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Fetal Lambs (fetal + lamb)
Selected AbstractsSinusoidal heart rate pattern: Reappraisal of its definition and clinical significanceJOURNAL OF OBSTETRICS AND GYNAECOLOGY RESEARCH (ELECTRONIC), Issue 3 2004Houchang D. Modanlou Abstract Objectives: To address the clinical significance of sinusoidal heart rate (SHR) pattern and review its occurrence, define its characteristics, and explain its physiopathology. Background: In 1972, Manseau et al. and Kubli et al. described an undulating wave form alternating with a flat or smooth baseline fetal heart rate (FHR) in severely affected, Rh-sensitized and dying fetuses. This FHR pattern was called ,sinusoidal' because of its sine waveform. Subsequently, Modanlou et al. described SHR pattern associated with fetal to maternal hemorrhage causing severe fetal anemia and hydrops fetalis. Both Manseau et al. and Kubli et al. stated that this particular FHR pattern, whatever its pathogenesis, was an extremely significant finding that implied severe fetal jeopardy and impending fetal death. Undulating FHR pattern: Undulating FHR pattern may be due to the following: (1) true SHR pattern; (2) drugs; (3) pre-mortem FHR pattern; (4) pseudo-SHR pattern; and (5) equivocal FHR patterns. Fetal conditions associated with SHR pattern: SHR pattern has been reported with the following fetal conditions: (1) severe fetal anemia of several etiologies; (2) effects of drugs, particularly narcotics; (3) fetal asphyxia/hypoxia; (4) fetal infection; (5) fetal cardiac anomalies; (6) fetal sleep cycles; and (7) sucking and rhythmic movements of fetal mouth. Definition of true SHR pattern: Modanlou and Freeman proposed the following definition for the interpretation of true SHR pattern: (a) stable baseline FHR of 120,160 bpm; (b) amplitude of 5,15 bpm, rarely greater; (c) frequency of 2,5 cycles per minute; (d) fixed or flat short-term variability; (e) oscillation of the sinusoidal wave from above and below a baseline; and (f) no areas of normal FHR variability or reactivity. Physiopathology: Since its early recognition, the physiopathology of SHR became a matter of debate. Murata et al. noted a rise of arginine vasopressin levels in the blood of posthemorrhagic/anemic fetal lamb. Further works by the same authors revealed that with chemical or surgical vagotomy, arginine vasopressin infusion produced SHR pattern, thus providing the role of autonomic nervous system dysfunction combined with the increase in arginine vasopressin as the etiology. Conclusion: SHR is a rare occurrence. A true SHR is an ominous sign of fetal jeopardy needing immediate intervention. The correct diagnosis of true SHR pattern should also include fetal biophysical profile and the absence of drugs such as narcotics. [source] Antenatal urodynamic studies in the fetal lamb: experimental protocol and preliminary resultsPRENATAL DIAGNOSIS, Issue 3 2003Renaud de Tayrac Abstract Objectives To set up a fetal lamb model for intrauterine fetal urodynamic studies. Methods Fourteen fetal lambs underwent placement of a bladder catheter at a mean gestational age of 87 days. Three fetuses also had a partial urethral obstruction by the simultaneous placement of a peri-urethral constricting ring. Urodynamic and ultrasound studies were performed weekly by the filling cystometry method. Results Hundred and six voiding cycles were recorded during 25 urodynamic studies between 84- and 133-days gestation. All voiding profiles were biphasic with a mean duration of 4.2 min (range 1,10), a mean voiding pressure of 23 cm of water (range 7,33) and a mean periodicity of 19.2 min (range 11,50). The obstructed animals had bladder overactivity. This correlated with ultrasound and post-mortem findings of megacystis and bilateral hydroureteronephrosis. The fetal mortality rate was 85.7% and the mean duration of survival post surgery was 45 ± 5.7 days. Conclusion Serial urodynamic studies could be performed in a fetal lamb model. Following partial urethral obstruction, bladder overactivity was observed. Copyright © 2003 John Wiley & Sons, Ltd. [source] Lentivirus vector-mediated gene transfer to the developing bronchiolar airway epithelium in the fetal lambTHE JOURNAL OF GENE MEDICINE, Issue 6 2007Ze-Yan Yu Abstract Background Development of effective and durable gene therapy for treatment of the respiratory manifestations of cystic fibrosis remains a formidable challenge. Obstacles include difficulty in achieving efficient gene transfer to mature airway epithelium and the need to stably transduce self-renewing epithelial progenitor cells in order to avoid loss of transgene expression through epithelial turnover. Targeting the developing airway epithelium during fetal life offers the prospect of circumventing these challenges. Methods In the current study we investigated vesicular stomatitis virus glycoprotein (VSVg)-pseudotyped HIV-1-derived lentivirus vector-mediated gene transfer to the airway epithelium of mid-gestation fetal lambs, both in vitro and in vivo. In the in vitro studies epithelial sheet explants and lung organ culture were used to examine transduction of the proximal and more distal airway epithelium, respectively. For the in vivo studies, vector was delivered directly into the proximal airway. Results We found that even during the early pseudoglandular and canalicular phases of lung development, occurring through mid-gestation, the proximal bronchial airway epithelium was relatively mature and highly resistant to lentivirus-mediated transduction. In contrast, the more distal bronchiolar airway epithelium was relatively permissive for transduction although the absolute levels achieved remained low. Conclusion This result is promising as the bronchiolar airway epithelium is a major site of pathology in the cystic fibrosis airway, and much higher levels of transduction are likely to be achieved by developing strategies that increase the amount of vector reaching the more distal airway after intratracheal delivery. Copyright © 2007 John Wiley & Sons, Ltd. [source] Myocardial growth before and after birth: clinical implications,ACTA PAEDIATRICA, Issue 2 2000AM Rudolph Perinatal changes in myocardial growth have recently evoked considerable interest with regard to cardiac chamber development with congenital cardiac lesions and to myocardial development in preterm infants. It is suggested that cardiac chamber development is influenced by blood flow. Experimental pulmonary stenosis in fetal lambs may induce either greatly reduced or markedly increased right ventricular volume. Ventricular enlargement appears to be associated with a large ventricular volume load resulting from tricuspid valve regurgitation. A small competent tricuspid valve is associated with reduced flow through the ventricle due to outflow obstruction and a small right ventricle. Postnatal growth of the ventricles in congenital heart disease is discussed. Increase in myocardial mass prenatally is achieved by hyperplasia, both during normal development and when myocardial mass is increased by right ventricular outflow obstruction. Postnatally, increases in myocardial mass with normal growth, as well as with ventricular outflow obstruction, are largely due to hypertrophy of myocytes. Myocardial capillary numbers do not increase in proportion with myocyte numbers in ventricular myocardium in association with outflow obstruction. The postnatal effects of these changes in congenital heart lesions are considered. Studies in fetal lambs suggest that the late gestational increase in blood cortisol concentrations is responsible for the change in the pattern of myocardial growth after birth. The concern is raised that prenatal exposure of the premature infant to glucocorticoids, administered to the mother to attempt to prevent hyaline membrane disease in the infant, may inhibit myocyte proliferation and result in a heart with fewer than normal myocytes. This would necessitate that each myocyte would have to hypertrophy abnormally to achieve a normal cardiac mass postnatally. [source] Sporadic fetal heart rate decelerations associated with electrocortical changes in fetal lambsJOURNAL OF OBSTETRICS AND GYNAECOLOGY RESEARCH (ELECTRONIC), Issue 2 2006Keiya Fujimori Abstract Aim: The purpose of this study was to determine a relationship between sporadic fetal heart rate (FHR) decelerations and fetal electrocortical changes in physiologically normal sheep fetuses. Materials and Methods: A total of 20 experimental observations were conducted on eight chronically instrumented fetal lambs. For electrocorticogram (ECoG) recording, two stainless steel electrodes were implanted bilaterally on the fetal parietal skull. Classifications of ECoG tracings were visually divided into periods of low, high, intermediate and transitional voltage. During day and night observations, sporadic FHR decelerations related to fetal ECoG changes were counted. Results: We found that 65% of the total sporadic FHR decelerations occurred in relation to fetal ECoG changes. The largest number of sporadic FHR decelerations was associated with a switch from low voltage to high voltage ECoG (37%). However, the greatest frequency of sporadic FHR decelerations occurred during intermediate ECoG periods (34%). Conclusion: The majority of sporadic FHR decelerations observed in physiologically normal sheep fetuses were associated with fetal ECoG changes. [source] Neuronal nitric oxide synthase does not contribute to the modulation of pulmonary vascular tone in fetal lambs with congenital diaphragmatic hernia (nNOS in CDH lambs),PEDIATRIC PULMONOLOGY, Issue 4 2008Anthony S. de Buys Roessingh MD Abstract Aim The aim of this study was to determine the presence of the neuronal nitric oxide synthase (nNOS) in near full-term lambs with congenital diaphragmatic hernia (CDH) and its role in the modulation of pulmonary vascular basal tone. Methods We surgically created diaphragmatic hernia on the 85th day of gestation. On the 135th, catheters were used to measure pulmonary pressure and blood flow. We tested the effects of 7-nitroindazole (7-NINA), a specific nNOS antagonist and of N -nitro- l -arginine (l -NNA), a nonspecific nitric oxide synthase antagonist. In vitro, we tested the effects of the same drugs on isolated pulmonary vessels. The presence of nNOS protein in the lungs was detected by Western blot analysis. Results Neither 7-NINA nor l -NNA modified pulmonary vascular basal tone in vivo. After l -NNA injection, acetylcholine (ACh) did not decrease significantly pulmonary vascular resistance (PVR). In vitro, l -NNA increased the cholinergic contractile-response elicited by electric field stimulation (EFS) of vascular rings from lambs with diaphragmatic hernia. Conclusion We conclude that nNOS protein is present in the lungs and pulmonary artery of near full-term lamb fetuses with diaphragmatic hernia, but that it does not contribute to the reduction of pulmonary vascular tone at birth. Pediatr Pulmonol. 2008; 43:313,321. © 2008 Wiley-Liss, Inc. [source] Antenatal urodynamic studies in the fetal lamb: experimental protocol and preliminary resultsPRENATAL DIAGNOSIS, Issue 3 2003Renaud de Tayrac Abstract Objectives To set up a fetal lamb model for intrauterine fetal urodynamic studies. Methods Fourteen fetal lambs underwent placement of a bladder catheter at a mean gestational age of 87 days. Three fetuses also had a partial urethral obstruction by the simultaneous placement of a peri-urethral constricting ring. Urodynamic and ultrasound studies were performed weekly by the filling cystometry method. Results Hundred and six voiding cycles were recorded during 25 urodynamic studies between 84- and 133-days gestation. All voiding profiles were biphasic with a mean duration of 4.2 min (range 1,10), a mean voiding pressure of 23 cm of water (range 7,33) and a mean periodicity of 19.2 min (range 11,50). The obstructed animals had bladder overactivity. This correlated with ultrasound and post-mortem findings of megacystis and bilateral hydroureteronephrosis. The fetal mortality rate was 85.7% and the mean duration of survival post surgery was 45 ± 5.7 days. Conclusion Serial urodynamic studies could be performed in a fetal lamb model. Following partial urethral obstruction, bladder overactivity was observed. Copyright © 2003 John Wiley & Sons, Ltd. [source] Lentivirus vector-mediated gene transfer to the developing bronchiolar airway epithelium in the fetal lambTHE JOURNAL OF GENE MEDICINE, Issue 6 2007Ze-Yan Yu Abstract Background Development of effective and durable gene therapy for treatment of the respiratory manifestations of cystic fibrosis remains a formidable challenge. Obstacles include difficulty in achieving efficient gene transfer to mature airway epithelium and the need to stably transduce self-renewing epithelial progenitor cells in order to avoid loss of transgene expression through epithelial turnover. Targeting the developing airway epithelium during fetal life offers the prospect of circumventing these challenges. Methods In the current study we investigated vesicular stomatitis virus glycoprotein (VSVg)-pseudotyped HIV-1-derived lentivirus vector-mediated gene transfer to the airway epithelium of mid-gestation fetal lambs, both in vitro and in vivo. In the in vitro studies epithelial sheet explants and lung organ culture were used to examine transduction of the proximal and more distal airway epithelium, respectively. For the in vivo studies, vector was delivered directly into the proximal airway. Results We found that even during the early pseudoglandular and canalicular phases of lung development, occurring through mid-gestation, the proximal bronchial airway epithelium was relatively mature and highly resistant to lentivirus-mediated transduction. In contrast, the more distal bronchiolar airway epithelium was relatively permissive for transduction although the absolute levels achieved remained low. Conclusion This result is promising as the bronchiolar airway epithelium is a major site of pathology in the cystic fibrosis airway, and much higher levels of transduction are likely to be achieved by developing strategies that increase the amount of vector reaching the more distal airway after intratracheal delivery. Copyright © 2007 John Wiley & Sons, Ltd. [source] |