摄入氯化铝后大鼠某些器官内铝含量的变化

用原子吸收分光光度计测定摄入含铝饲料和饮水的大鼠大脑、小脑、肾、肝和骨的铝含量变化。发现染铝14天后,各器官铝含量显著上升;25天后仅骨铝含量明显增高;40天后肝和骨铝含量亦上升明显。停止染铝8天后,各器官铝含量均未降至正常,且小脑及骨铝含量仍有轻微上升。表明摄入铝后,铝可在体内蓄积,尤其是小脑和骨。     

颅脑损伤后去骨瓣减压术的并发症及预防

严重颅脑损伤是临床常见的脑外伤，这类损伤病情重，变化快，继发性损伤（如脑内出血、脑水肿）也很严重，其颅内压增高是当前颅脑损伤救治的重点和难点，临床治疗困难，预后差。现在常用去骨瓣减压作为治疗不能控制的颅内压增高及术中突然发生的脑肿胀及脑膨出。尽管其减压效果满意，但也有一定的并发症，本研究就其并发症及其预防进行总结。     

22例重型颅脑损伤去骨瓣减压术后护理

重型颅脑损伤后由于急性颅内压增高 ,常造成继发性脑损害在药物无法控制下行去骨瓣减压术为目前临床救治急性脑损伤及脑内血肿的主要方法之一 ,而去骨瓣术后护理对提示医生实施抢救方案及降低病死率、残存率 ,预防手术后副作用有积极意义。现将行去骨瓣减压术后的护理体会及病情观察要点介绍如下。1　临床资料我科自 1999年 1月至 2 0 0 3年 3月重型颅脑损伤 (哥拉斯哥评分 5～ 8分 )并行去骨瓣减压手术者 2 2例 ,其中男 18例 ,女 4例 ;年龄最小 19岁 ,最大 6 5岁。临床诊断均为脑挫裂伤、脑内血肿或硬膜下血肿 ,10例合并颅骨骨折。行去骨瓣…     

标准大骨瓣减压手术在颅脑外伤治疗中的应用

目的:探讨对重型颅脑损伤行标准大骨瓣减压术的应用.方法:对2006年3月～2009年12月行标准大骨瓣减压手术48例重型颅脑损伤患者的治疗过程及其结果进行分析.结果:脑肿胀及不可控的脑水肿颅内压增高仍是主要致死原因,术后近期大部分患者的减压效果满意,部分患者术后出现急性脑肿胀膨出及减压性颅内出血情况等.结论:标准大骨瓣减压手术如果掌握好手术适应证,把握手术时机及操作规范,不但可以挽救大部分患者的生命,减少脑神经损伤,尽可能保留脑功能,而且可以使多数存活患者获得较好的生存质量.     

颅脑损伤术后顽固性脑膨出的护理

重型颅脑损伤手术时常去骨瓣减压.由于各种原因所致的颅内压升高使脑组织从颅骨缺损口向外膨出如蕈状,称为脑膨出,也称为脑蕈.颅脑损伤术后常伴有不同程度的脑膨出,突出的脑组织不断膨出、嵌顿、坏死、感染,继而又造成颅内相邻脑组织的瘀血、水肿、坏死,使颅内压增高进一步加剧,脑膨出更加严重,如果没有及时有效的处理,势必危及病人的生命.现将我科自1998年12月至2002年7月期间所遇到的颅脑损伤并发顽固性脑膨出病例进行回顾性分析.     

天幕裂孔切开联合大骨瓣减压术对重型颅脑损伤患者血清PA、MBP水平及颅内压的影响

<正>重型颅脑损伤属于神经外科急重症,多由外界暴力伤害所致,对患者脑组织产生的伤害较大,会因颅内压增高与脑灌注压降低,形成脑组织缺血-颅内压增高的恶性循环,而发生死亡[1,2]。标准大骨瓣减压术是重型颅脑损伤常用的治疗方式,但手术切口大、术后易并发免疫功能抑制、颅内感染等[3]。经天幕裂孔切开术可将重型颅脑损伤患者的颅内血肿清除,加快脑组织恢复,利于患者预后恢复。该研究旨在分析天幕裂孔切开联合大骨瓣减压术对重型颅脑损伤患者血清PA、MBP水平及颅内压的影响,现报告如下。     

150例颅脑手术患者手术室术中有效降压的护理

<正>颅内压(ICP)指颅腔的脑组织、脑脊液、血液3种内容物使颅腔内保持一定的压力,正常成人颅内压为5.0～13.5mmHg(1mmHg=0.133kPa),持续超过14.2mmHg即为ICP增高,ICP增高是神经外科常见的病理、生理综合征,是使患者病情恶化的原因之一。术中颅内压增高可导致急性脑膨出、脑移位、脑血流量减少,严重者可引起脑疝、库兴反应等影响手术操作及手术效果[1]。在开颅手术过程中严密     

排除铝减轻老年性痴呆症

铝是否为老年性痴呆症(Alzheimer'sdisease)的病因本已是探讨及争论的课题。老年性痴呆症患者脑内的铝含量较其他患者明显增高,但也有研究者认为这增高仅属偶然。在英国和法国某些地区,饮水中铝浓度较高,老年性痴呆症的发病率也有所增高。新近在加拿大安大略卫生部会议上,有报告称患者注射去铁胺(desferroxamine)以排除铝,可防止铝对细胞的非可逆性损害。将48名老年性痴呆症患者分为两组试验,一组注射去铁胺,一组不给药。去铁胺可与铝结合。经过二年以后,不给药组病情迅速恶化,有的患者死亡,有的必须住院;而给药组仍能自己料理生活,并与他人交往。这结果进一步说明铝与老年性痴呆症的联系。可能由于遗传     

额颞部继发性脑损伤病人临床救治分析

额颞部继发性脑内血肿、水肿可造成脑组织移位 ,使垂体柄及门脉血管受到牵拉损伤。还因灰结节下移疝入鞍膈开口内 ,使门脉血管在鞍膈的游离缘受压而发生垂体前叶梗塞坏死 ;下丘脑移位使供给下丘脑的血管损伤而发生循环障碍 ,使下丘脑发生梗塞坏死。从而引起脑肿胀 ,颅内压进一步增高 ,形成恶性循环。故采用外科综合治疗 ,打断这一恶性循环 ,是改善预后的关键。我科于 2 0 0 2年共收治外伤性额颞部脑挫裂伤、脑内血肿病人共计 37例 ,现报道如下。1　临床资料1.1　一般资料37例中男 2 9例 ,女 8例 ,年龄 6～ 70岁。病因 :车祸 2 0例 ,坠落伤 1…     

他下肢疼痛,原来祸起高血压

高血压对心、脑、肾等重要脏器会造成损伤,这一点很多人都知道,但长期高血压还可造成肢体损伤和胸痛腹痛,严重的使人致残,却常常被人们所忽视。     

Effects of arsenite on central monoamines and plasmatic levels of adrenocorticotropic hormone (ACTH) in mice

We studied the effects of chronic arsenic exposure on brain monoamines and plasma levels of adrenocorticotropic hormone (ACTH) of mice. After weaning, mice received arsenic (0, 20, 40, 60 or 100 ppm) in drinking water over a period of 9 weeks. Monoamine content was quantified in different brain regions, arsenic was quantified in brain tissue and ACTH levels in plasma. Brain arsenic concentrations up to 200 ng/g showed a significant correlation with exposure levels and produced slight modifications in regional monoamine levels. ACTH plasma levels were significantly associated with norepinephrine (NE) concentrations in the medulla and pons, but not with hypothalamic NE levels. ACTH levels were significantly higher in the group exposed to 20 ppm. Dopamine showed significant dose-related decreases in the hypothalamus. These results show that chronic sodium arsenite exposure produces changes in central monoamines, which are not associated on a dose-dependent basis with major alterations in plasma ACTH.     

Comparison of tissue dosimetry in the mouse following chronic exposure to arsenic compounds

Several chronic bioassays have been conducted in multiple strains of mice in which various concentrations of arsenate or arsenite were administered in the drinking water without a tumorigenic effect. However, one study (Ng et al., 1999) reported a significant increase in tumor incidence in C57Bl/6J mice exposed to arsenic in their drinking water throughout their lifetime, with no tumors reported in controls. A physiologically based pharmacokinetic model for arsenic in the mouse has previously been developed (Gentry et al., 2004) to investigate potential differences in tissue dosimetry of arsenic species across various strains of mice. Initial results indicated no significant differences in blood, liver, or urine dosimetry in B6C3F1 and C57Bl/6 mice for acute or subchronic exposure. The current work was conducted to compare model-predicted estimates of tissue dosimetry to additional kinetic information from the (C57Bl/6 xCBA)F1 and TgAc mouse. The results from the current modeling indicate that the pharmacokinetic parameters derived based on information in the B6C3F1 mouse adequately describe the measured concentrations in the blood/plasma, liver, and urine of both the (C57Bl/6 x CBA)F1 and TgAc mouse, providing further support that the differences in response observed in the chronic bioassays are not related to strain-specific differences in pharmacokinetics. One significant finding was that no increases in skin or lung concentrations of arsenic species in the (C57Bl/6 x CBA)F1 strain were observed following administration of low concentrations (0.2 or 2 mg/U of arsenate in the drinking water, even though differences in response in the skin were reported. These data suggest that pharmacodynamic changes may be observed following exposure to arsenic compounds without an observable change in tissue dosimetry. These results provided further indirect support for the existence of inducible arsenic efflux in these tissues.     

Two‐year drinking water carcinogenicity study of methyl tertiary‐butyl ether (MTBE) in Wistar rats

Methyl tertiary‐butyl ether (MTBE) has been used as a gasoline additive to reduce tailpipe emissions and its use has been discontinued. There remains a concern that drinking water sources have been contaminated with MTBE. A two‐year drinking water carcinogenicity study of MTBE was conducted in Wistar rats (males, 0, 0.5, 3, 7.5 mg ml^?1; and females, 0, 0.5, 3, and 15 mg ml^?1). Body weights were unaffected and water consumption was reduced in MTBE‐exposed males and females. Wet weights of male kidneys were increased at the end of two years of exposure to 7.5 mg ml^?1 MTBE. Chronic progressive nephropathy was observed in males and females, was more severe in males, and was exacerbated in the high MTBE exposure groups. Brain was the only tissue with a statistically significant finding of neoplasms. One astrocytoma (1/50) was found in a female rat (15 mg ml^?1). The incidence of brain astrocytomas in male rats was 1/50, 1/50, 1/50 and 4/50 for the 0, 0.5, 3 and 7.5 mg ml^?1 exposure groups, respectively. This was a marginally significant statistical trend, but not statistically significant when pairwise comparisons were made or when multiple comparisons were taken into account. The incidence of astrocytoma fell within historical control ranges for Wistar rats, and the brain has not been identified as a target organ following chronic administration of MTBE, ethyl tert‐butyl ether, or tertiary butyl alcohol (in drinking water) to mice and rats. We conclude that the astrocytomas observed in this study are not associated with exposure to MTBE. Copyright © 2011 John Wiley & Sons, Ltd.     

EVALUATION OF THE IMMUNOMODULATORY EFFECTS OF THE DISINFECTION BY-PRODUCT,SODIUM CHLORITE,IN FEMALE B6C3F1 MICE: A DRINKING WATER STUDY

Sodium chlorite is an inorganic by-product of chlorine dioxide formed during the chlorination of drinking water. Relatively little is known about the adverse health effects of exposure to sodium chlorite in drinking water. In this study, we evaluated sodium chlorite's immunomodulatory properties using female B6C3F1 mice and a panel of immune assays that were designed to evaluate potential changes in innate and acquired cellular and humoral immune responses. Female B6C3F1 mice were exposed to sodium chlorite in their drinking water (0, 0.1, 1, 5, 15, and 30 mg/L) for 28 days, and then evaluated for immunomodulation. Overall, minimal toxicological and immunological changes were observed after exposure to sodium chlorite. Increases in the percentages of blood reticulocytes, and the relative spleen weights were both observed at different sodium chlorite treatment levels; however, these increases were not dose-dependent. An increasing trend in the number of spleen antibody-forming cells was observed over the range of sodium chlorite concentrations. This increase was not, however, significant at any individual treatment level, and was not reflected by changes in serum IgM levels. A significant increase (26%) in the total number of splenic CD8⁺ cells was observed in mice treated with 30 mg/L of sodium chlorite, but not at the other concentrations. Splenic mixed leukocyte response and peritoneal macrophage activity were unaffected by sodium chlorite. Lastly, exposure to sodium chlorite did not affect natural killer cell activity, although a decrease in augmented natural killer cell activity (42%) was observed at the lowest sodium chlorite treatment level. These results suggest that sodium chlorite, within the range 0.1–30 mg/L, produces minimal immunotoxicity in mice.     

Evaluation of the immunomodulatory effects of the disinfection by-product, sodium chlorite, in female B6C3F1 mice: a drinking water study.

Sodium chlorite is an inorganic by-product of chlorine dioxide formed during the chlorination of drinking water. Relatively little is known about the adverse health effects of exposure to sodium chlorite in drinking water. In this study, we evaluated sodium chlorite's immunomodulatory properties using female B6C3F1 mice and a panel of immune assays that were designed to evaluate potential changes in innate and acquired cellular and humoral immune responses. Female B6C3F1 mice were exposed to sodium chlorite in their drinking water (0, 0.1, 1, 5, 15, and 30 mg/L) for 28 days, and then evaluated for immunomodulation. Overall, minimal toxicological and immunological changes were observed after exposure to sodium chlorite. Increases in the percentages of blood reticulocytes, and the relative spleen weights were both observed at different sodium chlorite treatment levels; however, these increases were not dose-dependent. An increasing trend in the number of spleen antibody-forming cells was observed over the range of sodium chlorite concentrations. This increase was not, however, significant at any individual treatment level, and was not reflected by changes in serum IgM levels. A significant increase (26%) in the total number of splenic CD8+ cells was observed in mice treated with 30 mg/L of sodium chlorite, but not at the other concentrations. Splenic mixed leukocyte response and peritoneal macrophage activity were unaffected by sodium chlorite. Lastly, exposure to sodium chlorite did not affect natural killer cell activity, although a decrease in augmented natural killer cell activity (42%) was observed at the lowest sodium chlorite treatment level. These results suggest that sodium chlorite, within the range 0.1-30 mg/L, produces minimal immunotoxicity in mice.     

Neonatal lead exposure changes quality of sperm and number of macrophages in testes of BALB/c mice

BALB/c mice were exposed to 0.1 ppm lead acetate in the drinking water from postnatal day (PND) 1 for 6 weeks. Until PND21, lead exposure was from mother's milk; thereafter, it was directly from the drinking water. The blood lead levels were the highest in pups before weaning (59.5 ± 0.9 μg/dL) and significantly lower between PND21 and PND42 (20.3 ± 4.7 μg/dL). At PND42, lead-exposed male mice were tested for fertility, sperm DNA, and macrophage number. Mating of lead-treated males with non-treated females confirmed the reduction of fertility in the exposed males. Flow cytometric studies of testicular preparations indicated that the sperm count was not different between lead-exposed and control males; however, the lead-treated mice had a significant increase in the number of testicular cells having a <1n amount of DNA, which coincided with a decrease in the number of testicular cells with a 2n and 4n amount of DNA. The number of testicular macrophages also was decreased in lead-exposed males, which could reflect altered levels of CSF-1 or response to CSF-1, as previously reported [Kowolenko, M., Tracy, L., Lawrence, D.A., 1989. Lead-induced alterations of in vitro bone marrow cell responses to colony stimulating factor-1. J. Leukoc. Biol. 45, 198–206]. Our study showed that exposure to 0.1 ppm of lead during the neonatal and adolescent period is sufficient to reduce fertility in adult male mice; however, it did not affect sperm count on PND42. The presence of an increased number of apoptotic (<1n amount of DNA) testicular cells may be diagnostic of defective sperm function. Thus, an administered dose of 0.1 ppm via drinking water ingestion by neonatal male BALB/c mice sufficient to produce PbB of 20–60 mg/dL compromised reproductive function in these mice as adults.     

Comparison of the effects of hexavalent chromium in the alimentary canal of F344 rats and B6C3F1 mice following exposure in drinking water: implications for carcinogenic modes of action

Exposure to high concentrations of hexavalent chromium (Cr[VI]) in drinking water is reported to induce oral mucosa tumors in F344 rats and intestinal tumors in B6C3F1 mice. To investigate the modes of action underlying these tumors, 90-day drinking water studies (with interim necropsy at day 8) were conducted with concentrations of 0.1-182 mg/l Cr(VI), administered as 0.3-520 mg/l sodium dichromate dihydrate. Blood and tissue samples were analyzed for chromium content, oxidative stress, iron levels, and gross and microscopic lesions. Results for the F344 rats are described herein and compared with results from B6C3F1 mice published previously. After 90 days of exposure, total chromium concentrations in the rat and mouse oral mucosae were comparable, yet significant dose-dependent decreases in the reduced-to-oxidized glutathione ratio (GSH/GSSG) were observed only in rats. In the duodenum, changes in GSH/GSSG were only observed in mice. Levels of 8-hydroxydeoxyguanosine were not increased in the oral or duodenal mucosae of either species. Glutathione levels were increased in the duodenum but decreased in the jejunum of both species, indicating potential differential responses in the intestinal segments. Histiocytic infiltration was observed in the duodenum of both species, yet duodenal cytokines were repressed in mice but increased in rats. Serum and bone marrow iron levels were more decreased in rats than mice. Collectively, these data suggest that Cr(VI)-induced carcinogenesis in the rodent alimentary canal involves oxidative stress; however, differences in histopathology, cytokines, and iron status suggest potential contributions from other factors as well.     

Irreversible effects of trichloroethylene on the gut microbial community and gut‐associated immune responses in autoimmune‐prone mice

The developing immune system is particularly sensitive to immunotoxicants. This study assessed trichloroethylene (TCE)‐induced effects on the gut microbiome and cytokine production during the development in mice. Mice were exposed to TCE (0.05 or 500 μg/mL) at the levels that approximate to environmental or occupational exposure, respectively. Mice were subjected to a continuous developmental exposure to these doses encompassing gestation, lactation and continuing directly in the drinking water postnatally for 154 days (PND154) or PND259. To observe persistence of the effect TCE was removed from the drinking water in a subset of mice on PND154 and were provided regular drinking water until the study terminus (PND259). Abundance of total tissue‐associated bacteria reduced only in mice exposed to TCE until PND259. The ratio of Firmicutes/Bacteroidetes did not alter during this continuos exposure; however, cessation of high‐dose TCE at PND154 resulted in the increased abundance Bacteroidetes at PND259. Furthermore, high‐dose TCE exposure until PND259 resulted in a lower abundance of the genera Bacteroides and Lactobaccilus and increased abundance of genus Bifidobactrium and bacterial family Enterobacteriaceae. TCE exposure until PND154 showed significant changes in the production of interleukin‐33; that might play a dual role in maintaining the balance and homeostasis between commensal microbiota and mucosal health. At PND259, interleukin‐3, granulocyte‐macrophage colony‐stimulating factor and Eotaxin were altered in both, the continuous exposure and cessation groups, whereas only a cessation group had a higher level of KC that may facilitate infiltration of neutrophils. The irreversible effects of TCE after a period of exposure cessation suggested a unique programming and potential toxicity of TCE even at the environmental level exposure.     

Combined in utero and juvenile exposure of mice to arsenate and atrazine in drinking water modulates gene expression and clonogenicity of myeloid progenitors

The effects of arsenate (As) and atrazine (Atr) on myeloid progenitors (colony-forming unit-granulocyte/macrophage, CFU-GM) cells derived from bone marrow were studied in male and female mice after combined in utero and juvenile exposure. Female adult mice were treated with arsenate in drinking water during gestation. Then, separate groups of males and females' offspring were exposed for 4 months to atrazine, to additional arsenate or to co-exposure of atrazine and arsenate together in drinking water. In male mice, arsenate and the combined exposure did not modulate the percentage of CFU-GM progenitors, whereas atrazine significantly decreases the clonogenicity of myeloid cells. In females, the percentage of CFU-GM significantly decreased after atrazine exposure did not change with arsenate treatment, but dramatically increased after the combined exposure. The expression of estrogen receptors alpha (ERalpha) and beta (ERbeta) in bone marrow cells was investigated, and an up-regulation of receptor beta was observed in both genders. A gene expression profile was generated using nylon membranes spotted with 1185 cancer-related genes. Results from microarrays indicate that atrazine alone did not stimulate the expression of any of the genes analysed in both male and female. Arsenic induced gene expression modulation only in female. Major significant changes on the gene expression resulted following the co-exposure to arsenic and atrazine in both male and female.