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A reação inflamatória nas meninges desencadeada pela punção subaracnoidea através da pele tatuada pode evoluir para aracnoidite adesiva?Silva, Ronaldo Antonio da. January 2019 (has links)
Orientador: Eliana Marisa Ganem / Resumo: Justificativa e objetivo: Cada vez mais o anestesiologista se depara com a necessidade de decidir por realizar ou não bloqueio de neuroeixo através da pele tatuada, já que o número de pessoas com tatuagem tem aumentado. Neste estudo foi avaliado se a punção subaracnoidea sobre área tatuada provoca alterações inflamatórias agudas nas meninges e medula espinal e se pode evoluir para aracnoidite adesiva. Material e Método: 42 coelhos machos foram divididos, aleatoriamente, em 3 grupos de 14 animais: G1, punção subaracnoidea através de pele não tatuada e injeção de solução salina, cativeiro 30 dias; G2, punção subaracnoidea através de pele tatuada e injeção de solução salina, cativeiro 30 dias; G3, punção subaracnoidea através de pele tatuada e injeção de solução salina, cativeiro 360 dias. Os animais foram anestesiados com cloridrato de xilazina e cloridrato de cetamina e realizou se punção subaracnoidea, guiada por ultrassom, no espaço intervertebral entre S1 – S2, com injeção de solução salina 0,2mL. Após período de cativeiro os animais foram sacrificados, sob anestesia, por decapitação e a porção lombossacra da medula espinal foi removida para análise histológica. Resultados: Nenhuma alteração histológica foi encontrada nos animais do grupo 1. Onze animais do grupo 2 apresentaram focos de infiltrado inflamatório linfocitário perivascular na pia-máter e/ou aracnoide. No grupo 3, oito coelhos apesentaram infiltrado inflamatório linfocitário ou linfoplasmocitário perivascular e ... (Resumo completo, clicar acesso eletrônico abaixo) / Abstract: Background and Objectives: As the number of people with tattoos has been increasing, anesthesiologists are more and more faced with the decision to perform a neuraxial blockage through tattooed skin. In this study, we evaluated the possibility of puncture through tattooed skin determines acute inflammatory changes in the meninges and spinal cord and later evolve into adhesive arachnoiditis. Method: Forty-two male rabbits were randomized into 3 equal groups of 14: G1, spinal puncture through non-tattooed skin and saline solution injection; G2, spinal puncture through tattooed skin and saline solution injection, captive for 30 days; G3, spinal puncture through tattooed skin and saline solution injection, captive for 360 days. The animals were anesthetized and ultrasound-guided spinal puncture was performed in the intervertebral spaces between S1–S2. During the period of captivity, the animals were clinically assessed for sensitivity and motor function. After that, they were sacrificed and the lumbosacral portion of the spinal cord was excised for histological analysis. Results: No histological changes were found on group 1. Eleven animals from group 2 presented with foci of perivascular lymphocytic inflammatory infiltrate in the pia mater and/or arachnoid. In Group 3, 8 rabbits presented with inflammatory changes in the meninges, which were associated with thickening and/or adhesion of the pia mater and arachnoid in some cases and 5 rabbits presented only thickening of pia-mate... (Complete abstract click electronic access below) / Doutor
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Evaluation of the Use of a Bioengineered Hydrogel Containing Hyaluronan to Reduce Inflammation and Scarring following Spinal Cord Injury Associated with ArachnoiditisAustin, James W. 10 December 2012 (has links)
Background: Spinal cord injury (SCI) is heterogeneous in nature and can be complicated by inflammation and scarring in the subarachnoid space (arachnoiditis). The constellation of traumatic injury and arachnoiditis can lead to extensive intraparenchymal cysts or post-traumatic syringomyelia (PTS), due to alterations in fluid flow and pressure dynamics in the subarachnoid space.
Hypothesis: Intrathecal injection of a bioengineered hydrogel containing hyaluronan (HA) will improve functional recovery following severe spinal cord injury associated with arachnoiditis.
Methods: Acute to subacute pathophysiological events were characterized in non-injured sham rats, rats receiving a clip compression/contusion injury (SCI), rats receiving an intrathecal kaolin injection (Arachnoiditis) and in rats receiving SCI plus kaolin injection (PTS). Next, a HA containing hydrogel (HAMC) or artificial cerbralspinal fluid (aCSF) control was injected into the subarachnoid space 24 hours following PTS injury. To assess treatment efficacy, subacute pathophysiology was assessed as was long-term neurobehavioural and neuroanatomical recovery. Finally, in vitro studies examined the effect of HA on TLR4 activation using lipopolysaccharide in primary rat microglial cultures.
Results: PTS animals exhibited a greater parenchymal injury response as compared to the sum of SCI alone or arachnoiditis alone. Injection of HAMC reduced the extent of scarring and inflammation in the subarachnoid space and improved neurobehavioural and neuroanatomical recovery relative to aCSF controls. These improvements were associated with reduced chondroitin sulfate proteoglycan and IL-1α expression and a trend towards and axonal preservation. In vitro studies demonstrated that HA is capable of reducing TLR4 mediated inflammation in microglia.
Conclusions: Acute arachnoiditis potentiates the intensity of intraparenchymal inflammatory and scarring events following SCI. When HAMC was injected intrathecally following PTS injury, it mitigated some of the pernicious effects of arachnoiditis. Part of the therapeutic action of HAMC can be attributed to the ability of HA to reduce TLR4 mediated inflammation in microglia, possibly through an extracellular mechanism.
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Evaluation of the Use of a Bioengineered Hydrogel Containing Hyaluronan to Reduce Inflammation and Scarring following Spinal Cord Injury Associated with ArachnoiditisAustin, James W. 10 December 2012 (has links)
Background: Spinal cord injury (SCI) is heterogeneous in nature and can be complicated by inflammation and scarring in the subarachnoid space (arachnoiditis). The constellation of traumatic injury and arachnoiditis can lead to extensive intraparenchymal cysts or post-traumatic syringomyelia (PTS), due to alterations in fluid flow and pressure dynamics in the subarachnoid space.
Hypothesis: Intrathecal injection of a bioengineered hydrogel containing hyaluronan (HA) will improve functional recovery following severe spinal cord injury associated with arachnoiditis.
Methods: Acute to subacute pathophysiological events were characterized in non-injured sham rats, rats receiving a clip compression/contusion injury (SCI), rats receiving an intrathecal kaolin injection (Arachnoiditis) and in rats receiving SCI plus kaolin injection (PTS). Next, a HA containing hydrogel (HAMC) or artificial cerbralspinal fluid (aCSF) control was injected into the subarachnoid space 24 hours following PTS injury. To assess treatment efficacy, subacute pathophysiology was assessed as was long-term neurobehavioural and neuroanatomical recovery. Finally, in vitro studies examined the effect of HA on TLR4 activation using lipopolysaccharide in primary rat microglial cultures.
Results: PTS animals exhibited a greater parenchymal injury response as compared to the sum of SCI alone or arachnoiditis alone. Injection of HAMC reduced the extent of scarring and inflammation in the subarachnoid space and improved neurobehavioural and neuroanatomical recovery relative to aCSF controls. These improvements were associated with reduced chondroitin sulfate proteoglycan and IL-1α expression and a trend towards and axonal preservation. In vitro studies demonstrated that HA is capable of reducing TLR4 mediated inflammation in microglia.
Conclusions: Acute arachnoiditis potentiates the intensity of intraparenchymal inflammatory and scarring events following SCI. When HAMC was injected intrathecally following PTS injury, it mitigated some of the pernicious effects of arachnoiditis. Part of the therapeutic action of HAMC can be attributed to the ability of HA to reduce TLR4 mediated inflammation in microglia, possibly through an extracellular mechanism.
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