Gastrostomia e jejunostomia: aspectos da evolução técnica e da ampliação das indicações

O acesso à luz do estômago e do jejuno proximal por meio de gastrostomia e jejunostomia, respectivamente, de forma temporária ou definitiva, está indicado diante da necessidade prolongada de descompressão digestiva ou de suporte alimentar. O emprego desses procedimentos expandiu-se nos últimos25 anos com a introdução da gastrostomia endoscópica, especialmente em pacientes com afecçõesneurológicas de evolução progressiva e neoplasias avançadas. Este artigo aborda aspectos conceituaisda gastrostomia e jejunostomia, as principais indicações, as vias de acesso preferenciais em diferentes cenários clínicos e as modalidades técnicas frequentemente empregadas. O manejo dessasestomias, os resultados e as potenciais complicações também são enfatizados. Finalmente, os fundamentos éticos e legais da ampliação da indicação da gastrostomia e da jejunostomia como procedimentos paliativos são discutidos.A temporary or permanent access to the stomach or jejunum, through a gastrostomy or jejunostomy, isindicated whenever nutritional support or prolonged decompression of the upper alimentary tract isneeded.  With the introduction of endoscopic gastrostomy, the utilization of these procedures has increased in the last 25 years, specially in patients with progressive neurologic diseases and in those withadvanced cancer.  This article deals with the conceptual aspects of gastrostomies and jejunostomies, itsprimary indications, the preferential means of access in different clinical scenarios as well as the technical modalities most frequently used.  The management of the stomas, the results and potential complications are also highlighted. Finally, the ethical and legal implications of greater utilization of theseprocedures in a palliative setting are also discussed

Ethanol intake-induced apoptosis in glial cells and axonal disorders in the cerebellar white matter of UChA rats (voluntary ethanol consumers)

Ethanol intake may cause alterations in cellular metabolism altering motricity, learning and cognition. The cerebellum is one of the most susceptible organs to ethanol-related disorders during development, and is associated with oxidative stress-induced apoptosis being crucial for pathogenic consequences. The UChA variety is a special strain of Wistar rat genetically selected and represents a rare model for the studies related to genetic, biochemical, physiological, nutritional, and pharmacological effects of ethanol. We evaluated the structure and apoptosis in the cerebellar white matter of UChA rats. There were two groups of 09 rats: a control group that did not consume ethanol, and an experimental group of UChA rats that consumed ethanol at 10% (v/v) (<2 g ethanol/kg body weight/day). At 120 days old, rats were anaesthetized followed by decapitation, and their cerebella were collected and fixed. Cerebellar sections were subjected to immunohistochemistry for Caspase-3 and XIAP and transmission electron microscopy (TEM). The UChA group showed more glial cells immunoreactive for caspase-3 and less for XIAP than control group. Alcohol consumption affected myelin integrity. Severe ultrastructural damages in UChA group were observed such as disruption of the myelin sheath, disorganization and deformation of its components, and an increase in the interaxonal spaces. In conclusion, our data demonstrated that ethanol induced apoptosis in the glial cells and promoted an intense change in the myelin sheath of UChA rats, which may cause functional disorders.Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP

Apoptosis of Purkinje and Granular Cells of the Cerebellum Following Chronic Ethanol Intake

Ethanol alters motricity, learning, cognition, and cellular metabolism in the cerebellum. We evaluated the effect of ethanol on apoptosis in Golgi, Purkinje, and granule cells of the cerebellum in adult rats. There were two groups of 20 rats: a control group that did not consume ethanol and an experimental group of UChA rats that consumed ethanol at 10 % (<2 g ethanol/kg body weight/day). At 120 days old, rats were anesthetized and decapitated, and their cerebella were collected and fixed. Cerebellar sections were subjected to immunohistochemistry for terminal deoxynucleotide transferase dUTP nick end labeling (TUNEL), caspase-3, X-linked inhibitor of apoptosis protein (XIAP), and insulin-like growth factor 1-receptor (IGF-1R); real-time PCR (RT-PCR) to determine caspase-3, XIAP, and IGF-1R gene expression; and transmission electron microscopy (TEM). We identified fragmentation of DNA and an increase in caspase-3 protein and XIAP in Purkinje cells, whereas granule cells exhibited increased caspase-3 and XIAP. IGF-1R expression was unchanged. There was no significant difference in gene expression of caspase-3, XIAP, and IGF-1R. There were an increase in lipid droplets, a reduction in the cellular cytoplasm in electrondense nuclei, and changes in the myelin sheath in the cerebellar cortex. In conclusion, our data demonstrated that ethanol induced apoptosis in the Purkinje and granule cells of the cerebellum of adult UChA rats.Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP

Nitric Oxide Synthase in Heart and Thoracic Aorta After Liver Ischemia and Reperfusion Injury: An Experimental Study in Rats

Objectives: We tested the effects of liver reperfusion in the immunohistochemical expression of nitric oxide synthase on the thoracic aorta and the heart. Materials and Methods: We randomized 24 male Wistar rats into 3 groups: (1) control; (2) R2 group, with 60 minutes of partial (70%) liver ischemia and 2 hours of global liver reperfusion; (3) and R6 group, with 60 minutes of partial liver ischemia and 6 hours of global liver reperfusion. Results: In the heart, there was little, diffuse immunohistochemical endothelial staining; immunohistochemical inducible nitric oxide synthase staining was expressed in the adventitia layer of intramyocardial vessels in both cases, with a time-dependent but not statistically significant increase. In the thoracic aorta, a time-dependent decrease in endothelial nitric oxide synthase expression in the muscular layer after reperfusion, which was statistically significant in R6 versus the control. Positive immunostaining for inducible nitric oxide synthase was seen in the muscular and endothelial layers, and this varied from moderate in the control group, to light in the endothelium in groups R2 and R6. Conclusions: We observed changes that may be implicated in heart injury and impairment of aortal tone after liver ischemia and reperfusion injury