Prenatal dexamethasone rescues heart hypoplasia in fetal rats with congenital diaphragmatic hernia

BACKGROUND/PURPOSE: Patients and rats with congenital diaphragmatic hernia (CDH) have lung and heart hypoplasia. Prenatal steroids improve lung hypoplasia in CDH rats. The current study tests the hypothesis that prenatal dexamethasone could rescue heart hypoplasia in rats with CDH. METHODS: Timed pregnant rats received intragastrically either 100 mg nitrofen or oil on day 9.5, and other animals had the same treatment with, in addition, either 0.25 mg/kg dexamethasone intraperitoneally or no treatment on days 19 and 20. Fetuses were recovered on day 21, and heart weight to body weight ratios, heart DNA, protein, and glycogen were measured in fresh specimens. Left-to-right ventricular diameter and aortic-to-pulmonary diameter ratios were measured after formalin fixation. RESULTS: Wet heart weight to body weight, left-to-right ventricular diameter, and aortic-to-pulmonary root diameter ratios, which were lower in fetuses exposed only to nitrofen than in their oil controls, were similar in those exposed to nitrofen plus dexamethasone than in their corresponding oil plus dexamethasone controls. Total heart DNA, which was decreased in fetuses exposed to nitrofen with CDH in comparison with their controls, was increased in those receiving nitrofen and dexamethasone in comparison with theirs. Protein to DNA ratio was decreased in all rats with CDH irrespective of their exposure or not to dexamethasone. Glycogen to DNA ratio was higher in all dexamethasone-treated fetuses than in those without this treatment. No gross histologic differences were seen among groups. CONCLUSIONS: Heart hypoplasia in rats with CDH is in part rescued by prenatal dexamethasone treatment as expressed by increased number of smaller myocytes with higher glycogen content. Prenatal steroids could modify heart involvement in human fetuses with CDH as well.     

Renal hemodynamics during pregnancy in chronically catheterized, conscious rats

Two types of experiments were performed, cross-sectional and longitudinal. In the cross-sectional studies, rats were mated, later prepared surgically, and then 5 or more days after surgery, each examined twice during days 11 to 15 or days 18 to 20 of gestation. Nonpregnant rats matched for age and prepregnant weight served as controls. In the longitudinal studies, rats were catheterized and, starting 6 days later, examined twice; then the same rats were mated and each was studied on days 5, 8, 12, 16, and 20 of gestation, as well as on day 5 postpartum. In the cross-sectional studies, glomerular filtration rate (GFR) and effective renal plasma flow (ERPF) were elevated by approximately 26% and 20%, respectively, above nonpregnant controls at 11 to 15 days of gestation (GFR, 2739 +/- 94 vs. 2181 +/- 134 microliters . min-1, P less than 0.005; ERPF, 9367 +/- 295 vs. 7785 +/- 422 microliters . min-1, P less than 0.01). By 18 to 20 days of gestation, GFR and ERPF had returned to levels that were not significantly different from nonpregnant values. The longitudinal studies confirmed these findings in every respect and further revealed that GFR and ERPF were elevated above nonpregnant values as early as day 5 of gestation (P less than 0.005). Thereafter, they rose to peak values, at 12 and 16 days of gestation, of 3122 +/- 144 and 10,584 +/- 541 microliters . min-1, and then returned to nonpregnant levels by day 20 of gestation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Congenital cystic adenomatoid malformation detected by prenatal sonography; report of 2 cases

We report 2 cases of congenital cystic adenomatoid malformation (CCAM) detected by prenatal sonography. The first CCAM was diagnosed by fetal sonography in a female fetus at 30 weeks' gestation. The infant was born at 37 weeks' gestation, with a body weight of 2,770 g. After birth, chest computed tomography (CT) showed a multicystic mass in the middle lobe of the lung. She remained asymptomatic until age 21 months, when she suffered pneumonia. Two months later, middle lobectomy was performed. The second CCAM was diagnosed by fetal sonography in a female fetus at 25 weeks' gestation. She was born at 39 weeks' gestation, with a body weight of 3,292 g. Four days after birth, CCAM type II was diagnosed by chest CT. The infant was asymptomatic, and left lower lobectomy was performed 11 months after birth.     

Does maternal stress induce abnormal descent of the testis in prepubertal rats?

OBJECTIVE: To investigate whether prenatal maternal stress, considered to alter plasma testosterone concentration and induce a lack of testosterone surge in male rat fetuses, has any effect on the growth of the processus vaginalis and testicular descent in male offspring. MATERIALS AND METHODS: Pregnant rats were divided into two groups. In group 1, the rats were placed three times daily for 60 min each session in Plexiglas rat holders (13x6x8 cm) illuminated by two 150-W flood lights from day 14 to day 18 of gestation during the dark phase of the animals' light (12 h) and dark (12 h) cycle. In group 2, pregnant females were not handled and acted as controls. After birth, the anogenital distance of both the male and female rats was measured, and the length of the processus vaginalis was measured at 7 days of age in some rats. Thereafter, at 21, 24, 27 and 30 days of age, testicular descent was assessed in the remaining male rats. RESULTS: In group 1, at 21, 24, 27 days of age, testicular descent was delayed in the stressed rats compared with the control rats. At 30 days of age, five of 36 stressed male offspring showed abnormal testicular descent; three testes were in the superficial inguinal position and two were above the scrotum. Both the anogenital distance and the length of the processus vaginalis were significantly less in the stressed male rats than in the controls. CONCLUSIONS: Maternal stress induced a female-like anogenital distance in male rat fetuses, and caused delayed and abnormal descent of the testis, by inhibiting the growth of the processus vaginalis after birth. Prenatal stress may therefore be involved in the delay of testicular descent in neonatal rats by inducing a mild anti-androgenic effect in the fetus.     

Prenatal ethanol exposure has differential effects on fetal growth and skeletal ossification

There is increasing evidence suggesting that the intrauterine environment may influence long-term bone health and the risk of developing osteoporosis in later life. Alcohol (ethanol) is one factor whose presence in the prenatal environment has long-term consequences for the offspring, including permanent growth retardation. Moreover, prenatal ethanol exposure retards both fetal and postnatal bone development. It is unknown if ethanol's effects on skeletal development result from generalized growth retardation or effects specific to skeletal development. Furthermore, the level of ethanol exposure required to produce skeletal effects is unknown. The objectives of this study were to determine (1) if ethanol exerts specific effects on fetal skeletal development that are independent from its effects on general growth, and (2) the level of prenatal ethanol exposure required to affect fetal growth and skeletal ossification. Rats were fed isocaloric diets with ethanol (15%, 25%, or 36% ethanol-derived calories (EDC), approximating low, moderate, and high exposure levels), or without ethanol (pair-fed, PF, or control, C groups), prior to and throughout 21 days of gestation. The degree of E-induced delay in development was determined by comparison of E fetuses on d21 gestation to C fetuses on d17-d21 gestation. Prenatal ethanol exposure at 36% EDC decreased fetal body weight, length, and skeletal ossification compared with PF and C fetuses on d21 gestation. Importantly, effects on ossification, but not body weight or length, were also seen at the more moderate dose of 25% EDC, and the number of bones affected and the severity of effects on ossification tended to increase with dose of ethanol. Comparison of E fetuses on d21 gestation with C fetuses from d17 to 21 gestation indicated that the ethanol-induced delay in development differed for weight and skeletal ossification, and was not uniform among skeletal sites. Taken together, these data suggest that prenatal ethanol exposure has effects on fetal skeletal development that are independent of those on overall fetal growth, and that these effects occur even at moderate levels of maternal drinking. Effects of prenatal ethanol exposure on fetal skeletal development could potentially increase the offspring's risk of osteoporosis later in life.     

Normal lactational environment restores nephron endowment and prevents hypertension after placental restriction in the rat

Uteroplacental insufficiency in the rat restricts fetal growth, impairs mammary development, compromising postnatal growth; and increases adult BP. The roles of prenatal and postnatal nutritional restraint on later BP and nephron endowment in offspring from mothers that underwent bilateral uterine vessel ligation (restricted) on day 18 of pregnancy were examined. Sham surgery (control) and a group of rats with reduced litter size (reduced; litter size reduced at birth to five, equivalent to restricted group) were used as controls. Offspring (control, reduced, and restricted) were cross-fostered on postnatal day 1 onto a control (normal lactation) or restricted (impaired lactation) mother. BP in male offspring was determined by tail cuff at 8, 12, and 20 wk of age, with glomerular number and volume (Cavalieri/Physical Dissector method) and renal angiotensin II type 1 receptor (AT(1)R) mRNA expression (real-time PCR) determined at 6 mo. Restricted-on-restricted male offspring developed hypertension (+16 mmHg) by 20 wk together with a nephron deficit (-26%) and glomerular hypertrophy (P < 0.05). In contrast, providing a normal lactational environment to restricted offspring improved postnatal growth and prevented the nephron deficit and hypertension. Reduced-on-restricted pups that were born of normal weight but with impaired growth during lactation subsequently grew faster, developed hypertension (+16 mmHg), had increased AT(1A)R and AT(1B)R mRNA expression (P < 0.05), but had no nephron deficit. Our study identifies the prenatal and postnatal nutritional environments in the programming of adult hypertension, associated with distinct renal changes. It is shown for the first time that a prenatally induced nephron deficit can be restored by correcting growth restriction during lactation.     

Inhibition of bone mineral loss during lactation by Cl2MBP

Summary Pregnant rats were injected subcutaneously with either saline or the bisphosphonate Cl₂MBP (dichloromethylenebisphosphonic acid) at a daily dose of 15 mg P/kg body weight on days 1 through 16 of gestation. Cl₂MBP treatment did not influence maternal body weight nor the number of pups born. When analyzed 1 day after birth, pups from Cl₂MBP-treated rats had a normal body weight but a 10% reduction in carcass calcium (Ca) content. The Cl₂MBP injections were resumed on day 1 postpartum and led to a 10% reduction in pup body weight gain and carcass Ca content at 16 days of age. In saline-injected rats, lactation resulted in slight hypocalcemia, greatly elevated serum levels of 1,25(OH)₂D₃, and loss of bone mineral, as indicated by a reduction in femur ash weight. In nonlactating rats, Cl₂MBP treatment produced slight hypercalcemia but had no effect on serum 1,25(OH)₂D₃ levels or bone mineral content. Compared to lactating rats receiving saline, Cl₂MBP-treated lactating rats were more hypocalcemic and had higher serum 1,25(OH)₂D₃ levels. However, the lactation-induced loss of bone mineral was completely inhibited by Cl₂MBP treatment.     

Elevated calcium, phosphorus, and magnesium retention in pregnant rats prior to the onset of fetal skeletal mineralization

Intestinal absorption and renal excretion rates of Ca, P, and Mg were compared in pregnant and control virgin rats fed a purified diet containing 0.55% Ca, 0.54% P, and 0.067% Mg. Four consecutive balance intervals of 5 days each were examined, beginning on day 1 of gestation. During days 6-10 of gestation, pregnant rats had elevated fractional intestinal absorptions of Ca (29.6 +/- 1.7 versus 20.6 +/- 1.5%), P (65.4 +/- 2.0 versus 59.9 +/- 0.9%), and Mg (54.3 +/- 1.5 versus 42.4 +/- 2.6%). Since urinary excretions of these elements did not change, the pregnant rats retained more Ca, P, and Mg than virgin rats. Fractional intestinal absorptions of these elements during pregnancy were similar to control values during days 1-5 and 11-15 of gestation and then rose for each element during days 16-20 of gestation. Presumably because of an increase in glomerular filtration rate, urinary excretions of Ca and Mg were elevated by 40 and 26% during days 16-20 of gestation. In contrast, urinary P excretion was decreased by 30% during days 11-20 of gestation. Analyses of uterine mineral contents indicated the increased maternal Ca and Mg retentions during pregnancy were balanced by the transfers of these elements to the fetuses. In contrast, pregnancy was associated with a net maternal retention of P. These data are consistent with previous observations of increased maternal skeletal mineralization during early pregnancy before the onset of fetal osteogenesis and subsequent enhanced maternal Ca intestinal absorption concurrent with fetal skeletal mineralization.     

Prenatal exposure to high level of glucocorticoids increases the susceptibility of renal proximal tubular cells to apoptosis induced by uropathogenic Escherichia coli toxins

Prenatal exposure to excessive glucocorticoids may alter the developing fetus inducing metabolic and endocrine imbalance in various organs, including the kidney. This study aimed at evaluating whether prenatal exposure to high levels of glucocorticoids adversely affects renal cell survival and predisposes to renal cell death. Pregnant rats were injected with 0.1 mg/kg dexamethasone (DEX) i.p. from day 1 of gestation. Renal proximal tubular cells (PTCs) were prepared from 20-day-old offspring in the DEX (DEX cells) and control groups (CON cells). After 4 days' culture, cells were exposed to uropathogenic Escherichia coli ARD6 toxins at concentrations known to induce apoptotic cell death. We found that cell death rate was significantly higher in DEX than in CON cells. Cells exhibited morphological and biochemical features of apoptosis. Conversely, the activity of the antioxidant enzyme catalase was significantly increased in renal cortex homogenate from 20-day-old DEX rats. The antioxidant vitamin E did not prevent apoptosis. These results indicate that prenatal exposure to high levels of glucocorticoids induces alterations in renal PTCs rendering them more sensitive to E. coli toxins via nonoxidative stress. With the increasing use of multiple doses of glucocorticoids in preterm infants, the possibility that antenatal glucocorticoids may lead to renal adverse consequences is of clinical relevance.     

先天性膈疝动物模型的制作

目的　制作先天性膈疝的动物模型 ,为进一步研究先天性膈疝合并肺发育不良的病理改变及其处理奠定基础。　方法　妊娠 9.5天的 SD大白鼠随机分成实验组和对照组。实验组经胃一次性灌入 2 ,4-二氯苯基 - P-硝基苯醚 ,对照组经胃灌入等量食用油。妊娠 2 1天时剖腹产取出胎鼠 ,放大镜下观察膈疝形成情况 ,并分别测定胎鼠体重及双肺重量 ,光学显微镜下观察肺的组织学发育情况。　结果　有 2 5只胎鼠制成先天性膈疝模型 ,成功率为 5 8.1% ,实验组胎鼠双肺重量降低 ,组织学显示肺发育不良。　结论　用 2 ,4-二氯苯基 - P-硝基苯醚制作胎鼠膈疝模型具有简便、成功率高的优点 ,是进一步研究膈疝合并肺发育不良的病理改变及其治疗的理想手段     

Increased angiotensin II receptor binding with age in isolated rat glomeruli

The current investigation was performed to determine whether there are changes in the renin-angiotensin system with increasing age in rats. Experiments were performed on male Sprague-Dawley rats (50 to 165 days old). There were no changes in plasma renin activity or angiotensin II concentrations, but the number of angiotensin II binding sites in isolated glomeruli increased with increasing age (r = 0.87, P less than 0.01). Since rat weight varies directly with age, we studied the possibility that the increase in receptor number was due to changes in glomerular morphometrics. In a separate group of experiments the diameter of isolated glomeruli was measured, and assuming spherical shape, glomerular volume and surface area were calculated. Glomerular diameter increased with age and weight of the rats (r = 0.99, P less than 0.001). There was a strong linear correlation between the changes in angiotensin II receptor number and glomerular surface area (r = 0.99, P less than 0.001). The number of receptors per unit surface area was independent of rat weight or age (1224 receptors/micron 2). To test the hypothesis that the apparent increase in glomerular angiotensin II receptor sites with increasing age was due to the shape of the glomerulus, additional binding studies were performed on membranes prepared from isolated glomeruli. There were no differences in the number of angiotensin II receptors in membranes from 63 and 112 day-old rats (888 +/- 115 vs. 925 +/- 128 fmol/mg). In additional experiments the effects of increasing age on angiotensin modulation of renal function were studied.(ABSTRACT TRUNCATED AT 250 WORDS)     

Glucocorticoid activates glomerular antioxidant enzymes and protects glomeruli from oxidant injuries

We examined the effect of glucocorticoid on intrinsic glomerular antioxidant enzyme (AOE) activities. Munich-Wistar rats were treated with daily i.p. injection of vehicle or methylprednisolone [MP, 15 mg/kg body wt, (MP15)] either for three days or nine days. Glomeruli isolated from rats given MP15 had significantly higher activities of total (T-) and manganese (Mn-) superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase than vehicle-treated rats (P less than 0.05). MP15-treated rats were subjected to intrarenal arterial infusion of hydrogen peroxide (35 mumol over 1 hr). Values for urinary protein excretion rate (UprV) after hydrogen peroxide infusion were markedly lower in rats pretreated with MP15 for both three days and nine days than in untreated rats (109 +/- 18 and 55 +/- 24 vs. 416 +/- 73 micrograms/min, respectively, both P less than 0.005). To test whether the same therapeutic intervention attenuates reactive oxygen species (ROS)-mediated glomerular injury in another model, rats given a single i.v. dose of puromycin aminonucleoside (PAN) (50 mg/kg body wt) were treated with daily i.p. injection of vehicle or MP15. Two days after PAN administration, when compared to vehicle-treated controls, PAN rats given MP15 had significantly higher activities of Mn-SOD, GSH-Px and catalase. After eight days of PAN injection, T- and Mn-SOD activities were, likewise, significantly higher in MP15- than vehicle-treated PAN rats. PAN rats given MP15 also had substantially less proteinuria, compared to PAN rats given vehicle alone, UprV averaging 32.3 +/- 9.4 versus 159.0 +/- 13.8 mg/24 hr (P less than 0.05). Elevated glomerular malondialdehyde (MDA) level characteristic of PAN rats was absent in rats treated with MP15. Moreover, epithelial foot process fusion and cell vacuolization seen in vehicle-treated PAN rats were markedly attenuated in MP15-treated PAN rats. These data indicate that the mechanism for therapeutic effect of glucocorticoids on ROS-mediated renal injuries includes an enhancement of endogenous glomerular AOE activities, which attenuates lipid peroxidation of glomerular tissue.     

Disturbed pituitary-testicular axis inhibits testicular descent in the prenatal rat

OBJECTIVE: To investigate whether prenatal stress affects the pituitary-testicular axis in relation to testicular descent in rat fetuses, as maternal stress can alter the plasma testosterone concentration and inhibit testicular descent in male rat fetuses. MATERIALS AND METHODS: Pregnant rats were divided into two groups and kept in reverse light-dark cycles, with lights-off at 08.00 hours and on at 20.00 hours. In group 1, 15 pregnant females were placed three times daily for 60 min each session in plastic rat-holders (13 x 6 x 8 cm) illuminated by two 150-W flood lights during the dark phase, from day 14 to 18 of gestation. In group 2, 10 pregnant females were not handled and thus were used as controls. At 19 days of gestation, five pregnant rats had a Caesarean section in each group, and both testes and the pituitary gland were removed from male fetuses at 10.00-11.00 hours. The tissue homogenates were analysed for testicular testosterone and pituitary luteinizing hormone (LH) by a radioimmunoassay. Thereafter, at 21 and 30 days of age, testicular descent was assessed in the remaining male offspring. Student's t- and the chi-square test were used to assess the results. RESULTS: The mean (sd) concentration of fetal testicular testosterone was significantly lower in group 1, at 312.9 (26.2) pg/mg, than in group 2, at 532.5 (18.2) pg/mg (P < 0.05); that of pituitary LH was also significantly lower in group 1, at 130.6 (22.7) and 295.6 (35.2) pg/mg, respectively (P < 0.05). The completion rate of testicular descent was 14% in group 1 (36 male rats) and 64% in group 2 (28 male rats) at 21 days old, and thereafter they were 81% and 100%, respectively, at 30 days old (P < 0.05). CONCLUSION: Maternal stress might inhibit the pituitary-testicular axis, thereby resulting in abnormal testicular descent in male fetuses.     

Body composition and bone measurements in intra-uterine growth retarded and early postnatally undernourished male and female rats at the age of 6 months: comparison with puberty

Undernutrition in early life may permanently change body structure, physiology and metabolism and leads to chronic diseases in later life. To test whether malnutrition during different critical time periods around birth in the rat has long-lasting effects on body composition and skeletal growth, we examined body weight and body composition in pubertal rats and adult rats of 6 months after pre- and postnatal malnutrition. Prenatal malnutrition or intra-uterine growth retardation (IUGR) was induced by ligation of the uterine arteries on day 17 of gestation and postnatal food restriction (FR) by litter enlargement to 20 pups per mother from day 2 after birth until weaning (day 24). Pubertal markers were balanopreputial separation (BPS) in the male and vaginal opening (VO) in the female. IUGR as well as FR resulted in a persistent growth retardation. From birth in IUGR rats and from day 4 after birth in FR rats until 6 months of age body weight in male and female rats was significantly lower compared with controls (P < 0.01 and P < 0.05). Although total body bone mineral content (TBBMC) did not differ between male IUGR rats and controls at BPS, at the age of 6 months TBBMC was significantly lower (P < 0.01) compared with controls. At BPS as well as at 6 months of age, TBBMC was significantly lower in male FR rats compared with controls (P < 0.05 and P < 0.01). In the female IUGR rats TBBMC was significantly lower compared with controls at VO (P < 0.01) and 6 months (P < 0.05). TBBMC in the female FR rats was significantly lower at VO (P < 0.01), but did not differ from controls at the age of 6 months. For both IUGR and FR male and female rats these differences disappeared after adjusting for body weight. Body composition in terms of total fat mass, percentage fat and percentage lean did not differ from controls in male and female IUGR rats at 6 months and the same results were observed in the female FR rats. However, in the male FR rats, total fat mass and percentage fat were significantly lower compared with controls (P < 0.01 and P < 0.05), while the percentage lean mass was significantly higher (P < 0.05). We conclude that different critical time periods of malnutrition around birth have different effects later in life on growth, which do not disappear at least after 6 months of life. With respect to body composition, only in the FR male rats, differences are found in total fat mass and the balance of percentage fat mass and lean mass. At time of puberty and at the age of 6 months bone mass adjusted for body weight does not seem to be affected by perinatal undernutrition.     

Age as a factor influencing the power and sensitivity of experiments for assessing body weight, testis size, and spermatogenesis in rats

Data from 25 rats aged 60, 150, or 240 days (n = 75) were used to determine the number of observations per rat and or rats per treatment group needed to provide future experiments of known power and sensitivity. End points examined included body weight, testicular weight, number of resistant elongated spermatids, yields of germ cells from their younger progenitors, and germ cell:Sertoli cell ratios. Requirements differed in relation to the experimental power and sensitivity desired. However, the replication needed for detecting equivalent treatment effects on paired testes weight or the number of spermatids per gram of testis increased with age, and was twice as great for 240- vs 60-day-old rats. In contrast, approximately twice as many 60-day-old rats were required for detecting treatment effects on the number of spermatids per Sertoli cell than when 150- or 240-day-old rats were used.     

Techniques of spinal cord surgery in fetal rats

These experiments were done to develop techniques to expose and manipulate the spinal cord in fetal rats, techniques that could be used to study spinal cord regeneration and transplantation. Adequate maternal anesthesia required a mixture of acepromazine-ketamine supplemented by thiopental. Fetal rats were operated on at 16 to 22 days of gestation. Fetal mortality increased as the age of the fetus decreased. Microsurgical techniques were developed to expose, divide, and transplant the distal spinal cord.     

产前产后一体化诊治大动脉转位畸形5例

目的 总结产前和产后一体化诊治大动脉转位畸形(TGA)的经验.方法 5位孕妇在产前诊断中心确诊胎儿TGA,愿意继续妊娠.孕妇平均年龄(28.4±3.0)岁,产前诊断时胎龄(28.4±4.4)孕周.妊娠(36.5±1.8)孕周分娩,新生儿体重(2468±442)g.新生儿接受超声心动图复查,TGA合并室间隔缺损2例,室间隔完整3例.针对严重缺氧患儿,给予前列腺素和呼吸机辅助呼吸.完善术前准备,均在中低温体外循环下完成大动脉调转术,同时矫治合并心脏畸形.结果 患儿生后2～19天,平均(9.0±6.2)天手术.生存3例.死亡2例,1例早产低体重(1770 g)儿,术后第2天心搏骤停,复苏失败;1例Apgar评分低早产儿术前使用呼吸机和前列腺素,生后第2天急诊手术,术后顽固性低心排血量,第3天死亡.结论 TGA产前和产后一体化诊治有利于减少患儿术前缺氧,避免长途转运,但是需要多科室合作,任何环节的不足将会抵消产前诊断给TGA患儿带来的益处.

Abstract：

Objective To summarize primary experiences of integrated fetal diagnosis and postnatal treatment for the transposition of the great arteries (TGA). Methods Five fetus were diagnozed as TGA at(28.4 ±4.4) weeks of gestation via fetal echocardiography. The mean age of the pregnant women was (28.4 ±3.0) years old. Delivers were taken by caesarean at (36.5 ±1.8) weeks of gestation. The body weight of neonates was (2468 ±442) grams. All neonates were transported to the department of neonatology and re-checked by echocardiography. 3 cases were TGA with intact ventricular septum, 2 cases were TGA with ventricular septal defect. Prostaglandin and mechanical ventilation were applied if oxygen saturation was lower. The standard arterial switch procedure was performed under cardiopulmonary bypass with moderate hypothermia. Results The mean age for patients at surgery was (9. 0 ±6. 2) days ( ranged 2-19 days). Three neonates survived, 2 preterm neonates died. One with body weight 1770 g, 2 days after operation was died of sudden heart arrest and failure of resuscitation. Another was treated by mechanical ventilation and prostaglandin after delivery and underwent operation at the second postnatal day, the neonate appeared low cardiac output and high serum lactate postoperatively and died in the third day. Conclusion The integrated fetal diagnosis and postnatal treatment for TGA could prevent severe cyanosis and emergency transportation after parturition. The lack of any link in the cooperation among the multidisciplinary team could affect the benefits for the TGA neonates provided by prenatal diagnosis.     

Is there an association between level of adult blood pressure and nephron number or renal filtration surface area?

BACKGROUND: Reductions in renal filtration surface area (FSA) have been linked to development of hypertension. This study investigated whether there are direct relationships, in the adult rat, between levels of blood pressure and nephron number or total renal FSA. METHODS: F1 and F2 offspring were generated from a spontaneously hypertensive rat (SHR)/Wistar Kyoto (WKY) rat cross. Tail-cuff systolic blood pressure was measured twice weekly from 5 to 15 weeks of age and mean arterial blood pressure determined prior to sacrifice. At 15 weeks of age, the rats were perfusion-fixed and glomerular (and thereby nephron) number, glomerular size, total length, and surface area of glomerular capillaries and total renal FSA were determined using unbiased stereologic techniques. RESULTS: In F1 offspring, blood pressure levels were midway between the SHR and WKY rats. Nephron number was significantly higher in the WKY rats compared to the SHR and F1 offspring. However, there was no difference in nephron number between the F1 rats and SHR and no difference in renal FSA between the three groups. In the F2 generation, where there is random segregation of the SHR and WKY genes, there was no significant correlation between either nephron number and adult blood pressure (r2= 0.16, P= 0.11) or total renal FSA and adult blood pressure (r2= 0.02, P= 0.58). There was a significant inverse correlation between nephron number and glomerular size (r2= 0.49, P= 0.0043). CONCLUSION: There is not a direct corollary between nephron number or renal FSA and level of blood pressure in this rat model.     

Time-specific effects of mono-n-butyl phthalate on the transabdominal descent of the testis in rat fetuses

OBJECTIVE: To determine the time-specific effects of mono-n-butyl phthalate (MBP) on the transabdominal migration of the testis in fetal rats. Materials and methods Three groups of pregnant rats were administered MBP by stomach-tube feeding when the fetus was at 7-10 days of gestation in group 1, 11-14 days in group 2, and 15-18 days in group 3; controls (group 4) were given vehicle only from 7-18 days. At 20 days of gestation the fetuses were obtained by Caesarean section, and the position of the testes, the development of the gubernaculum, cranial suspensory ligament and the epididymis were examined. RESULTS: The timed intervals of MBP administration showed that the maximum inhibition of transabdominal testicular descent was at 15-18 days of gestation. There was an elongated gubernaculum and hypertrophic cranial suspensory ligament in the MBP-treated rat fetuses. Furthermore, the epididymis showed a few small ducti deferentia, although there were no remarkable changes in either the Sertoli and Leydig cells in these testes. The mean (SEM) content of testicular testosterone was significantly less (P < 0.001) in the MBP-treated rats, at 50.9 (3.8) pg/testis, than in the controls, at 676 (33.3) pg/testis. CONCLUSIONS: These findings indicate that a brief exposure to MBP during fetal development can inhibit the transabdominal migration of the testis and reduce testosterone content in rats, although the relationship between migration and the testicular testosterone content remains unknown.