減輕,羥脯氨酸和丙二醛含量減少(Plt;0.05),與對(duì)照組相比總超氧化物歧化酶無(wú)明顯變化(Pgt;0.05)。結(jié)論:貫葉連翹提取物對(duì)百草枯誘導(dǎo)的大鼠肺纖維化模型有抑制作用,其機(jī)制可能與抑制脂質(zhì)過(guò)氧化有關(guān)。
目的:觀察百草枯中毒大鼠血漿和肺組織勻漿中的內(nèi)皮素-1的動(dòng)態(tài)變化,探討大鼠PQ中毒肺損傷的可能機(jī)制。方法:將雄性Wistar大鼠隨機(jī)分成百草枯中毒組和生理鹽水對(duì)照組,分別給予16mg/kg百草枯或等體積生理鹽水腹腔內(nèi)注射,并在給藥后6、12、24和72 h處死大鼠,觀察其一般表現(xiàn)、肺的病理變化。測(cè)定肺系數(shù)、肺組織勻漿和血漿中內(nèi)皮素-1的含量。結(jié)果: 百草枯中毒后大鼠出現(xiàn)呼吸困難,活動(dòng)能力下降,肺系數(shù)增加,并隨時(shí)間變化,光鏡下表現(xiàn)為肺出血、水腫等不同程度的肺損傷改變。血漿和組織勻漿中內(nèi)皮素-1在中毒后與對(duì)照組大鼠比較明顯升高,并隨時(shí)間變化(Plt;0.01)。結(jié)論:在百草枯中毒肺損傷中,內(nèi)皮素-1可能發(fā)揮了重要作用。
百草枯中毒所致急性肺損傷是目前臨床上百草枯中毒致死的主要因素,近年來(lái)對(duì)于其損傷機(jī)制的研究不斷深入,但其具體機(jī)制尚不完全明確。現(xiàn)對(duì)近年來(lái)百草枯中毒肺損傷在炎癥反應(yīng)、氧化損傷、基因異常表達(dá)等方面的機(jī)制研究進(jìn)行綜述,以期為臨床醫(yī)生對(duì)百草枯中毒致肺損傷的治療提供依據(jù)。
目的分析百草枯中毒死亡的臨床及病理學(xué)特點(diǎn),探討百草枯中毒致肺纖維化的損傷機(jī)制。 方法對(duì)2010年1月-2013年12月涉及百草枯中毒的3例死亡案例進(jìn)行回顧性分析,觀察對(duì)比急慢性百草枯中毒死亡的臨床特點(diǎn)及病理學(xué)改變。 結(jié)果百草枯中毒的臨床及病理表現(xiàn)主要是以肺為靶器官的多器官損傷,急性中毒死亡者肺損傷主要為肺水腫及肺透明膜形成,慢性中毒死亡者肺損傷主要為肺透明膜形成及廣泛肺間質(zhì)纖維化。 結(jié)論臨床上應(yīng)加深百草枯中毒表現(xiàn)及損傷機(jī)制的認(rèn)識(shí)以對(duì)患者進(jìn)行早期診治。而法醫(yī)學(xué)鑒定應(yīng)結(jié)合案情、臨床資料、毒物分析及解剖結(jié)果進(jìn)行綜合分析而得出正確的鑒定結(jié)論。