Dilazep dihydrochloride acts as an adenosine uptake inhibitor. It promotes cerebral and coronary vasodilation by amplifying adenosine's effects. Additionally, Dilazep dihydrochloride prevents ischemic injury, platelet clumping, and the cellular uptake of nucleosides[1][2]. In vitro studies have thoroughly examined the uptake mechanism, revealing that Dilazep, NBI, and Dipyridamole can all inhibit adenosine absorption in various cell types. Among these, Dilazep and NBI demonstrate nearly ten-fold greater potency compared to Dipyridamole. Moreover, Dilazep is unique in its water solubility, eliminating the need for any solubility-enhancing organic solvents when preparing its aqueous solution[1].
Dilazep 2HCl 动物研究
Animal study
Post-Dilazep administration, even at minimal dosages ranging from 0.04 to 0.1 mg/kg/min, the introduction of external adenosine markedly enhances superior mesenteric arterial conductance (SMAC) and boosts the concentration of adenosine in arterial plasma. There is a strong correlation between the rise in adenosine and the percentage increase in SMAC, with Rmax and EC50 values recorded at a 193.4% change in SMAC and 2.8 μM, respectively. The administration of 8-phenyltheophylline in bolus doses negates Dilazep's vasodilatory potentiation effect, yet it does not interfere with the relaxation induced by isoproterenol[1].
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