Browsing by Author "Correia-Pinto, J."
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- In utero meconium exposure increases spinal cord necrosis in a rat model of myelomeningocelePublication . Correia-Pinto, J.; Reis, J.; Hutchins, G.; Baptista, M.; Estevão-Costa, J.; Flake, A.; Leite-Moreira, A.Abstract BACKGROUND/PURPOSE: The rationale for in utero repair of myelomeningocele has been supported experimentally by the observation of preserved neural function after prenatal closure of surgically created defects compared with nonrepaired controls. The mechanism of injury to the exposed neural elements is unknown. Postulated mechanisms include trauma to the herniated neural elements or progressive injury from amniotic fluid exposure as gestation proceeds. A component of amniotic fluid that may contribute to neural injury is meconium. In the current study the effect of human meconium on the exposed spinal cord in a fetal rat model of myelomeningocele was examined. METHODS: Twenty time-dated pregnant rats underwent laparotomy at 181/2 days of gestation. The exposed uterus was bathed in ritrodrine for tocolysis. The amniotic cavity was opened over the dorsal midline of the fetal rat, and, under a dissecting microscope (x25), a 2- to 3-level laminectomy was performed. Under magnification (x40), the translucent dura was opened using a 25-gauge needle as a knife. Two fetuses per dam were operated on. In the control group, the amniotic fluid was restored with saline solution, whereas in the experimental group a solution of Human meconium diluted (10%) in saline was used to restore the amniotic fluid. Fetuses were harvested by cesarean section at 211/2 days' gestational age. The liveborn pups were then killed and fixed in 10% formaline. Sections 10 micrometer thick were stained with H&E and studied by light microscopy for evidence of spinal cord injury. RESULTS: Seven of 20 (35%) experimental rat pups and 6 of 20 (30%) control rat pups were liveborn. All liveborn pups had severe paralysis of the hindlimbs and tail, so that functional differences between the 2 groups could not be detected. Histologic examination of 13 spinal cords at the site of surgical exposure showed that necrosis of neural tissue in 5 of 7 meconium-exposed rat pups was increased when compared with that observed in the 6 fetuses exposed to amniotic fluid without meconium. In general, inflammation was greater and repair processes appeared delayed in meconium-exposed rat pups. CONCLUSIONS: Exposure of the spinal cord of fetal rats to amniotic fluid by surgically created myelomeningocele leads to severe functional impairment. Histologically recognizable necrosis of neural elements was increased in those animals that were exposed to diluted human meconium in the amniotic fluid. The results support the hypothesis that meconium may contribute to the pathophysiology of spinal cord injury observed in myelomeningocele.
- In utero topographic analysis of astrocytes and neuronal cells in the spinal cord of mutant mice with myelomeningocele.Publication . Reis, J.L.; Correia-Pinto, J.; Monteiro, M.P.; Hutchins, G.M.Abstract OBJECT: Myelomeningocele (MMC) is the most severe form of spina bifida causing severe neurological deficits. Injury to the placode has been attributed to in utero aggression. In this study, glial and neuronal cell changes in both number and topography in mice with MMC were investigated during gestation. METHODS: The curly tail/loop-tail mice model of MMC was used, and fetuses were harvested using caesarean surgery at Days 14.5, 16.5, and 18.5 (full gestation at 19 days). Immunohistochemical analyses of the MMC placodes and the normal spinal cords from the control group were performed using anti-glial fibrillary acidic protein (astrocytes) and mouse anti-neuronal nuclear (neurons) antibodies. Light microscopy was used along with computer-assisted morphometric evaluation. Progressive increases in astrocytes in the spinal cord of all mouse fetuses were found between Days 14.5 and 18.5 of gestation. This increase was significantly higher in the placodes of mice with MMC than in those of normal mice, particularly in the posterior region. Neuronal labeling at Day 14.5 of gestation was similar between mice with MMC and control mice. At Day 16.5 of gestation there was a deterioration of neural tissue in MMC fetuses, mainly in the posterior region, progressing until the end of gestation with a marked loss of neurons in the entire MMC placode. CONCLUSIONS: This study delineated the quantitative changes in astrocytes and neurons associated with MMC development during the late stages of gestation. The detailed topographic analysis of the MMC defines the timing of the intrauterine insult and how the placode lesions progress. This study supports the current concept of placode protection through in utero surgery for fetuses with MMC. PMID: 17566405 [PubMed - indexed for MEDLINE]
- TRANSESOPHAGEAL RIGHT UPPER PULMONARY LOBECTOMY - IN VIVO PORCINE EXPERIMENTAL STUDYPublication . Moreira-Pinto, J.; Ferreira, A.; Miranda, A.; Rolanda, C.; Correia-Pinto, J.TRANSESOPHAGEAL RIGHT UPPER PULMONARY LOBECTOMY - IN VIVO PORCINE EXPERIMENTAL STUDY João Moreira-Pinto, MD1,2,3; Aníbal Ferreira, MD1,2,4; Alice Miranda, DVM1,2; Carla Rolanda, MD, PhD1,2,4; Jorge Correia-Pinto, MD, PhD1,2,5 1Surgical Sciences Research Domain, Life and Health Sciences Research Institute (ICVS), School of Health Sciences, University of Minho, Braga, Portugal; 2ICVS/3B’s - PT Government Associate Laboratory, Braga/Guimarães, Portugal; 3Pediatric Surgery division, Centro Hospitalar do Porto, Porto, Portugal; 4Department of Gastroenterology, Hospital de Braga, Braga, Portugal; 5Pediatric Surgery division, Hospital de Braga, Braga, Portugal. Background and Study Aims Video-assisted thoracoscopic surgery (VATS) has been widespread as the better approach to carry out pulmonary lobectomy. Natural Orifice Transluminal Endoscopic Surgery (NOTES) is being assessed as an alternative to the transthoracic endoscopic surgery. We designed this study to test the feasibility of peroral transesophageal right upper pulmonary lobectomy with the assistance of a single transthoracic trocar. Material and Methods In ten anesthetized pigs (35-45 Kg), we performed right upper pulmonary lobectomy using a forward viewing single-channel gastroscope (introduced perorally) and an operative thoracoscope with a 5 mm working channel (introduced through a single-transthoracic 10 mm port) (Karl Storz). After introducing the gastroscope throughout an oroesophageal overtube into the esophagus, a 1 cm transverse esophagotomy was carried out in the upper third using an ESD-knife under thoracoscope control. Anatomic dissection of the right upper hilum was performed using flexible (gastroscope) and rigid (thoracoscope) instruments. After individual dissection, right upper pulmonary arteries, veins and correspondent bronchus were independently stapled using a 45-mm long, linear endostapler (EndoPath®, Ethicon Endo-Surgery) introduced through the oroesophageal overtube. After completing the lobe resection using an endoscopic snare with cautery, the specimen was extracted retrogradely through the mouth. The esophagotomy was stitched and tied using Endo Stitch™ (Covidien) and a long knot-pusher, which were handled through the oroesophageal overtube. Results Esophagotomy was performed safely in all animals. Dissection of the right upper lobe hilum elements (arteries, veins and bronchus) was also carried out in all animals without significant problems. Oroesophageal handling of the endostapplers for independent ligation of the hilum elements under transthoracic imaging was surprisingly feasible, reasonably easy to perform and reliable in 7 cases. In two cases ligation of the vessels was en bloc. In one case, severe hemorrhage occurred from incomplete vein ligation, although we could control it using electrocoagulation. Esophagotomy closure was feasible but its reliability was not tested in survival studies. All but one animal were kept alive until the end of the acute experiment when they were sacrificed. Conclusions Transesophageal right upper pulmonary lobectomy using single transthoracic trocar assistance is feasible and it may represent a step towards scarless pulmonary lobectomy. Additional survival studies are necessary to test the reliability of this procedure. Apresentador: João Moreira-Pinto, Médico Interno de Cirurgia Pediátrica, CHP.
- Vascular and apoptotic changes in the placode of myelomeningocele mice during the final stages of in utero developmentPublication . Reis, J.L.; Correia-Pinto, J.; Monteiro, M.P.; Costa, M.; Hutchins, G.M.JOAQUIM L. REIS, M.D., PH.D.,1,2 JORGE CORREIA-PINTO, M.D., PH.D.,3,4 MARIANA P. MONTEIRO, M.D., PH.D.,1 MADALENA COSTA, B.SC.,1 AND GROVER M. HUTCHINS, M.D.5 1Department of Anatomy, Abel Salazar Institute for the Biomedical Sciences and Unit for Multidisciplinary Biomedical Research, University of Porto; 2Department of Neurosurgery, Santo António General Hospital; 4Department of Pediatric Surgery, São João Hospital, Porto; 3Life and Health Sciences Research Institute, School of Health Sciences, University of Minho, Braga, Portugal; and 5Department of Pathology, Johns Hopkins School of Medicine, Baltimore, Maryland Object. Myelomeningocele (MMC) is a primary neurulation defect that is associated with devastating neurological disabilities in affected newborns. To better characterize the in utero neurodegenerative process of MMC, the authors investigated the changes in vascular organization, apoptosis, and the presence of inflammatory cells during gestation by using a mutant mouse model of MMC. Methods. The curly tail/loop tail (ct/lp) mutant mouse model of MMC was chosen to obtain fetuses at different stages of gestation. Mouse fetuses harboring MMC were harvested by caesarean section at embryonic Days 14.5, 16.5, and 18.5 (complete mouse gestation at 19 days, 6 mice/group); littermate fetuses with the same gestational age but without an MMC were used as controls. Samples of the MMC placode or normal spinal cord were stained for immunocytochemical labeling with caveolin antibody (endothelium marker) and activated caspase-3 antibody (apoptosis marker). Samples were morphometrically analyzed with a computer-assisted image analyzer. Results. The MMC mice presented with an increase in vascular density from embryonic Days 16.5–18.5 and an enhanced number of apoptotic cells at embryonic Day 18.5, compared with controls. There were scarce signals of an inflammatory reaction in the MMC placode, as a few infiltrating neutrophils were seen only at embryonic Day 18.5. Conclusions. Fetal placodes in MMC mice showed evidence of increased vascular density since embryonic Day 16.5 and increased apoptosis at embryonic Day 18.5. These new data support the view that in utero changes of the MMC placode, occurring during the last stages of gestation, contribute to the neuropathological manifestations in fullterm newborns with MMC. (DOI: 10.3171/PED/2008/2/8/150)