The nutritional status modulates preservation-reperfusion injury in rat fatty liver
| Autor: | Giuseppe Palasciano, Mauro Bernardi, Ignazio Grattagliano, Marco Domenicali, Paolo Caraceni, Elisabetta Maiolini, Anna Maria Pertosa, A. Principe, Franco Trevisani |
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| Přispěvatelé: | Caraceni P., Domenicali M., Pertosa A.M., Maiolini E., Grattagliano I., Principe A., Palasciano G., Trevisani F., Bernardi M. |
| Rok vydání: | 2004 |
| Předmět: |
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medicine.medical_specialty Prostaglandin In Vitro Techniques medicine.disease_cause Rats Sprague-Dawley chemistry.chemical_compound Internal medicine medicine Animals Viaspan EXPERIMENTAL LIVER TRANSPLANTATION Liver injury Glycogen biology business.industry PRESERVATION INJURY Fatty liver Alanine Transaminase Fasting Organ Preservation NUTRITIONAL STATUS medicine.disease Rats Fatty Liver Endocrinology Glucose Biochemistry chemistry Alanine transaminase Liver Reperfusion Injury Dietary Supplements biology.protein Prostaglandins Surgery Animal Nutritional Physiological Phenomena business Reperfusion injury Oxidative stress |
| Zdroj: | The Journal of surgical research. 127(2) |
| ISSN: | 0022-4804 |
| Popis: | Background Microcirculation disturbances are essential factors of preservation injury in fatty liver. However, hepatocyte injury is also markedly excessive in fatty liver resulting, at least in part, from energy metabolism impairment and oxidative stress. Thus, this study aimed to determine whether nutritional status influences preservation injury in fatty liver and whether energetic substrate supplementation, alone or with a vasodilator, is protective. Materials and methods Normal or fatty livers induced by a choline-deficient diet were isolated from fed and fasted rats, preserved in University of Wisconsin solution at 4°C for 18 h, and then reperfused with Krebs–Henseleit solution at 37°C for 120 min. Fasted rats with fatty liver were also treated as follows: (1) Glucose supplementation : rats had access to a glucose solution for 18 h prior procurement; (2) Prostaglandin (PG) : alprostadil was continuously infused during reperfusion; (3) Combined treatment : Glucose supplementation + PG. Results Fasting-induced liver injury was significantly greater in fatty than normal liver. In fatty livers from fasted rats, all treatments reduced the alanine aminotransaminase release. Hepatic oxygen consumption improved in the glucose and glucose + PG groups, while PG infusion had no effect. Glucose supplementation did not affect portal pressure, which, in contrast, was reduced in livers receiving PG. Finally, all treatments lowered oxidative injury. Conclusions Preservation injury in fatty liver is greatly related to nutritional status. Energetic substrate supplementation may represent a clinically feasible protective strategy and a multistep approach adding vasodilators could offer further benefit by acting on different pathogenetic mechanisms. |
| Databáze: | OpenAIRE |
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