Revue: | Annals of hepatology |
Base de datos: | PERIÓDICA |
Número de sistema: | 000411685 |
ISSN: | 1665-2681 |
Autores: | Nedredal, Geir I1 Elvevold, Kjetil2 Chedid, Marcio F3 Ytrebo, Lars M4 Rose, Christopher F5 Sen, Sambit6 Smedsrod, Bard2 Jalan, Rajiv7 Revhaug, Arthur1 |
Instituciones: | 1University Hospital of Northern Norway, Department of Digestive Surgery, Troms, Tromso. Noruega 2University of Tromso, Department of Medical Biology, Troms, Tromso. Noruega 3Hospital de Clinicas de Porto Alegre, Unidade de Cirurgia, Porto Alegre, Rio Grande do Sul. Brasil 4University Hospital of Northern Norway, Department of Anesthesia and Intensive Care, Troms, Tromso. Noruega 5Universite de Montreal, Hepato-Neuro Laboratory, Montreal, Quebec. Canadá 6Luton & Dunstable University Hospital, Department of Gastroenterology, Luton. Reino Unido 7Royal Free Hospital, Institute of Liver and Digestive Health, Londres. Reino Unido |
Año: | 2016 |
Periodo: | May-Jun |
Volumen: | 15 |
Número: | 3 |
Paginación: | 427-435 |
País: | México |
Idioma: | Inglés |
Tipo de documento: | Artículo |
Enfoque: | Experimental, analítico |
Resumen en inglés | Pulmonary complications are common in acute liver failure (ALF). The role of the lungs in the uptake of harmful soluble endogenous macromolecules was evaluated in a porcine model of ALF induced by hepatic devascularization (n = 8) vs. controls (n = 8). In additional experiments, pulmonary uptake was investigated in healthy pigs. Fluorochrome-labeled modified albumin (MA) was applied to investigate the cellular uptake. Results. Results. As Results. compared to controls, the ALF group displayed a 4-fold net increased lung uptake of hyaluronan, and 5-fold net increased uptake of both tissue plasminogen activator and lysosomal enzymes. Anatomical distribution experiments in healthy animals revealed that radiolabeled MA uptake (taken up by the same receptor as hyaluronan) was 53% by the liver, and 24% by the lungs. The lung uptake of LPS was 14% whereas 60% remained in the blood. Both fluorescence and electron microscopy revealed initial uptake of MA by pulmonary endothelial cells (PECs) with later translocation to pulmonary intravascular macrophages (PIMs). Moreover, the presence of PIMs was evident 10 min after injection. Systemic inflammatory markers such as leukopenia and increased serum TNF-α levels were evident after 20 min in the MA and LPS groups. Conclusion. Significant lung uptake of harmful soluble macromolecules compensated for the defect liver scavenger function in the ALF-group. Infusion of MA induced increased TNF-α serum levels and leukopenia, similar to the effect of the known inflammatory mediator LPS. These observations suggest a potential mechanism that may contribute to lung damage secondary to liver disease |
Disciplinas: | Medicina |
Palabras clave: | Gastroenterología, Neumología, Insuficiencia hepática aguda, Síndrome de respuesta inflamatoria sistémica, Acido hialurónico, Células endoteliales, Hígado, Macrófagos, Pulmones |
Keyword: | Medicine, Gastroenterology, Pneumology, Acute liver failure, Systemic inflammatory response syndrome, Hyaluronic acid, Endothelial cells, Liver, Macrophages, Lungs |
Texte intégral: | Texto completo (Ver PDF) |