血液灌流联合血液滤过治疗急性百草枯中毒患者的临床分析

目的探讨血液灌流联合血液滤过治疗急性百草枯中毒的临床疗效。方法选取我院2011年1月至2014年7月急诊收治的78例急性百草枯中毒患者,随机分为对照组及治疗组,每组各39例。对照组采取血液灌流治疗,治疗组采取血液灌流联合血液滤过治疗。结果治疗组患者的治愈率、病死率均优于对照组,差异具有统计学意义(P<0.05)。治疗组患者急性肾功能衰竭(ARF)、急性呼吸窘迫综合征(ARDS)、多器官功能障碍(MODS)发生率低于对照组(P<0.05)。结论血液灌流联合血液滤过治疗急性百草枯中毒,可短时间内清除体内的毒物,减轻肝肾功能损害,减少ARDS、MODS的发生,降低病死率,有利于改善中毒患者的预后。     

急性百草枯中毒临床治疗分析

目的总结分析急性百草枯(PQ)中毒的临床治疗效果。方法收集近几年来急性百草枯中毒患者32例,给予彻底洗胃、白淘土灌胃、血液灌流、早期大剂量激素20mg/kg冲击治疗,保护重要脏器,严密监测血气分析、肺CT、肝肾功能等,一旦上述指标出现异常,提示有肺纤维化形成时,立即再次给予大剂量激素20mg/kg冲击治疗,阻止肺纤维化形成。结果服毒量在20ml以下24h以内给予彻底洗胃等以上治疗措施的,临床疗效好。服毒量在20ml以上未能及时给予洗胃的,虽采取上述治疗措施,临床疗效差,死亡率高。结论急性百草枯中毒目前尚无特效解毒剂,彻底洗胃、白淘土灌胃吸附、血液灌流、早期大剂量激素20mg/kg冲击治疗,防止肺纤维化形成及早实施,是急性百草枯中毒抢救成功的关键。     

煤燃烧排放的细颗粒物对大鼠肺的免疫损伤

目的研究燃煤细颗粒物(PM_(2.5))对大鼠肺部的免疫损伤。方法采集空气动力学直径≤2.5μm的PM_(2.5)并分析测试其化学成分,研究因燃煤而产生的PM_(2.5)对大鼠肺部的免疫损伤。将40只雄性6周龄Wistar大鼠随机分为4组,分别对4组大鼠气管滴注生理盐水、低浓度(1.5 mg/kg·bw)、中浓度(7.5 mg/kg·bw)及高浓度(37.5 mg/kg·bw)PM_(2.5)悬液,分别于24和48 h后处死动物,检测其血常规和肺泡灌洗液(BALF)中白介素-6(IL-6)、肿瘤坏死因子(TNF-α)及转化生长因子(TGF-β1)等氧化炎症因子,并制作肺组织病理切片。结果一定的染毒时间和染毒剂量可明显提高大鼠白细胞数(WBC)、明显降低红细胞数(RBC)。急性染毒48 h后,低浓度组和高浓度组染毒使大鼠肺组织中TNF-α升高(P0.05)。对大鼠肺部病理观察显示,急性染毒导致大鼠肺部产生病理变化,特别是中浓度和高浓度染毒24和48 h后,大鼠肺泡严重压缩、溃不成形,血管和支气管内产生结晶,炎细胞浸润。结论燃煤PM_(2.5)急性染毒24 h后,导致大鼠血液WBC升高、激发TNF-α的分泌,大鼠表现出积极的免疫应对;急性染毒48 h后,大鼠血液WBC和RBC数量降低,大鼠表现出免疫系统调节能力降低。随着染毒污染物浓度的升高,大鼠肺部组织的不利影响逐渐加重。     

不同血液净化方式对脓毒症合并急性肾损伤炎性因子表达和预后效果的影响研究

目的分析不同血液净化方式治疗脓毒症合并急性肾损伤的效果。方法选取我院以血液净化治疗的99例脓毒症合并急性肾损伤患者作为研究对象,将接受连续性血液净化的45例患者作为连续组,将接受间歇性血液净化的44例患者作为间歇组,对比组间在炎性因子表达以及预后效果的不同。结果血液净化后,连续组IL-6(4.52±1.24)pg/m L、IL-8(7.42±1.28)pg/m L、hs-CRP(3.16±0.75)mg/L、TNF-α(29.04±8.78)pg/m L明显低于间歇组(P<0.05),而总有效率(91.11%)显著高于间歇组(P<0.05)。结论与间歇性血液净化相比,连续性血液净化对炎性反应的抑制作用更佳,治疗脓毒症合并急性肾损伤的效果更显著。     

舒脑欣滴丸对寒凝气滞血瘀证大鼠血小板聚集和血液流变学指标的影响

目的探讨舒脑欣滴丸对急性血瘀模型大鼠血小板聚集和血液流变学指标的影响。方法选取70只Wistar大鼠,随机分为对照组,模型组,舒脑欣滴丸13、26、52 mg/kg组,阳性药脑心通胶囊(15 mg/kg)、阿司匹林肠溶片(15 mg/kg)和藻酸双脂钠片(90 mg/kg)组,连续ig给药7 d,1次/d,末次给药后1 h,采用sc 0.1%肾上腺素加在冰水中游泳的方法,制备大鼠急性血瘀模型,观察舒脑欣滴丸对不同血小板聚集诱导剂二磷酸腺苷(ADP)、花生四烯酸(AA)和胶原(CG)引起的大鼠血小板聚集影响;通过检测血液流变学指标、凝血功能评价舒脑欣滴丸对血瘀模型大鼠的作用。结果舒脑欣滴丸对3种不同血小板聚集诱导剂引起的血小板聚集均有不同程度的抑制作用,可显著降低全血黏度,延长血瘀模型大鼠凝血酶原时间(PT)、活化部分凝血活酶时间(APTT)。结论舒脑欣滴丸13、26、52 mg/kg具有明显活血化瘀作用,能降低血液黏度,抑制多种诱导剂引起的血小板聚集,具有一定抗凝活性。     

6%羟乙基淀粉急性高容量血液稀释对老年食管癌患者的影响

急性高容量血液稀释(AHH)具有减少术中失血和异体血用量、操作简便、节约时间、降低费用和减少血液污染机会等优点[1].老年患者由于心血管等系统的衰老退变,而AHH存在增加容量负荷及对凝血功能的影响,因而在老年患者实施AHH有所顾虑[2].我们观察了AHH对围术期食管癌老年患者的血液动力学和凝血功能的影响.     

依达拉奉对百草枯中毒大鼠急性肺损伤治疗作用

目的研究依达拉奉对百草枯中毒急性肺组织损伤的治疗作用及可能机制。方法将96只雄性SD大鼠随机分为对照组(Con组)、模型组(Mod组)、依达拉奉治疗组(ED组)和地塞米松治疗组(Dex组),每组再根据染毒时间分为6h、24h、48h和72h等4个亚组,每组6只。采用腹腔注射20%百草枯溶液(25mg/kg)制备百草枯中毒急性肺损伤模型,Con组腹腔注射等容积生理盐水。染毒后1h开始,ED组和Dex组分别给予腹腔注射依达拉奉(3mg/kg)和地塞米松(3mg/kg),2次/日,Con组和Mod组给予等容积生理盐水。分别在染毒后6h、24h、48h和72h,观察大鼠一般状况变化,然后处死大鼠,经心脏采集血液标本检测血清SOD活性和MDA含量,并行HE染色观察肺组织病理变化。结果与Con组比较,Mod组、ED组及Dex组各时间点血清SOD活性明显下降(P<0.05或P<0.01),血清MDA水平均明显增加(P<0.01),肺组织病理示急性肺损伤改变,炎症细胞浸润,肺泡萎缩塌陷,甚至结构消失,且随时间进展加重;与Mod组相比,ED组和Dex组血清SOD活性明显上升(P<0.05或P<0.01),血清MDA含量明显下降(P<0.05或P<0.01),肺组织病理改变明显减轻;而ED组和Dex组间差异无统计学意义(P>0.05)。结论依达拉奉和地塞米松对百草枯中毒引起的急性肺损伤均有治疗作用,其治疗作用和减轻自由基损伤有关。     

血液灌流与联合血液透析治疗百草枯中毒疗效比较

目的：观察血液灌流联合血液透析治疗百草枯中毒患者的疗效,寻找治疗的有效途径。方法：回顾分析血液灌流(HP)与血液灌流加透析(HD)抢救治疗58例急性百草枯中毒患者的疗效。结果：血液灌流加透析联合组死亡率、白细胞109/L、血肌酐、血谷丙转氨酶、血肌酸激酶等指标均显著低于血液灌流组(P＜0.05)。结论：血液灌流联合血液透析是抢救急性百草枯中毒有效安全治疗手段。     

血液灌流治疗急性有机磷中毒并呼吸肌麻痹的疗效分析

急性有机磷中毒是基层医院常见急症之一,合并呼吸肌麻痹的中毒患者,病死率高.我科自1999年6月开始采用血液灌流(HP)治疗该类病人,现将资料整理并与常规治疗作对比分析.     

血液灌流和纳洛酮治疗氯氮平中毒效果观察

目的 探讨血液灌流和纳洛酮治疗氯氮平中毒的临床效果.方法 将内蒙古医科大学附属医院2007年8月至2014年4月救治的41例急性氯氮平中毒患者据治疗方式不同分为常规治疗组（20例）、血液灌流和纳洛酮治疗组（21例）.常规治疗组患者入院后给予洗胃、利尿、导泻、保护脏器功能等治疗,血液灌流和纳洛酮治疗组患者在上述常规治疗基础上,用HA230灌流器以150 ～ 200 ml/min流速血液灌流2h,血液灌流后在4h内静脉滴注纳洛酮0.5 mg/kg.观察并比较2组患者治疗5d后病死率、昏迷时间和并发症发生率.结果 常规治疗组和血液灌流和纳洛酮治疗组病死率分别为10.0％ （2/20）和4.7％（1/21）,组间差异无统计学意义（P＞0.05）;昏迷时间分别为（30±14）h和（19±10）h,组间差异有统计学意义（P＜0.05）.常规治疗组中有8例患者（44.4％）出现吸入性肺炎,血液灌流和纳洛酮组中仅有1例（6.2％）出现吸入性肺炎,组间差异有统计学意义（P＜0.05）.血液灌流和纳洛酮组和常规治疗组其他并发症如肝功能异常、心肌酶学异常、心功能不全、低血压、癫（痫）发作、深静脉穿刺部位出血、血小板减少发生率,差异均无统计学意义[19.0％（4/21）比25.0％（5/20）,38.1％（8/21）比35.0％（7/20）,19.0％（4/21）比15.0％（3/20）,23.8％ （5/21）比10.0％（2/20）,9.5％（2/21）比10.0％（2/20）,23.8％ （5/21）比0.0,9.5％（2/21）比0.0]（均P＞0.05）.结论 血液灌流和纳洛酮联合治疗可缩短氯氮平中毒患者昏迷时间,降低吸入性肺炎并发症发生率.     

Circulation,respiration, and blood homeostasis in cyanide-poisoned dogs after treatment with 4-dimethylaminophenol or cobalt compounds

The effects of intravenously injected 4-dimethylaminophenol-HCl (DMAP), Co₂EDTA, and Co(histidine)₂ on the survival rate and several physiological parameters were studied on dogs after acute intravenous poisoning with the double lethal dose of potassium cyanide.All dogs survived when the antidotes were administered 1 min after poisoning. When the therapy began 4 min after poisoning more dogs were rescued in the DMAP group than in the cobalt groups. DMAP, Co₂EDTA, and Co(histidine)₂ restored circulation and respiration of the surviving animals in a similar manner.The increase in the plasma concentrations of glucose and lactate was much higher in the Co₂EDTA group than in the DMAP group. The injection of Co₂EDTA produced a sharp rise in the lactate-to-pyruvate ratio. The lactate-to-pyruvate ratio stayed unchanged for some 15 min after injection of DMAP before also rising. The total dose of KCN (4 mg/kg) was bound to the ferrihemoglobin formed by DMAP. The arterial pO₂ increase, caused by liberation of oxygen from oxyhemoglobin during the formation of ferrihemoglobin, was less when the cyanide could act on the tissues for a longer period of time before the therapy with DMAP began.DMAP is more appropriate for the therapy of cyanide poisoning than Co₂EDTA, since the latter adds its inhibitory effects on the metablism to those of cyanide.     

Effects of 4-dimethylaminophenol,Co2EDTA,or NaNO2 on cerebral blood flow and sinus blood homeostasis of dogs in connection with acute cyanide poisoning

The effects of the cyanide antidotes DMAP, Co₂EDTA, and NaNO₂ on cerebral blood flow (CBF) and cerebral blood gases were investigated in connection with acute poisoning of dogs by cyanide. The substances were injected intravenously. Local CBF as measured with thermocouples in the cingulum increased by 100–200% after a non-lethal dose of KCN (1 mg/kg) and by 50% after injection of NaNO₂ (15 mg/kg), that oxidized some 20% of the total hemoglobin to ferrihemoglobin. Co₂EDTA (10 mg/kg) induced a decrease in local CBF of 30% and in brain temperature of 0.5°C. The temperature diminished also after poisoning by KCN, but it rose by 0.15°C after the administration of NaNO₂. Local CBF and sinus sagittalis blood flow increased by 60–160% for about 15 min, and the brain temperature decreased by 0.4–0.5°C when DMAP (3.25 mg/kg) or Co₂EDTA (15 mg/kg) was injected 1 min after poisoning by cyanide (4 mg/kg), a dose that always caused respiratory arrest. Immediately after injection of DMAP the brain temperature rose transiently by 0.1–0.2°C. Co₂EDTA did not exert such an effect. In the sinus sagittalis blood of artificially ventilated animals pCO₂ decreased rapidly by 10–20 mmHg after poisoning and approached the initial level after treatment with DMAP or Co₂EDTA. The highest value of pO₂ was about 80 mmHg and 50 mmHg after injection of DMAP and Co₂EDTA, respectively; thereafter pO₂ declined to 20 mmHg or 40 mmHg at 20 min. The lactate concentration increased by 60–70% without tendency to return to normal.     

The experimental treatment of cyanide poisoning with a methemoglobin solution]

The stroma-free methemoglobin solution proved to be an effective antidote against acute cyanide poisoning in experiment. The poisoning was induced by intraperitoneal administration to rats of cyanide solutions in doses of 5, 10 and 15 mg/kg. Methemoglobin solutions were injected intravenously in doses of 2 and 4 g/kg. All the rats given methemoglobin solution after the administration of cyanide survived. Spectrophotometry of rat urine demonstrated rapid excretion of methemoglobin cyanide.     

The effect of prior treatment with 4-dimethylaminophenol (DMAP) on animals experimentally poisoned with hydrogen cyanide

Six dogs were given sufficient oral 4-dimethylaminophenol (DMAP) to produce a peak methaemoglobin level of 12–15%. Five out of the six dogs then survived an intravenous injection of approximately 2 LD₅₀'s of hydrogen cyanide given when the methaemoglobin had reached 8–10%. The sixth dog died after 44 min. When the same dose of hydrogen cyanide was given to dogs, not previously given DMAP, all three died within 11/2 min. It was concluded that prior treatment with oral DMAP provided a large measure of protection against cyanide poisoning. Comparison of cyanide levels in whole blood and plasma in the two groups of dogs lent support to the hypothesis that methaemoglobin complexed with cyanide in the erythrocytes causing the plasma cyanide to remain lower than it did in unprotected animals.     

Zur Beurteilung der Blausäure-Antidote

The effect of various antidotes on the exhalation of hydrocyanic acid has been measured in guinea pigs and cats poisoned with cyanide. This procedure permits evaluation of both the speed of action and the capacity of the agents tested to detoxify hydrocyanic acid, and therefore allows an exact judgement as to therapeutic value of various antidotes to cyanide poisoning. The results were as follows:

1. Cobaltous histidine at a dose of 20 mg/kg was distinguished among the compounds tested by its rapid action in both species. Its detoxifying capacity was not adequate however. Treatment of severe cyanide poisoning in man with Co (his)₂ would appear to be reasonable, but only when combined with sodium thiosulfate.
2. The same rapid action as with cobaltous histidine was achieved in cats by intravenous injection of 2.25 mg/kg p-dimethylaminophenole (DMAP) leading to a methemoglobin formation of 30%. A dose of 0.75 mg/kg DMAP forming 10% methemoglobin reduced HCN-exhalation by an equivalent amount only after a 2.4 min delay. The capacity of DMAP to detoxify hydrocyanic acid was considerably greater than that of cobaltous histidine but still was far inferior to that of sodium thiosulfate.
3. The high capacity of sodium thiosulfate to detoxify hydrocyanic acid was likewise demonstrated by the new method employed here in both animal species. However, the onset of its effect was always very delayed. In clinical practice, this agent should never be omitted, but in treatment of severe poisonings it will only be successful when combined with a more rapid-acting antidote such as cobaltous histidine or DMAP.
4. Sodium nitrite, even when applied in relatively high doses, did not act rapidly enough nor did it demonstrate a satisfactory capacity to detoxify hydrocyanic acid. Therefore, it no longer fulfills the requirements that presently should be demanded of an antidote to hydrocyanic acid.

     

The in vivo effects of cyanide and its antidotes on rat brain cytochrome oxidase activity.

The in vivo effects of sodium cyanide and its antidotes, sodium nitrite, sodium thiosulfate and 4-dimethylaminophenol (DMAP), as well as the alpha-adrenergic blocking agent phentolamine, on rat brain cytochrome oxidase were studied. The course of inhibition was time-dependent and a peak of 40% was attained between 15 and 20 min after the s.c. injection of 1.3 LD50 (12 mg/kg) of cyanide. Pronounced dose-dependence was observed in the inhibition of the enzyme, at this relatively low, but lethal dose. Further observation was impossible because of rapidly lethal effects of cyanide. In animals artificially ventilated with room air, observation was possible up to 60 min. However, maximum inhibition was also 40%. When antidotes were applied 30 min after 20 mg/kg of cyanide, marked reactivation of cytochrome oxidase activity was observed with all antidotes (particularly with thiosulfate) except for phentolamine which had no effect. Prevention of methemoglobin forming with toluidine blue did not affect the reactivating ability of nitrite or DMAP, thus suggesting more complex protective mechanisms then simple methemoglobin formation. The high efficacy of thiosulfate may be attributed to its rhodanese catalyzed, direct binding to free blood cyanide, leading thus to its dissociation from cytochrome oxidase. The theory that cytochrome oxidase inhibition is a basic mechanism of cyanide toxicity could not be disproved.     

Effects of 4-dimethylaminophenol and Co2EDTA on circulation, respiration, and blood homeostasis in dogs.

The effects of intravenously injected 4-dimethylaminophenol and Co2EDTA on peripheral circulation, respiration, acid-base balance, and several other physiological and biochemical parameters were studied on dogs. DMAP increased the respiratory minute volume and mean arterial pressure, diminished the lactate-to-pyruvate ratio, and induced an increase in arterial oxygen pressure caused by liberation of oxygen from oxyhemoglobin during the formation of ferrihemoglobin. A study in vitro of the fate of the oxygen during the reaction between DMAP and oxyhemoglobin showed that only 30--40% of the oxygen released by the formation of ferrihemoglobin appeared in the gas phase. Co2EDTA caused circulatory depression, hyperventilation, and metabolic acidosis resulting in a decrease in base-excess and pH. The concentrations of lactate, pyruvate, potassium, and urea nitrogen and the hemoglobin content were increased by Co2EDTA. The side effects of Co2EDTA in therapeutic doses were more serious than those of DMAP. Thus the latter is superior in the therapy of cyanide poisoning, all the more since it detoxifies more cyanide.     

Sodium thiosulfate for acute cyanide poisoning: study in a rat model

Unlike practices in the United States where it is associated with other antidotes, sodium thiosulfate is not used for emergency therapy for cyanide poisoning in France. The purpose of this study was to develop a rat model using intraperitoneal injections of sodium thiosulfate at a dose of 225 mg/kg to test its therapeutic efficacy for acute cyanide poisoning. Efficacy was assessed directly by quantifying arterial blood cyanide and indirectly using markers of hypoxia: serum lactate and arteriolization of venous blood gases. Cyanide poisoning induced intense biological anomalies which were persistent (serum lactate) or transient (blood gases). Sodium thiosulfate was found to be an effective antidote in the rat enabling rapid normalization of hypoxia markers and clearing of cyanide from arterial blood.