An Experimental Study on the Mechanism of Anisodamini Hydrobromidum in Treating Acute Ischemic Renal Failure

Althoughthepathogenesisofacuteischemicrenalfailurehasvarioushypotheses,theischemicinjuryoftubulirenalesholdsaleadingpostduringthewholeattackprocess.ManystudiesindicatedthattheintracellularCa2 levelchangeplaysakeyroleinischemicinjury.WhentheintracellularfreeCa2 (Ca' j,)concentrationisconstantlyelevatedtopresentCaZ --overload,theirreversibleinjuryoftubulirenalesendothelialcellsisusuallyinduced.Theresearchesalsoindicatedthattheintracellularinositoltriphosphate(lP,)levelplayedanimportantroleint…

An experimental study on the mechanism of anisodamini hydrobromidum in treating acute ischemic renal failure

In order to explore the mechanism of anisodamini hydrobromidum (654-2) in treating acute ischemic renal failure, the model of acute ischemic renal failure in white New Zealand rabbits was established to dynamically observe and statistically analyze the intracellular concentration changes of free calcium(Ca(2 )]i) and inositol triphosphate (IP3). The results showed that the levels of Ca(2 )], and IP3 in acute renal failure group were higher than those in control group (P<0. 01). However, the levels of Ca(2 )]i and IP3 in 654-2 treated group were significantly lower than those in acute renal failure group (P<0. 001). It was concluded that 654-2 could alleviate Ca(2 )-overload in renal histocytes in acute ischemic renal failure. The protective mechanism is associated with intracellular reduction of IP3.