Hepatectomy including more than half of liver volume with intermittent portal triad occlusion.

INTRODUCTION: Liver resections over 50% of hepatic volume can be achieved with a low morbi-mortality, although occasionally they are followed by severe complications. Postoperative evolution and complications after this type of hepatic resections with intermittent occlusion of the portal triad have been studied. PATIENTS AND METHODS: 13 right hepatectomies, 5 enlarged right hepatectomies and 2 enlarged left hepatectomies were performed consecutively, with intraoperative ultrasound evaluation and intermittent portal triad occlusion. RESULTS: Maximum time of continuous hepatic hilum occlusion was 15 minutes, with a mean isquemia time of 25 +/- 8.6 minutes. Peak of disturbance of hepatic function was at 24 hours and recovered totally at 7th postoperative day. Nine of the 20 patients (45%) did not need intraoperative transfusion and the average of transfusion was 1.8 +/- 1.9 blood units. Four biliary leaks (20%), with no severe hepatic disfunction were observed during postoperative period, and there was no hospital mortality. CONCLUSIONS: Intermittent portal triad occlusion during hepatic resections in more than 50% of liver volume is a safe surgical maneuver.

Decreases in the size and proliferation rate of VIP-immunoreactive cells induced in vitro by testosterone are associated with decreases in VIP release.

As in vitro study was carried out to determine whether testosterone directly inhibits the secretion of pituitary vasoactive intestinal peptide (VIP). A study was also conducted to elucidate the repercussions of treatment with 10(-6) M testosterone of monolayer cultures in the size and proliferation rate of pituitary VIP-immunoreactive cells, using double immunocytochemical labelling for proliferating cell nuclear antigen (PCNA) and VIP. Testosterone decreased the in vitro release of VIP from pituitary cells. It also decreased the percentage of pituitary VIP-immunoreactive and PCNA- and VIP-immunoreactive cells and decreased the size of the cellular and nuclear areas of these cells. Our results suggest that the inhibition of pituitary VIP secretion induced by testosterone could be exerted at pituitary level and that testosterone could act as a modulator of the proliferation rate of rat pituitary VIP-immunoreactive cells.