Acute and chronic mammary periprosthetic histological changes of the muscle.

Background: Augmentation mammoplasty with subpectoral prosthesis implantation is a frequent performed procedure in plastic surgery for reconstructive and aesthetic purposes. Although prosthesis implantation in a pocket under the major pectoralis muscle has been related to volumetric and functional alterations, there is not much information about the associated short- and long-term histological changes. Therefore, the aim of our study was to describe the acute and chronic histological muscle alterations associated with subpectoral prosthesis implantation. Materials and Method: We collected samples from patients with breast tissue expander (<6 months after implantation) and prosthesis (>1 year after implantation) and from patients without implantation as a control group. The samples were processed for assessing their histological, histochemical and immunohistochemical properties. Results: In the control group, no relevant histological findings were identified. Additionally, in the patients with expander, we observed mild augmentation of the internalised nuclei, normal morphology, significant muscle atrophy and fibrosis, whereas in the patients with prosthesis considerable augmentation of internalised nuclei, significant muscle atrophy, fibrosis and alteration of normal muscle morphology were observed. Conclusion: Prosthesis implantation induces histological changes in the periprosthetic striated muscle. Chronic fibrosis and inflammation play key roles in this process, which should be characterised in more detail from the histological and molecular biological perspective.

Utilidad de la ECMO sobre el injerto pulmonar disfuncionante en un modelo porcino estandarizado de trasplante unipulmonar / [Usefulness of ECMO on dysfunctional lung graft in a standardized porcine model of one-lung transplant]

Objetivo: Establecer un modelo de muerte encefálica y trasplante pulmonar y analizar el posible papel protector del oxigenador de membrana extracorpóreo (ECMO).Métodos: Se emplearon 20 cerdos hembras, 10 donantes y 10 receptoras. Las receptoras del Grupo A (n = 5) fueron sometidas a un trasplante unipulmonar izquierdo (Tx-UPI) sin ECMO. Las receptoras del Grupo B (n = 5) se sometieron a un Tx-UPI con ECMO venoarterial (ECMO-VA). Se recopilaron datos funcionales e histológicos en situación basal, a los 10 minutos de clampar el hilio derecho (Tiempo 1) y a las 2 horas (Tiempo 2). Se analizó la expresión proteica de marcadores de inflamación y de la ruta de hipoxia.Resultados: El modelo de muerte encefálica empleado, seguido de un tiempo de isquemia frío prolongado (20 horas) dio lugar a la aparición de un edema pulmonar severo. Tras el implante, 3 receptores del grupo A sobrevivieron hasta el Tiempo 2, falleciendo 2 por edema pulmonar masivo. Por el contrario, todos los animales del Grupo B sobrevivieron, siendo la PaO2 en ese momento de 462,72 mmHg. Hubo un incremento de la expresión de IL6, TNF, PCR, AC IX y el VEGF, así como un descenso en la expresión de IL8 y GLUT1, al usar la ECMO.Conclusiones: Se ha desarrollado un modelo porcino estandarizado y reproducible de muerte encefálica, que simula el proceso clínico de la donación pulmonar. Este modelo puede servir de plataforma para investigar posibles dianas terapéuticas. (AU)

Objective: Establish a model of brain death and lung transplantation and analyze the possible protective role of extracorporeal membrane oxygenation (ECMO).Methods: 20 female pigs were used, 10 donors and 10 recipients. Group A recipients (n = 5) underwent left-sided single- lung transplantation (LUCT-Tx) without ECMO. Group B recipients (n = 5) underwent ICU-Tx with venoarterial ECMO (VA-ECMO). Functional and histological data were collected at baseline, 10 minutes after clamping the right hilum (Time 1) and 2 hours (Time 2). Protein expression of inflammation markers and the hypoxia pathway was analyzed.Results: The brain death model used, followed by a prolonged cold ischemia time (20 hours) gave rise to the appearance of severe pulmonary edema. After implantation, 3 group A recipients survived until Time 2, with 2 dying from massive pulmonary edema. In contrast, all the animals in Group B survived, with PaO2 at that time being 462.72 mmHg. There was an increase in the expression of IL6, TNFα, CRP, AC IX and VEGF, as well as a decrease in the expression of IL8 and GLUT1, when using ECMO.Conclusions: A standardized and reproducible porcine model of brain death has been developed, which simulates the clinical process of lung donation. This model can serve as a platform to investigate possible therapeutic targets. (AU)