Maternal nicotine effects on vascular endothelial growth factor expression and morphometry in rat lungs

Aims

Maternal smoking during pregnancy may impair pulmonary function in infants, and the exact mechanisms underlying these changes are unknown. We evaluated the effects of maternal nicotine exposure on lung VEGF expression and morphometry during the postnatal period in rats.

Methods and results

Timed pregnant Sprague–Dawley rats were injected subcutaneously with nicotine at a dose of 2 mg/kg/day from Day 3 to Day 21 of gestation. A control group was injected with saline. Body weight, lung weight, and lung volume were comparable between control and nicotine-exposed rats. Plasma vascular endothelial growth factor (VEGF) levels and lung VEGF mRNA expression decreased with advancing age, and nicotine exposure insignificantly decreased plasma VEGF levels and lung VEGF mRNA expression, compared with the control rats during the study period. Nicotine exposure caused a significant decrease in vascular endothelial growth factor receptor (VEGFR)-2 mRNA expression, compared with the level of the control rats on Postnatal Day 1. On Postnatal Day 1, nicotine-exposed rats exhibited a significantly lower volume fraction of alveolar airspace and alveolar surface area and a significantly higher alveolar wall volume fraction than did the control rats.

Conclusions

Maternal nicotine exposure during pregnancy decreases VEGF and VEGFR-2 mRNA expression and alters lung structure in the lungs of postnatal rats. Because angiogenesis is vital for alveolarization during normal lung development, these results suggest that decreased VEGF expression might be involved in the structural alterations of the developing lung after exposure to antenatal nicotine.     

Aortic intima–media thickness in nicotine-exposed rat pups during gestation and lactation period

There have been several studies confirming an association between maternal smoking during pregnancy and low birth weight. The detrimental effect of nicotine exposure beginning in fetal life continues during lactation, in infancy and in the early childhood period. In our previous studies, we found increased aortic intima–media thickness (aIMT) as a preatherosclerotic lesion in neonates with intrauterine growth restriction and in infants of smoking mothers. We aimed to evaluate histopathologically the effect of nicotine exposure during pregnancy and lactation period on fetal growth and aIMT at postnatal 45 days of age (end of the mid-adolescent period) in rat pups living in the same conditions. Gravid rats were assigned into three groups. In nicotine A, pregnant rats received 6 mg/kg/day nicotine intraperitoneally during pregnancy from 1 to 21 days of gestation and lactation (until postnatal day 21). Nicotine B received 3 mg/kg/day nicotine for the same period. Control pregnant rats received only saline intraperitoneally. Abdominal aIMT was studied histopathologically at postnatal 45 days of age. Nicotine exposure resulted in decreased birth weight and pregnancy weight gain. The mean aIMT values of the rat pups exposed to nicotine in both nicotine A and B groups were higher than those of the control group (103.78 ± 21.33 μm, 99.11 ± 30.12 μm, and 62.56 ± 7.18 μm, respectively). In conclusion, the detrimental effect on birth weight of nicotine exposure that began in fetal life is dose dependent. Nicotine exposure during intrauterine life and the lactation period causes increased aIMT in rat pups.     

钳夹子宫血管致宫内生长迟缓幼鼠肝及脑组织变化的研究

目的　建立简便可靠的大鼠宫内发育迟缓(IUGR)模型,观察其幼鼠肝及脑重量和病理变化。方法　将大鼠分为2组:钳夹组于孕17d 行双侧子宫血管钳夹术30m in;对照组行同期开关腹术,但不钳夹子宫血管。随机获得孕21d 剖宫产及自然分娩两队。结果　剖宫产队:钳夹组幼鼠体重、肝重、脑重均明显低于对照组(P< 0.05),肝及脑组织光镜下有明显的病理形态学异常。自然分娩队:生后d6 两组幼鼠体重无明显差异(P> 0.05),但钳夹组幼鼠肝及脑重仍明显低于对照组(P<0.05),光镜下脑的异常改变部分恢复,肝的形态学改变恢复正常。结论　钳夹子宫血管法能造成IUGR模型,且IUGR幼鼠出现可测定的肝及脑损伤,生后6d 肝损伤恢复,脑损伤部分恢复     

Effect of malnutrition and chronic use of nicotine during pregnancy on lung phospholipid concentration in neonate rats

OBJECTIVE: The aim of the present study was to determine whether lung phospholipid concentration is affected in neonate rats "Wistar EPM-1" following a continuous 21-day gestational exposure to nicotine. METHODS: Eighty rats "Wistar EPM-1" were randomly divided in four control (diet free and water "ad libitum") groups (10 rats each): 1 - Control, 2 - Physiologic Solution (infused with 0.15ml of NaCl 0.9%), 3 - Nicotine 1 (infused with 900 micro g/kg/day of nicotine bitartrate 95%), and 4 - Nicotine 2 (infused with 2.700 micro g/kg/day of nicotine bitartrate 95%), and four undernourished (diet 13g/day and water ad libitum) groups (10 rats each), that received the same kind of treatment as the control groups. The infusion of nicotine was subcutaneous. The offspring were divided in eight groups according to their origin. RESULTS: A significant high lung phospholipid concentration was observed in the non-undernourished nicotized group which was injected with a high dose of nicotine. In the other groups, there was no alteration in that concentration. CONCLUSION: We conclude that gestational exposure to nicotine increases lung phospholipid concentration in neonate rats, and that the nutritional state also influences this lung phospholipid concentration.     

Nicotine and Cotinine Concentrations in the Nursing Mother and Her Infant

ABSTRACT. Twenty-two smoking mothers and their healthy newborn infants (mean postnatal age of 3.7 days) was studied in the maternity ward. A close correlation was found (r=0.94) between nicotine concentrations in the mothers' plasma and milk after smoking, the milk: plasma ratio being 2.9. The amount of nicotine transferred to the infant increased from 0.09 to 1.03 μg/kg infant body weight when mothers smoked before breast-feeding. The daily dose of nicotine via the mothers' milk was 6 μg per kg infant body weight. Cotinine but not nicotine concentrations in the plasma and milk of the mothers and the urine of the infants reflected the smoking habits of the mothers during pregnancy. There was no correlation between nicotine and cotinine concentrations in the infant's urine and the amount of nicotine given to the infant via the mother's milk.     

Studies on Carbohydrate Metabolism in Infants with Congenital Heart Disease Part II. Effects of hypoxia on growth, hepatic glycogen storage, and transaminase activities in serum and liver, of rats

To ascertain the harmful effects of hypoxia on liver function and growth, an experimental study was performed using young female rats. Body weight, food intake, hepatic glycogen content, and GOT, GPT and LDH in the serum and liver of rats reared in a hypoxic condition were compared with those of controls. The following results were obtained.

• 1) Although the food intake of rats in a hypoxic condition was almost equal to that of the controls, the mean weight gain of hypoxic rats was lower than that of the controls.
• 2) Glycogen storage in the liver of rats in a hypoxic condition was significantly deficient when compared with that of the controls.
• 3) GOT and GPT activity in serum and liver of hypoxic rats were elevated.
• 4) The deficiency of glycogen storage in the liver was histologically demonstrated. To sum up, hypoxia induced growth retardation, deficiency of glycogen storage in the liver of rats, and hepatic dysfunction. Hypoxia in infants with congenital heart disease may be one of the most important causes of their growth retardation. (Acta Paediatr Jpn 23(2): 172–176 1981)

     

Nicotine and cotinine concentrations in the nursing mother and her infant

Twenty-two smoking mothers and their healthy newborn infants (mean postnatal age of 3.7 days) were studied in the maternity ward. A close correlation was found (r = 0.94) between nicotine concentrations in the mothers' plasma and milk after smoking, the milk: plasma ratio being 2.9. The amount of nicotine transferred to the infant increased from 0.09 to 1.03 micrograms/kg infant body weight when mothers smoked before breast-feeding. The daily dose of nicotine via the mothers' milk was 6 micrograms per kg infant body weight. Cotinine but not nicotine concentrations in the plasma and milk of the mothers and the urine of the infants reflected the smoking habits of the mothers during pregnancy. There was no correlation between nicotine and cotinine concentrations in the infant's urine and the amount of nicotine given to the infant via the mother's milk.     

Picolinic carboxylase activity in rat liver and kidney. I. Influence of growth, sex, gestation, lactation, and nutritional imbalance

Picolinic acid (PA) is a metabolite of tryptophan that chelates trace metals, including zinc. Several recent observations have suggested a role for PA in zinc metabolism. The enzyme responsible for its formation is picolinic carboxylase (PC). We have measured PC in rats under a variety of conditions, using tissues that play a role in zinc metabolism. PC activity was demonstrated in liver and kidney and was not detectable in pancreas and brain. Activity was most pronounced in kidney. In male suckling rats, PC increased gradually, reaching maximum levels on the 21st day of life. Only liver PC showed marked variations under different physiological conditions. Liver PC was higher on the 21st day of life than in adulthood. It was higher in female than in male adult rats. In pregnant rats, liver PC decreased gradually toward the end of gestation, reaching the lowest point near delivery; however, a 12-fold increase occurred during lactation. Liver PC activity of rats with symptoms of pellagra showed a fivefold increase over controls with similar body weight, whereas liver PC of chronically starved rats showed only a twofold increase over controls with twice their body weight.     

Effects of maternal nicotine exposure during lactation on breast-fed rat pups

BACKGROUND: Nicotine is known to be associated with adverse effects in infants and children. It is concentrated in breast milk and is absorbed by the infant. The aim of this study was to investigate the effects on breast-fed rat pups of maternal nicotine exposure during lactation. METHODS: In the experimental group (n = 6), nicotine was given to lactating dams (2 mg/kg/day) after delivery and continued for 10 days during lactation. Control animals (n = 4) received saline for the same duration. The suckling rats were weighed and killed on postnatal day 10, and samples were taken from the lung, liver, kidney, spleen and small intestine for histopathological examination. Superoxide dismutase (SOD), catalase (CAT) activities and malondialdehyde (MDA) levels were measured in the liver of the dam and the offspring. RESULTS: Histopathological changes in the liver of the nicotine-exposed group showed portal inflammatory infiltrate, ballooning degeneration of hepatocytes, and focal necrosis in the parenchyma. Thickening of alveolar walls because of interstitial inflammation was noted in the lungs. Histopathological examination of kidney, spleen and small intestine tissue did not reveal any abnormality. In the experimental group, SOD and CAT activities were significantly decreased (p <0.001) but MDA levels were significantly increased (p <0.001) compared with the control group. CONCLUSION: These results indicate that maternal nicotine exposure induces oxidative stress and causes detrimental histopathological changes in the lung and liver of lactating offspring.     

Effect of guanidinoethyl sulfonate on taurine concentrations and fetal growth in pregnant rats

Guanidinoethyl sulfonate (GES), a transport antagonist of taurine, was given to pregnant rats from day 11 to 21 of gestation as a 1% solution in drinking water. On day 21 of gestation in GES-treated pregnant rats, the concentration of taurine markedly decreased in the fetal whole body (54% of the control), the fetal liver (37%), the fetal whole brain (87%), the placenta (32%), the maternal liver (33%), the maternal whole brain (32%), and the maternal plasma (46%). The wet weight of fetal whole body, liver and brain of fetus, and placenta also showed a significant drop. But there were no differences of weight gain, in the liver and brain weights of the mother of the control and GES-treated pregnant rats. The urinary excretion of taurine in pregnant rats treated with GES was much higher than that of the controls. These results suggest that the administration of GES to pregnant rats induces much urinary taurine excretion with a resulting decrease in the tissue taurine content and readily produces taurine-deficient fetal rats.     

表没食子儿茶素-3-没食子酸酯对宫内生长受限大鼠肝脏脂代谢的影响和机制

目的 探讨表没食子儿茶素-3-没食子酸酯（EGCG）对宫内生长受限（IUGR）大鼠肝脏脂代谢的影响和机制。方法 采用母鼠孕期全程限食法建立IUGR大鼠模型，随机分为IUGR组和EGCG组，EGCG组大鼠在离乳后用含EGCG的饮用水喂养至10周，同时设立正常对照组，每组8只。13周龄时，测量各组大鼠体重后，采集大鼠血液及肝脏组织标本，检测各组大鼠血清空腹总胆固醇（TC）、甘油三酯（TG）、游离脂肪酸（FFA）、血糖（FPG）、胰岛素（FINS）和肝脏脂质水平，计算稳态模型评估胰岛素抵抗（HOMA-IR）和脂肪组织胰岛素抵抗（adipo-IR），观察肝脏组织病理切片，并采用实时荧光定量PCR法检测肝脏相关基因的相对表达水平。结果 13周龄时，各组大鼠体重比较差异无统计学意义（P=0.067）。各组间的FPG、FFA、FINS、HOMA-IR和adipo-IR水平比较差异均有统计学意义（P < 0.05）。各组间的血清TC和TG水平比较差异无统计学意义（P > 0.05），但在肝脏中IUGR组TC和TG水平均明显高于EGCG组（P < 0.05）。油红染色结果提示，IUGR大鼠的肝脏脂肪储积明显增加，而EGCG能够改善该现象。PCR结果显示，与对照组相比，IUGR组的Ampk mRNA及Adipor1 mRNA表达水平降低，Srebf1 mRNA表达水平增加（P < 0.05），EGCG能逆转IUGR大鼠Ampk mRNA及Srebf1 mRNA的表达水平，且与对照组比较差异无统计学意义（P > 0.05）。结论 早期EGCG干预可能通过Ampk/Srebf1通路下调脂肪酸的从头合成，并通过改善肝细胞的胰岛素抵抗，从而降低IUGR大鼠的肝脏脂肪积累。     

The relationship of diaphragmatic defect,liver growth,and lung hypoplasia in nitrofen-induced congenital diaphragmatic hernia in the rat

Reduced lung size (lung hypoplasia, LH) is the main cause of mortality in newborns with congenital diaphragmatic hernia (CDH). However, it is unclear which mechanisms lead to LH. To assess this, we analyzed the relationship of LH and liver mass in correlation to the size of the diaphragmatic defect in rats with nitrofen-induced CDH. A total of 266 newborn Sprague-Dawley rats (30 litters) were exposed to nitrofen on day 11.5 of pregnancy. After spontaneous delivery at term (22 days), all newborns were microdissected. Using a computerized morphometric device, the area of the thoracic cavity, the lung, the intrathoracic liver, and the diaphragmatic defect were measured. The lungs, the intrathoracic, and the extrathoracic portion of the liver were weighed. After nitrofen exposure, 160 newborn rats presented with CDH (60.2%). They were divided into five groups according to the intrathoracic content of intraabdominal organs. We observed a significant increase of the total liver and decrease of the lung weight in the severely affected groups. A significant correlation between the size of the defect and the weight of the intrathoracic part of the liver could be demonstrated. Nitrofen alone had no effect on liver weight. Our results indicate that (1) the presence of liver inside the thoracic cavity is not the result of dislocation but rather of growth of liver tissue through the defect, and (2) the observed correlation between the size of the defect and the intrathoracic liver weight may be part of the pathogenesis of LH in CDH.     

Effect of somatocrinin and a somatostatin antiserum on liver growth in the rat

This study examines the effects of somatocrinin (GRF) and somatostatin antiserum (ASS) alone, and in combination, on liver growth. Twenty-four-day-old rats were injected s.c. twice daily for 14 days with either saline or GRF (4 and 20 micrograms X kg-1). ASS was given i.p. every 2 days. GRF alone had no effect on liver weight, but produced hyperplasia and increased RNA content. ASS alone had no effect on RNA, DNA, and protein contents. Potentiation of the effects of GRF by ASS was observed on liver weight and DNA content. Indeed, this combined treatment resulted in increased organ weight and hyperplasia at an intermediary level of GRF. These data indicate that a strong interaction exists between GRF and ASS on the control of liver growth, possibly through the release of growth hormone (GH).     

新生大鼠在1-氨基-3,5-二甲基金刚烷盐酸急性毒理实验中的病理学变化

目的从病理学角度探讨1-氨基-3,5-二甲基金刚烷(美金胺)对新生大鼠各主要脏器可能造成的毒性影响。方法新生大鼠68只随机分为7组,分别腹腔注射不同剂量的美金胺和注射用水,对所有死亡新生大鼠及时尸解,存活新生大鼠在给药7 d后断头处死,取肝、肾、脑、心、肺、脾进行病理检查,评估不同剂量的美金胺对重要脏器的可能毒性改变。结果1.用药组死亡新生大鼠脑、肝的脏体较正常7日龄新生大鼠相应脏器的脏体比显著增高,脾脏较正常7日龄新生大鼠相应脏器的脏体比显著减低。2.镜下病理检查结果显示,脑组织有神经元变性,肝组织有淤血和细胞变性,余脏器病变不明显。3.新生大鼠的病理变化程度及死亡率与美金胺的剂量呈正相关。结论美金胺对新生大鼠的脑和肝脏影响较大。     

大鼠不同时期高脂饮食对子代糖脂代谢的影响及机制研究

目的 探讨Sprague-Dawley母鼠不同时期高脂饮食对子代糖脂代谢的影响及相关机制。 方法 根据孕前及孕期哺乳期饮食的不同,将母鼠随机分为4组（n=9）：CC组（孕前、孕期哺乳期均正常饮食）、HC组（孕前高脂饮食、孕期哺乳期正常饮食）、CH组（孕前正常饮食、孕期哺乳期高脂饮食）、HH组（孕前、孕期哺乳期均高脂饮食）;子代生后3周断奶后,全部给予正常饮食。记录母鼠孕前、孕期体重及仔鼠体重。取各组幼年期（3周）、成年期（12周）雄性仔鼠,检测空腹血糖（glucose,GLU）、胰岛素（insulin,INS）及肝脏三酰甘油（triglyceride,TG）、总胆固醇（total cholesterol,TC）水平,计算胰岛素抵抗指数（homeostasis model assessment of insulin resistance,HOMA-IR）、糖耐量试验（glucose tolerance test,GTT）及胰岛素耐量试验（insulin tolerance test,ITT）的曲线下面积（area under the curve,AUC）;取肝脏组织行苏木精-伊红染色和油红O染色,观察肝脏脂质沉积;检测肝脏糖脂代谢关键基因IR、IRS、AKT和FASN、SREBP1c、PPARα的mRNA及其蛋白表达水平。 结果 孕前高脂饮食组（HC组、HH组）母鼠体重较正常饮食组（CC组、CH组）显著增加（P<0.001）;HC组、CH组、HH组母鼠孕期增重较CC组显著增加（P<0.001）。生后3周时,HC组、CH组、HH组的仔鼠体重、肝脏TG及TC含量,以及FASN、SREBP1c、PPARα的mRNA及其蛋白表达水平均较CC组显著增加（P<0.05）,肝脏脂质沉积增加,其中HH组增加最显著;HH组的空腹GLU及INS水平、HOMA-IR、GTT-AUC、ITT-AUC及肝脏p-IRS蛋白表达水平均较CC组显著增加,肝脏IR、IRS的mRNA及其蛋白表达水平均较CC组显著降低（P<0.05）。生后12周时,HC组、CH组、HH组的仔鼠体重、空腹GLU及INS水平、HOMA-IR、GTT-AUC、ITT-AUC、肝脏TG及TC含量、p-IRS蛋白表达水平,以及FASN、SREBP1c、PPARα的mRNA及其蛋白表达水平均较CC组显著增加（P<0.05）,肝脏脂质沉积增加,其中HH组增加最显著;HC组、CH组、HH组IR、IRS、AKT的mRNA水平均较CC组显著降低,IR、IRS、p-AKT蛋白表达水平均较CC组显著降低（P<0.05）。HC组与CH组在不同时期的糖脂代谢水平未见显著性差异（P>0.05）。 结论 大鼠怀孕前后不同时期的高脂饮食对子代的糖脂代谢具有不同的影响,孕前、孕期、哺乳期全程高脂饮食对子代糖脂代谢影响最大;大鼠高脂饮食对其子代糖脂代谢的影响考虑与糖脂代谢基因的表达改变有关。 引用格式:     

宫内生长迟缓和高脂饮食对大鼠血脂及肝脏相关基因转录水平的影响

目的 探讨宫内生长迟缓(IUGR)和高脂饮食对大鼠生长、脂代谢及肝脏相关基因的作用。方法 采用母鼠孕期全程限食法建立IUGR 大鼠模型。断奶后,将32 只正常子鼠和24 只IUGR 子鼠随机分配到标准饮食组和高脂饮食组。10 周龄时,测量空腹血糖、血脂,观察肝脏组织病理切片,并测定肝脏相关基因转录水平。结果 IUGR 大鼠与正常大鼠比较,10 周龄时,标准饮食下两者体重差异有统计学意义,而高脂饮食下两者体重差异无统计学意义。和正常大鼠相比,两种饮食下的IUGR 大鼠均出现能量摄入增加、空腹血糖、总胆固醇和甘油三酯水平升高。无论在正常大鼠还是IUGR 大鼠,高脂饮食均降低了血清甘油三酯浓度。IUGR和高脂饮食均加重了肝脏的脂肪堆积。双因素方差分析显示,10 周龄时,与正常大鼠比较, IUGR 大鼠肝脏脂代谢相关基因PGC-1α、CPT-1、SREBF-2、HMGR、LDLR 和SREBF-1 的表达差异有统计学意义;与标准饮食比较,高脂饮食增加了正常大鼠和IUGR 大鼠PPARα、SREBF-1、SREBF-2、ABCG5 和CYP7A1 的表达;IUGR 和高脂饮食对LDLR 水平存在交互作用。结论 IUGR 大鼠呈现出高血脂和肝脏脂肪堆积,可能与IUGR 大鼠的食欲增强和转录水平上脂肪酸氧化相关基因调节紊乱有关。高脂饮食可加重大鼠的肝脏脂肪堆积,可能与转录水平上调节脂肪酸合成的相关基因表达增加和甘油三酯分泌减少相关。     

小于胎龄鼠肝脏肥胖基因Lipin2的表达及其意义

目的 探讨小于胎龄(SGA)鼠肝脏中肥胖基因lipin2表达的动态变化及其意义.方法 选取健康成年SD大鼠,建立孕期全程低蛋白SGA鼠模型,随机分为适于胎龄(AGA)组和SGA组,每组24只仔鼠.选择1d、7d、21 d和56 d作为观察点,测定其体质量及头臀长,留取肝脏组织,采用反转录(RT) -PCR和蛋白质免疫印迹技术(Western blot)检测其肝组织中lipin2 mRNA和蛋白的动态表达.结果 1.体质量指数(BMI):1 dSGA鼠BMI较AGA组降低(P ＜0.05)；56 d SGA鼠的BMI较AGA组升高(P＜0.01).2.lipir2 mRNA和蛋白的表达:1 d SGA组低于AGA组(Pa＜0.05),7d和56 d SGA组均高于AGA组(Pa＜0.05).3.BMI与56 d大鼠lipin2蛋白表达量呈高度正相关(r=0.713,P=0.009).结论 SGA鼠出生时体态瘦小,后出现追赶生长,青春期末期成年大鼠表现出肥胖倾向.lipin能敏感地反映不同阶段宫内发育迟缓仔鼠肝脏物质代谢情况,提示其参与了SGA鼠的糖脂代谢紊乱过程,lipin基因表达的改变可能为SGA鼠引起成年期代谢综合征发病机制之一. .     

Mitochondrial Changes and Carnitine Status in Fasting Rats

To elucidate mitochondrial morphology and related pathophysiology in the fasting state, liver mitochondrial area, plasma levels of carnitine and non-esterified fatty acids were measured in fed (N = 30) and fasted for 5 days (N = 28) rats. The rats were divided into three groups according to body weight: 100g-group (aged 5 weeks), 200g-group (aged 7–8 weeks), 400g-group (aged 15–16 weeks). Electron microscopy of the liver revealed mitochondrial enlargement in fasted rats. There were significant differences in mitochondrial area measured by digitizer, between fasted groups with 100g and 200g body weights and the compatible fed groups. The grade of mitochondrial swelling was inversely proportional to the body weight (i.e. the age). The fasting induced decreased plasma levels of free carnitine and increased plasma levels of acylcarnitine. Plasma free carnitine levels in all fed rats appeared to be directly correlated to the body weight. The above mitochondrial swelling and abnormal carnitine status are hallmarks of Reye's syndrome (RS). These changes are not specific to RS but might be attributable to fasting.     

控制食谱联合有氧运动对实验性肥胖大鼠血管内皮功能的影响

目的观察控制食谱联合有氧运动对实验性肥胖大鼠血管内皮功能的影响。方法24只雄性Wis-tar大鼠随机分为普通饮食组和高脂饮食组,喂养8周后肥胖大鼠造模成功。肥胖大鼠随机分为2组:实验组,基础饲料 游泳运动;高脂组,继续高脂饮食;原普通饮食组作为正常组,继续饲予基础饲料。干预12周后处死大鼠,测定Lee指数、心重、肝重;总胆固醇(TC)、甘油三脂(TG),血浆内皮素(ET)、血清一氧化氮(NO)、血浆血管性假血友病因子(v WF);免疫组化法检测腹主动脉细胞间粘附分子1(ICAM-1)蛋白的表达,RT-PCR法检测腹主动脉ICAM-1mRNA的表达,并进行组间比较。结果实验组Lee指数、肝重、TC、TG、ET、v WF、动脉ICAM-1蛋白和mRNA表达水平均显著低于高脂组,心重、NO显著高于高脂组。结论控制食谱联合有氧运动可改善实验性肥胖大鼠的高脂血症及血管内皮舒缩、凝血和粘附功能。     

Narcotic and nicotine effects on the neonatal auditory system

To evaluate narcotic and nicotine effects on the neonatal auditory system, brain stem auditory evoked responses were recorded in 15 infants prenatally exposed to both narcotics and nicotine (median gestational age 38.4 weeks, median birth weight 2820 g), in 15 nicotine exposed infants (gestational age 40.0 weeks, birth weight 3000 g) and in 24 healthy term infants (gestational age 40.1 weeks, birth weight 3310 g) who served as controls. Whereas nicotine-exposed and control infants were similar in all brain stem auditory evoked response measurements, narcotic/nicotine infants had bilaterally increased wave V latencies (left: p = 0.005; right: p = 0.04) and I-V intervals (left: p = 0.02; right: p = 0.01) when compared to controls. Our findings suggest that prenatal narcotic but not nicotine exposure negatively affects maturation or integrity of the neonatal auditory brain stem tract and that neither narcotic nor nicotine exposure is associated with hearing loss in the neonate.