Folinic Acid Potentiates the Liver Regeneration Process after Selective Portal Vein Ligation in Rats.

Liver resection remains the gold standard for hepatic metastases. The future liver remnant (FLR) and its functional status are two key points to consider before performing major liver resections, since patients with less than 25% FLR or a Child-Pugh B or C grade are not eligible for this procedure. Folinic acid (FA) is an essential agent in cell replication processes. Herein, we analyze the effect of FA as an enhancer of liver regeneration after selective portal vein ligation (PVL). Sixty-four male WAG/RijHsd rats were randomly distributed into eight groups: a control group and seven subjected to 50% PVL, by ligation of left portal branch. The treated animals received FA (2.5 m/kg), while the rest were given saline. After 36 h, 3 days or 7 days, liver tissue and blood samples were obtained. FA slightly but significantly increased FLR percentage (FLR%) on the 7th day (91.88 ± 0.61%) compared to control or saline-treated groups (86.72 ± 2.5 vs. 87 ± 3.33%; p < 0.01). The hepatocyte nuclear area was also increased both at 36 h and 7days with FA (61.55 ± 16.09 µm2, and 49.91 ± 15.38 µm2; p < 0.001). Finally, FA also improved liver function. In conclusion, FA has boosted liver regeneration assessed by FLR%, nuclear area size and restoration of liver function after PVL.

Antioxidant-Based Therapy Reduces Early-Stage Intestinal Ischemia-Reperfusion Injury in Rats.

Intestinal ischemia-reperfusion injury (i-IRI) is a rare disorder with a high mortality rate, resulting from the loss of blood flow to an intestinal segment. Most of the damage is triggered by the restoration of flow and the arrival of cytokines and reactive oxygen species (ROS), among others. Inactivation of these molecules before tissue reperfusion could reduce intestinal damage. The aim of this work was to analyze the preventive effect of allopurinol and nitroindazole on intestinal mucosal damage after i-IRI. Wag/RijHsd rats were subjected to i-IRI by clamping the superior mesenteric artery (for 1 or 2 h) followed by a 30 min period of reperfusion. Histopathological intestinal damage (HID) was assessed by microscopic examination of histological sections obtained from injured intestine. HID was increased by almost 20% by doubling the ischemia time (from 1 to 2 h). Nitroindazole reduced HID in both the 1 and 2 h period of ischemia by approximately 30% and 60%, respectively (p < 0.001). Our preliminary results demonstrate that nitroindazole has a preventive/protective effect against tissue damage in the early stages of i-IRI. However, to better understand the molecular mechanisms underlying this phenomenon, further studies are needed.

Modificación de la distribución de la 3H-atropina por la administración de etanol en un modelo animal / Modification of 3H-atropine by ethanol administration in an animal model

Se estudió la biodistribución de la 3H-atropina en ratones albinos machos heterocigóticos por administraciòn conjunta de atropina y etanol y de atropina solamente. Se observó un comportamiento cualitativamente similar en el perfil de distribución, pero se encontraron diferencias significatiovas entre los niveles de 3H-atropina en la sangre y en la casi totalidad de los tejidos, incluídos el cerebro, que es el órgano donde se producen los principales efectos. Los niveles incrementados de la atropina en la sangre y en los tejidos no parecen proceder de la modificación de su enlazamiento a las proteínas plasmáticas, sino más bien, entre otras causas, al efecto de estimulación circulatoria que produce el etanol favoreciendo la llegada de mayores cantidades de atropina a los tejidos y como consecuencia al sitio de acción, lo que provoca una respuesta más intensa que justifica el efecto de potenciación que se produce por la administración conjunta de etanol y atropina