Abstract
An animal model resembling clinical cases with extrahepatic portal vein obstruction was developed. The changes in hepatic mitochondrial function and the hepatic hemodynamics including hepatic regional blood flow, portal venous pressure, and portogram were evaluated to assess the effect of portal vein obstruction in the model.
Portal vein ligation in this model was a simple and easy maneuver and could produce collateral veins to the liver—cavernomatous transformation—which were obviously seen in clinical patients with extrahepatic portal obstruction. Hepatic blood flow was significantly decreased until 5 days after portal vein ligation; however, hepatic blood flow was gradually increased and reached the normal value at 3 weeks after portal vein ligation due to the formation of the collateral veins to the liver. Respiratory parameters of mitochondria were gradually decreased and reached the lowest levels at 5 days after portal vein ligation, while they recovered to normal values in accordance with increasing hepatic blood flow at 3 weeks after portal vein ligation.
In extrahepatic portal obstruction, although the liver is temporarily deteriorated by portal vein obstruction such as portal vein thrombosis, hepatic blood flow and the liver functions are to be normally improved with the formation of collateral veins to the liver.
Résumé
Un modèle expérimental d'obstruction portale extrahépatique resemblant à la clinique humaine a été créé chez l'animal. On a évalué les modifications de la fonction mitochondriale et les constantes hémodynamiques, y compris le débit hépatique, la pression portale, et les résultats de la portographie. La ligature de la veine porte est un geste simple et crée une circulation collatérale périhépatique avec cavernome, situation qui peut très bien se voir chez l'homme ayant un bloc extrahépatique. Après ligature, le débit hépatique a baissé de façon significative pendant 5 jours; cependant, le débit a ensuite augmenté pour atteindre une value normale 3 semaines après, grâce à la formation de la circulation collatérale. Les paramètres respiratoires mitochondriaux ont diminué après ligature pour retrouver leur valeurs du départ à 3 semaines, parallèlement à la normalisation du débit hépatique. Dans le bloc portal extrahépatique par thrombose porte par exemple, la fonction hépatique, bien que temporairement détériorée, revient à la normale progressivement au fur et à mésure du dévelopement de la circulation collatérale du foie.
Resumen
Hemos desarrollado un modelo animal que simula la condición clínica de la obstrucción extrahepática de la vena porta. Se valoraron los cambios en la hemodinamia hepática, incluyendo el flujo sanguineo regional hepático, la presión venosa portai, y la portografía con el objeto de determinar el efecto de la obstrucción de la vena porta en el modelo experimental.
La ligadura de la vena porta en el modelo es una maniobra simple y de sencilla ejecución y produce venas colaterales hacia el hígado y transformación cavernomatosa, lo cual es de observación obvia en pacientes con obstrucción portal extrahepática. El flujo sanguíneo hepático apareció significativamente disminuído hasta 5 días después de la ligadura de la vena porta; sinembargo, el flujo portal aumentó gradualmente y llegó a su valor normal a las 3 semanas después de la ligadura de la vena porta en virtud de la formación de venas colaterales en dirección al hígado. Los parámetras respiratorios mitocondriales resultaron gradualmente disminuídos y alcanzaron los niveles más bajos a los 5 días de la ligadura portai, pero se recuperaron para llegar a valores normales, de acuerdo con el creciente flujo hepático, a las 3 semanas después de la ligadura de la vena porta.
En la obstrucción portal extrahepática, aunque el hígado resulta temporalmente deteriorado por la obstrucción portal, tal como ocurre en la trombosis de la vena porta, el flujo sanguíneo y las funciones hepáticas se normalizan con la formación de venas colaterales en dirección del hígado.
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Omokawa, S., Asanuma, Y. & Koyama, K. Evaluation of hemodynamics and hepatic mitochondrial function on extrahepatic portal obstruction in the rat. World J. Surg. 14, 247–253 (1990). https://doi.org/10.1007/BF01664884
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DOI: https://doi.org/10.1007/BF01664884