重组人促红细胞生成素对新生大鼠急性高氧肺损伤保护作用的机制探讨

目的　探讨重组人促红细胞生成素 (recombinanthumanerythropoietin ,rHuEPO)的血管生长因子样作用对新生大鼠高氧肺损伤的影响。　方法　检测高氧暴露 6d后动物存活率、右肺湿重 /干重比值的变化、免疫组化法检测肺组织内皮细胞标志物—CD3 1的阳性面积比的表达变化。　结果　高氧暴露 6d后 ,与高氧对照组相比 ,肺水肿程度减轻( 5 .18± 0 .2 1vs 5 .5 4± 0 .3 1P <0 .0 5 ) ,肺组织CD -3 1的表达升高 ( 3 8.69%± 1.68%vs 3 3 .5 7%± 4.12 % ,P <0 .0 5 )。　结论　rHuEPO可能通过促进肺血管的发育和修复对新生鼠高氧肺损伤有保护作用。     

蔺草染土尘致大鼠肺部病变的实验研究

目的　研究蔺草染土粉尘的致尘肺作用。方法　SD雄性大鼠以非暴露式气管内染尘(5 0mg/只 ) ,于染尘后 3、6、12个月 ,取大鼠肺和肺淋巴结作病理和电镜观察 ,测定肺组织胶原蛋白和血清铜蓝蛋白 (CP)含量。结果　染尘后 12个月 ,蔺草染土尘组大鼠肺湿重 (2 .6 9± 0 .2 2 )g ,高于对照组 [(1.87± 0 .2 5 )g]和TiO2 组 [(2 .2 5± 0 .2 6 )g],但低于SiO2 组 [(11.4 1± 1.6 3)g];蔺草染土尘组大鼠肺干重 (0 .4 7± 0 .0 3)g ,高于对照组 [(0 .32± 0 .0 3)g]和TiO2 组 [(0 .4 1± 0 .0 8)g],但低于SiO2 组 [(2 .0 6± 0 .2 8)g];蔺草染土尘组大鼠肺胶原蛋白含量 [(10 3.0 8± 14 .79)mg]高于对照组 [(75 .96± 13.91)mg]和TiO2 组 [(85 .84± 17.6 2 )mg],但低于SiO2 组 [(497.5 0± 10 0 .80 )mg];蔺草染土尘组大鼠血清CP含量为 (18.0 3± 1.87)U/L ,高于对照组 [(15 .0 5± 2 .2 4 )U/L]和TiO2 组 [(16 .92± 1.6 7)U/L],但低于SiO2组 [(2 5 .37± 3.5 8)U/L]。以上各指标各组间的差异均有显著性 (P <0 .0 5或P <0 .0 1)。蔺草染土尘组大鼠病理观察可见肺巨噬细胞肺泡炎、Ⅱ型肺泡上皮细胞增多及肺泡间隔增宽 ,有 1～ 2级矽结节和少量胶原纤维性变。电镜下可见 ,蔺草染土尘组大鼠肺有初级和次级溶酶体及     

氨溴索对百草枯中毒大鼠肺组织损伤及肺表面活性蛋白-A的影响

目的探讨氨溴索(ambroxol)对百草枯(paraquat,PQ)中毒大鼠急性肺损伤及肺表面活性蛋白-A(SP-A)的影响。方法120只SD大鼠随机分为对照组(24只,腹腔注射生理盐水1．25 mg/kg)、PQ染毒组(PQ组,48只,腹腔注射PQ溶液25 mg/kg)和氨溴索治疗组(AT组,48只,对染毒大鼠腹腔注射氨溴索35 mg/kg),每组按1、3、5和7 d分为4个观察时段。观察不同处理后大鼠的死亡率、PaO_2、PaCO_2及肺组织湿/干重比(W/D)的变化,对肺组织行光镜及电镜检查,观察肺组织病理表现,用免疫组织化学方法检测肺组织SP-A的表达。结果PQ组和AT组7d时死亡率分别为50．0%和25．0%。AT组大鼠3、5 d时PaCO_2低于PQ组,高于对照组同时点的PaCO_2值,差异有统计学意义(P＜0．05)；AT组大鼠3、5、7 d时PaO_2高于PQ组,低于对照组同时点的PaO_2,差异有统计学意义(P＜0．05或P＜0．01)；PQ组肺组织W/D增加,明显高于对照组,差异有统计学意义(P＜0．01),AT组与PQ组各时点W/D比较均有明显下降,差异有统计学意义(P＜0．05或P＜0．01)。光镜及电镜病理观察,PQ组较对照组肺组织损伤程度明显加重,AT组肺组织损伤程度减轻。PQ组肺泡上皮细胞SP-A表达7 d时阳性细胞的百分数为13．22%±2．21%,明显低于对照组的21．82%±3．67%,差异有统计学意义(P＜0．06),AT组SP-A表达7 d时阳性细胞的百分数达到18．97%±0．91%,较PQ组明显增高,差异有统计学意义(P＜0．05)。结论氨溴索具有一定的促进SP-A合成及分泌的作用,能减轻PQ中毒所致急性肺损伤。     

染矽尘大鼠肺组织一氧化氮合酶的表达

目的　研究染矽尘大鼠早期炎性肺损伤过程中一氧化氮合酶 (NOS)的表达规律 ,为矽肺纤维化机制提供理论依据。方法　气管暴露法建立矽肺动物模型。测定支气管肺泡灌洗液 (BALF)中诱导型NOS(iNOS)的表达和总NOS的活力。在组织芯片上使用SP法检测大鼠肺组织iNOS的表达 ,并用Image ProPlus图像分析法对iNOS的表达进行定量测定。结果　iNOS主要表达在巨噬细胞和中性粒细胞胞浆内。与对照组相比 ,染矽尘大鼠肺组织中iNOS积分光密度于染尘后 3、7d时分别增加了1.47× 10 5 、2 .73× 10 5 ,2 8d时降低了 1.11× 10 5 ,差异均有显著性 (P <0 .0 5或P <0 .0 1)。大鼠BALF中iNOS活力在染尘后 3、7、14d时分别增加了 0 .86、1.89、0 .92U/ml ,差异均有显著性 (P <0 .0 5或P <0 .0 1)。BALF总NOS活力在染尘后 1、3、7、14d时分别增加了 1.43、2 .0 5、2 .61、2 .19U/ml,差异均有显著性 (P <0 .0 5或P <0 .0 1)。结论　在矽尘诱导下 ,大鼠肺组织中表达iNOS的细胞主要是肺泡巨噬细胞和中性粒细胞 ,其肺组织中iNOS的表达从染尘后 1d至 2 8d有一抛物线型的过程     

染矽尘小鼠肺组织中转化生长因子β1表达的免疫组织化学检测

目的　观察染矽尘小鼠肺组织转化生长因子 β1(TGF β1)蛋白水平的改变 ,研究其在矽肺发病中的意义。方法　采用暴露式气管内注入法给小鼠一次性染矽尘 (0 .2g/kg)。染尘后第 1、3、5、7、14、2 8天每组各处死 8只小鼠 ,取肺组织 ,用免疫组织化学技术检测TGF β1在小鼠肺组织蛋白水平的表达。结果　对照组小鼠肺组织中免疫组化染色呈弱阳性 (± ) ,可见少量TGF β1蛋白 ;染尘组小鼠肺TGF β1表达明显增强 ,免疫组化染色结果为 +～ +++,染尘后第 7～ 14天达高峰。染尘组小鼠肺出现TGF β1表达阳性肺泡巨噬细胞 ,第 5天达高峰 ,其阳性肺泡巨噬细胞百分率为 93.4 %± 2 .8% ,与对照组 (42 .2 %± 12 .0 % )相比 ,差异有显著性 (P <0 .0 1)。结论　TGF β1在矽肺早期的发生、发展过程中可能有重要作用。     

兴奋性氨基酸与1,2-二氯乙烷急性中毒性脑病关系的探讨

目的　探讨兴奋性氨基酸 (EAAs)与 1 ,2 二氯乙烷 (1 ,2 DCE)急性中毒性脑病的关系。方法　将SD大鼠随机分为 7组 :对照组、3个染毒组 (5 .0、1 0 .0、2 0 .0g/m31 ,2 DCE)和 3个时间组(1 0 .0g/m31 ,2 DCE染毒后 2、4、6h) ;连续静式吸入染毒 1 2h ;干湿重法测定大鼠脑皮质和髓质含水量 ;高效液相色谱法 (HPLC)检测脑组织中谷氨酸 (Glu)、天冬氨酸 (Asp)、甘氨酸 (Gly)及γ 氨基丁酸(GABA)含量的变化。结果　 (1 )大鼠脑皮质和髓质含水量 :不同剂量染毒组大鼠脑皮质含水量分别为 76 .1 0 %± 1 .41 %、76 .45 %± 0 .75 %、79.95 %± 1 .45 % ,均高于对照组 (74.2 2 %± 1 .77% ) ,差异有显著性 (P <0 .0 5 ,P <0 .0 1 ) ;髓质含水量仅 2 0 .0g/m3组 (71 .77%± 3 .0 7% )有明显升高 ,差异有显著性(P <0 .0 5)。染毒后 2、4、6h脑皮质含水量分别为 79.36 %± 2 .1 0 %、79.48%± 1 .2 1 %、80 .64 %±1 .93 % ,均高于 1 0 .0g/m3即刻组 ,差异有显著性 (P <0 .0 5)。 (2 ) 4种氨基酸递质含量 :不同剂量染毒组Asp含量分别为 (4.83± 0 .35)、(7.1 7± 0 .40 )、(1 0 .52± 0 .39) μmol/g ;Glu含量分别为 (2 3 .86± 0 .62 )、(31 .2 1± 2 .50 )、(2 8.2 3± 1 .58) μmol/g;Gly含量分别为 (5 .59±     

金属研磨尘染毒大鼠支气管肺泡灌洗液的变化

目的　观察金属研磨的混合粉尘对大鼠呼吸系统的损伤作用。方法　大鼠经支气管注入磨工粉尘染尘后饲养 2周 ,采用大鼠支气管肺灌洗技术 ,分析灌洗液中细胞含量、分类、存活率及乳酸脱氢酶 (LDH)、碱性磷酸酶 (ALP)活力的变化。结果　染尘大鼠肺泡灌洗液中细胞含量随磨工粉尘染尘剂量的加大而增大 ,且均高于SiO2 尘组。大鼠支气管肺泡灌洗液中性粒细胞比例 [SiO2 粉尘组为 (33 .83± 4 .54) % ,1 0、2 5、50mg/ml磨工粉尘组分别为 (2 6 .50± 3 .99) %、(36 .0 0± 3 .58) %和 (38.0 0±2 .1 0 ) % ]均较对照组 [(2 .83± 0 .75) % ]明显增加 ;巨噬细胞比例 [SiO2 粉尘组为 (62 .1 7± 4 .54) % ,1 0、2 5、50mg/ml磨工粉尘组分别为 (70 .83± 3 .66) %、(60 .83± 2 .1 4 ) %和 (58.1 7± 2 .48) % ]比对照组[(95 .67± 1 .2 1 ) % ]相应降低 ,差异均有显著性 (P <0 .0 1 )。对照组大鼠肺泡灌洗液细胞存活率达80 %以上 ,与磨工粉尘组、TiO2 组的差异有显著性 (P <0 .0 1 )。各染尘组大鼠肺灌洗上清液中LDH、ALP活力明显增加 ,与对照组的差异有显著性 (P <0 .0 1或P <0 .0 5) ,随磨工粉尘染尘剂量加大 ,LDH、ALP活力逐渐升高。结论　磨工粉尘对大鼠肺细胞有损害作用 ,进一步证实磨工粉尘可能对肺脏有致纤     

慢性苯染毒小鼠DNA损伤及体内抗氧化酶的变化

目的　了解苯对体内DNA的损伤作用、机制以及抗氧化酶体系的变化情况。方法　对小鼠进行静式吸入染毒 2个月 ,每天 4h ,采用单细胞凝胶电泳技术对骨髓细胞及外周血淋巴细胞DNA损伤进行检测 ;同时检测肝、脾、脑组织中超氧化物歧化酶 (SOD)、谷胱甘肽过氧化物酶 (GSH Px的活力及丙二醛 (MDA)含量。结果　低浓度组与高浓度组小鼠骨髓细胞及外周血淋巴细胞彗星百分率分别为骨髓细胞 (83.5 6 %± 10 .2 8% )、(92 .5 4 %± 15 .93% ) ;外周血淋巴细胞 (41.2 7%± 6 .0 3% )、(6 5 .79± 11.6 2 % ) ,明显高于对照组 (4.13%± 0 .5 2 %、2 .2 1%± 0 .31% ) ,差异有显著性 (P <0 .0 1) ,并呈剂量 -反应关系。高、低浓度组小鼠肝匀浆SOD活力 [(75 4 .33± 116 .30 )、(6 94 .2 6± 116 .30 )U/mgpro],GSH Px活力分别为 [(2 2 .5 2± 3.31)、(18.5 6± 4 .97)U/mgpro]均明显低于对照组分别为 [(999.92± 188.2 4 )、(35 .31± 6 .6 3)U/mgpro],差异有显著性 (P <0 .0 5 ) ,但两组间差异无显著性 (P >0 .0 5 ) ;高、低浓度组小鼠脾匀浆GSH Px活力分别为 [(31.38± 2 .71)、(2 5 .30± 7.4 4 )U/mgpro],均明显低于对照组 [(37.11± 3.4 2 )U/mgpro],差异有显著性 (P <0 .0 5 ) ,且组间差异有显著性 (P <0 .0 5 )     

芥子气对大鼠骨髓细胞DNA损伤的研究

目的　研究芥子气 (MG)对大鼠骨髓细胞DNA的损伤作用。方法　雄性SD大鼠随机分为 6组 ,腹腔注射生理盐水 (NS)、丙二醇、MG(0 .2、0 .4、0 .8、1.6mg/kg体重 ) ,分别于染毒后 0、2 4、4 8、72h处死各组的 5只大鼠 ,用单细胞凝胶电泳法分析大鼠骨髓细胞DNA的损伤情况。结果　在染毒后 0h各组的大鼠骨髓细胞DNA损伤差异无显著性 (P >0 .0 5 ) ;丙二醇组的大鼠骨髓细胞DNA迁移率和迁移度在染毒后 2 4、4 8、72h分别为 15 .4 %± 0 .2 1%、16 .0 %± 0 .19%、15 .7%± 0 .2 3%和 (11.4±0 .2 )、(13.5± 0 .3)、(12 .8± 0 .2 ) μm ,明显高于在同时刻的NS组水平 ,差异有显著性 (P <0 .0 5 ) ;各MG组的大鼠骨髓细胞DNA迁移率和迁移度在染毒后 2 4、4 8、72h分别高于在同时刻的NS组和丙二醇组水平 ,差异有显著性 (P <0 .0 5 )。结论　MG对大鼠骨髓细胞DNA有损伤作用 ,随剂量的增大损伤有上升的趋势 ,损伤呈时间依赖性。     

开胸手术对肺表面活性物质的影响研究

目的　探讨开胸手术对肺表面活性物质 (PS)的影响。方法　左侧开胸手术治疗的 10例食管癌患者 ,分别于术前、术后行左、右肺支气管肺泡灌洗 ,测定支气管肺泡灌洗液 (BALF)中PS活性水平 ,以右侧为对照组。结果　术前两侧BALF中的饱和卵磷脂 /总磷脂 (SatPC/TPL)比值以及饱和卵磷脂 /总蛋白 (SatPC/TP)比值统计学分析无显著性差异 ,术后左右侧SatPC/TPL也无显著性差异 ,然而 ,术后左侧SatPC/TP(6 0 9± 1 5 3) %较右侧SstPC/TP(7 89± 2 32 ) %减少 (P <0 0 5 )。结论　开胸手术后术侧肺会引起一定程度的损伤 ,该侧肺毛细血管通透性增加 ,肺泡内渗出的血浆蛋白增多 ,引起肺表面活性物质活性水平下降     

Increased rat mammary tissue vitamin A associated with increased vitamin A intake during lactation is maintained after lactation

Although increases in dietary vitamin A increase milk vitamin A, little is known about effects of vitamin A intake on mammary tissue vitamin A levels during and after the reproductive cycle. First, we measured vitamin A concentrations in milk, mammary tissue and liver of lactating rats fed 0, 4, or 50 micromol of vitamin A/kg diet during pregnancy and through d 12 of lactation. Liver vitamin A concentration was significantly affected by diet in lactating females and pups 12 d after parturition. Milk vitamin A concentrations were significantly higher (7.1 +/- 2.2 micromol/L, n = 8) in dams fed 50 micromol/kg than in those fed 0 or 4 micromol/kg (1.9 +/- 0.3, n = 5 and 2.9 +/- 0.7 micromol/L, n = 7; P < 0.001), as were mammary tissue vitamin A concentrations (5.1 +/- 1.1 versus 2.2 +/- 0.4 and 2.4 +/- 0.6 nmol/g; P < 0.001). Next, we maintained female rats on 50 or 10 micromol vitamin A/kg diet during pregnancy and lactation and then on 4 micromol/kg diet after pups were weaned on d 21. On d 21, mammary tissue vitamin A concentrations were 3.14 +/- 0.75 versus 1.52 +/- 0.21 nmol/g in dams fed 50 versus 10 micromol/kg (n = 4/group; P < 0.001). Mammary tissue vitamin A concentrations were not significantly affected by time from 7 to 49 d after lactation and averaged 8.5 +/- 0.4 and 4.9 +/- 0.8 nmol/g on d 49 in dams fed 50 versus 10 micromol/kg (n = 4; P < 0.001). We conclude that diet-induced differences in rat mammary tissue vitamin A developed during pregnancy and lactation are maintained for > or =7 wk after lactation.     

Particulate concentrations in pulmonary alveolar proteinosis.

Quantitative birefringent particle counts per 10 high-power fields in lung tissue were correlated with age, sex, and occupational exposure in 37 cases of pulmonary alveolar proteinosis. Counts were significantly higher in pulmonary alveolar proteinosis cases in both regions of alveolar proteinosis (47 +/- 11) and perivascular and peribronchiolar areas (dust retention areas) (275 +/- 65) than in 13 controls (5 +/- 3 and 79 +/- 23, respectively). Of a total of 8619 particles, 4817 were less than 1 micron, and 3771 were 1 to 10 microns in diameter. Fifty-nine percent were round, 19% fibrous, and 22% irregular. When analyzed individually, 20 of 37 cases (78%) had alveolar particle counts significantly higher than controls, and 10 of 26 cases had dust-retention area counts greater than controls (P less than 0.050). Known or possible occupational exposure was ascertained in 13 cases. In the remaining 24 cases insufficient occupational information was available. The mean age of the pulmonary alveolar proteinosis patients was 33 +/- 4 years, and of the controls, 40 +/- 7 years, and there was a male-to-female ratio of approximately 3:1. We propose that many cases of pulmonary alveolar proteinosis will ultimately be shown to be associated with environmental exposures to fine dusts or fumes.     

Probiotics enhance recovery from malnutrition and lessen colonic mucosal atrophy after short-term fasting in rats

OBJECTIVE: We investigated the effects of probiotics on nutritional status and gut mucosal atrophy after fasting. METHODS: Twelve rats were fasted for 3 d and then fed with rat chow (control group, n = 6) or an isoenergetic and isonitrogenous diet containing probiotics (probiotics group, n = 6; 10(6) colony-forming units/g of Bifidobacterium lactis BL and Streptococcus thermophilus) for 3 d. Twelve other rats were starved for 3 d (starved group) or normally fed with rat chow (sham group). At the end of the experiment, blood samples were collected for total protein and albumin analyses, and the colonic mucosa was weighed (in grams) and assayed for DNA content (milligrams per gram of tissue). RESULTS: Feeding efficiency was greater in the probiotic group than in the control and sham groups (P < 0.01). Animals in the probiotic group presented higher albumin than did those in the control group (P = 0.04). Colonic mucosa of the sham group (1.32 [range, 1.28-1.44]) was heavier than that of all other groups (probiotic, 1.20 [0.95-1.49], P = 0.03; control, 1.09 [0.96-1.21], P < 0.01; and starved, 1.03 [0.99-1.07], P < 0.01) and heavier in the probiotic than in the starved group (P = 0.03). The DNA content in probiotic rats (49.1 +/- 9.7) was similar to that in sham rats (53.9 +/- 5.9; P = 0.79) and higher than that in control (30.3 +/- 12.9; P = 0.01) and starved (34.4 +/- 6.5; P = 0.05) rats. CONCLUSIONS: Probiotics enhance the recovery of nutritional status and lessen gut mucosal atrophy after fasting.     

尾加压素Ⅱ在低氧性肺动脉高压中基因表达、合成、释放及意义的基础研究

目的探讨加压素Ⅱ（UⅡ）在低氧性肺动脉高压中基因表达合成释放的意义。方法本研究采用建立HPH大鼠模型，采用RIA观察不同低氧时间点大鼠血浆、支气管肺泡灌洗液（BALF）中UⅡ／、ADM含量的动态变化，从整体动物水平探讨低氧对UⅡ合成和释放的影响，以及UⅡ和ADM在HPH中的相互关系及意义；从而为揭示UⅡ在HPH中的病理生理作用提供实验依据。结果成功复制HPH动物模型；低氧促进肺组织UⅡ的表达、合成和释放；UⅡ参与HPH发病过程；在HPH发生发展过程中UⅡ和ADM之间存在正相关。结论两种血管活性肽具有相反的生理作用，推测二者之间的比例平衡对于调节肺循环和肺通气，稳定肺动脉压力具有非常重要的作用。     

博莱霉素致大鼠肺纤维化及与肺血管内皮细胞损伤的关系

目的 探讨血管内皮损伤与博莱霉素(BLM)致大鼠肺纤维化发生间的关系。方法 实验组大鼠经气管灌注BLM制作肺纤维化模型,采用免疫组化及图像分析系统对其肺组织中血管内皮细胞生长因子(VEGF)进行定性、定量分析。结果 (1)组织学观察:染BLM后3、7 d,大鼠肺泡腔及间隔水肿,炎细胞渗出,肺泡Ⅰ型及Ⅱ型上皮细胞变性、坏死,肺泡上皮细胞基底膜断裂,血管内皮细胞肿胀,核浓缩;7、14 d,大鼠肺泡Ⅱ型上皮细胞增生,肺泡间隔有较多成纤维细胞及新生毛细血管形成;28 d,大鼠肺泡间隔增厚,肺泡结构破坏,肺组织明显纤维化样改变。(2)VEGF免疫组化染色:对照组大鼠肺组织呈弱表达,主要分布于肺泡Ⅱ型上皮细胞、支气管黏膜上皮细胞、肺泡巨噬细胞及肺间质细胞。染BLM组大鼠VEGF呈明显高表达,其中,3 d至28 d,大鼠肺泡Ⅱ型上皮细胞VEGF持续高表达,表达量明显高于对照组,差异有统计学意义(P<0.05,P<0.01);7、14、28 d,大鼠肺间质细胞VEGF呈高表达;3 d至28 d,大鼠肺泡巨噬细胞VEGF表达均升高,与对照组的差异均有统计学意义(P<0.05,P<0.01)。结论 VEGF持续高表达与大鼠血管内皮细胞损伤有关,而血管内皮细胞的损伤可能是BLM诱发大鼠肺纤维化的重要启动因素之一。     

Chronic food restriction amplifies the effect of lactation on the duration of postpartum anestrus in rats.

We studied the effects of food intake and lactation on the duration of postpartum infecundability in rats. Sprague-Dawley rats were given free access to a purified diet (AIN-76A) or a similar diet (modified to contain twice the concentrations of vitamins and minerals) in amounts equal to 50% of that consumed by controls. At -65 d of age, animals were bred. At parturition, dams were allowed to nurse 4-5 pups, or all pups were removed. Thus, four groups were created: lactating control (n = 11), nonlactating control (n = 11), lactating food restricted (n = 8), and nonlactating food restricted (n = 10). Vaginal cytology was observed twice daily for the detection of proestrus, which occurred at 4.5 +/- 0.5 and 6.7 +/- 0.5 d (mean +/- SD) postpartum in nonlactating control and food restricted groups, respectively (P less than 0.005), and at 16.5 +/- 0.5 and 28.8 +/- 0.5 d postpartum in lactating control and food restricted groups, respectively (P less than 0.0001). The interaction between food intake and lactation was significant (P less than 0.0001). These results indicate that maternal food restriction exacerbates the effects of lactation in prolonging postpartum anestrus.     

Resting energy expenditure in patients with chronic obstructive pulmonary disease

Resting energy expenditure (REE) was measured in 68 patients with stable chronic obstructive pulmonary disease (COPD) and in 34 weight-stable, age-matched (65 +/- 8 y; means +/- SD) healthy control subjects. Fat-free mass (FFM) determined by bioelectrical resistance explained 84% of the variation in REE in the control group but only 34% in the COPD patients. REE could not reliably be predicted from regression equations either developed in healthy subjects or in COPD patients. REE adjusted for FFM was significantly higher (P less than 0.05) in weight-losing (n = 34) than in weight-stable (n = 34) patients (6851 +/- 781 and 6495 +/- 650 kJ/d, respectively). Pulmonary function was more compromised in weight-losing patients. Adjusted REE in weight-stable patients was significantly higher (P less than 0.01) than in the healthy control group (6131 +/- 405 kJ/d). In patients with COPD, factors in addition to FFM are important determinants of REE. A disease-related increase in REE develops, which may contribute to weight loss in COPD in combination with a lack of an adaptive response to undernutrition in weight-losing patients.     

Dietary vitamin A has both chronic and acute effects on vitamin A indices in lactating rats and their offspring

To further investigate the effect of dietary vitamin A (VA) intake on milk VA concentrations and pup VA status, female rats were fed 2 concentrations of VA [0 (n = 9) or 50 micromol/kg diet (n = 10)] during pregnancy and lactation. Plasma retinol concentrations were significantly higher (30-40%) during lactation than before pregnancy or after weaning but were not influenced by dietary VA. In rats fed VA, VA concentrations during lactation were significantly higher in milk (1.5-3 times), mammary tissue (>100%), liver (4 times), pup plasma (20-40%), and pup liver (1.1-6.7 times). In Expt. 2, when VA intake was switched on d 7 of lactation from 0 to 50 micromol/kg, milk VA concentrations (2.24 +/- 0.42 micromol/L; mean +/- SD, n = 6) increased significantly (1.7 times) by d 9 to the same level as in rats administered 50 micromol/kg (6.04 +/- 0.60 micromol/L; n = 6). When VA was removed from the diet on d 7, concentrations declined significantly (by 50%) and by d 11 were the same as those in rats given 0 micromol/kg. We conclude that the rapid effect of changes in dietary VA intake are attributable to changes in the delivery of chylomicron VA to mammary tissue and milk.     

Trace element supplementation after major burns modulates antioxidant status and clinical course by way of increased tissue trace element concentrations

BACKGROUND: After major burns, patients can develop nutritional deficiencies including trace element (TE) deficiencies. Various complications, such as infections and delayed wound healing, influence the clinical course of such patients. OBJECTIVES: We aimed to investigate the effects of large, intravenous doses of TE supplements on circulating and cutaneous TE tissue concentrations, on antioxidant status, and on clinical outcome after major burns. DESIGN: This was a prospective, randomized, placebo-controlled trial in 21 patients aged 35 +/- 11 y (x +/- SD) with burns on 45 +/- 21% of their body surface area. Intravenous copper, selenium, and zinc (TE group) or vehicle (V group) was given with a saline solution for 14-21 d. Blood and urine samples were collected until day 20, and skin biopsy specimens were collected on days 3, 10, and 20. RESULTS: The age of the patients and the severity of their burns did not differ significantly between the groups. Plasma TE concentrations were significantly higher in the TE group. In burned areas, skin contents of both selenium (P=0.05) and zinc (P=0.04) increased significantly by day 20. Plasma and tissue antioxidant status was improved by supplementation. The number of infections in the first 30 d was significantly lower in the TE group (P=0.015), with a median number of 2 versus 4 infections per patient in the TE and V groups, respectively, as a result of a reduction in pulmonary infections (P=0.03). Wound healing was improved in the TE group, with lower requirements for regrafting (P=0.02). CONCLUSIONS: TE supplementation was associated with higher circulating plasma and skin tissue contents of selenium and zinc and improved antioxidant status. These changes were associated with improved clinical outcome, including fewer pulmonary infections and better wound healing.