Proceedings of The Physiological Society
University College Dublin (2009) Proc Physiol Soc 15, C88
Restoration of bile bilirubin excretion rate after cessation of obstructive cholestasis is suppressed by hyperprolactinemia in rats
N. Kushnareva1, O. V. Smirnova2
1. Biological Department, Moscow State University, Moscow, Russia. 2. Biological Department, Moscow State University, Moscow, Russia.
Background: Key liver function is maintenance of bile flow and bilirubin excretion rate. Some liver pathologies (e.c., cirrhosis) are associated with alteration of bile flow and hyperprolactinemia. Female prevalence of obstructive cholestasis (OC) development was assumed is related to high prolactin (Prl) and its hepatic receptors level in women. Aims: to investigate Prl influence on liver bilirubin excretory activity using rat model of hyperprolactinemia combined with OC. Methods: Obstructive cholestasis was induced by common bile duct ligation and hyperprolactinemia by donor pituitary transplantation under kidney capsule of recipient. Surgical procedures were conducted under diethyl ether anesthesia. Bilirubin concentration in bile, blood, and urine, bile flow and bilirubin excretion rates in early (3 h) period of decompression (EPD) were tested. Results: OC induced elevation of bile bilirubin concentration in females and its depletion in males and elevation of blood and urine bilirubin level in both sex. Bile flow rate was elevated in EPD as comparied with normal conditions with male predominance so that bilirubin excretion rate was the same in both sex. OC combined with hyperprolactinemia (4 weeks) resulted in sharp decreasing of bile bilirubin level and appearance of “white bile” in females and additional decreasing in males. Bilirubin concentration in females was firstly elevated in blood and urine and then decreased in bile, in males there were no evident alterations of blood and urine bilirubin concentration. Depending on hyperprolactinemia duration restoration of bile flow after bile duct decompression was firstly suppressed and then not restored in females and essentially suppressed in males. Hyperprolactinemia without bile duct obstruction had no marked influence on investigated parameters. Conclusions: Hyperprolactinemia deteriorates liver functions suppressing bile flow restoration after OC cessation, however due to decreasing bilirubin entry into bile it may participate in redistribution of bilirubin pool and promote kidney bilirubin excretion.
Where applicable, experiments conform with Society ethical requirements