Renal Damage Induced By Iodinated Contrast Media In Acute Myocardial Infarction Rat Model

Background: The rate of Contrast-induced nephropathy (CIN) in acute myocardialinfarction (AMI) patient for primary percutaneous coronary intervention (PCI) ishigher than elective patients. We evaluated the nephrotoxicity of the low-osmolarcontrast media in the AMI SD rats.Methods: Forty male rats were randomly divided into four groups: control group(n=8), contrast media (CM) group (n=12), AMI group (n=8) and AMI+CM group(n=12). Velocity of renal artery blood flow (VRABF) was measured by ultrasound.CM group and AMI+CM group were examined by computer tomography (CT). Thelevel of serum creatinine was measured. Reactive oxidative species(ROS) in kidneytissue was determined by an oxidation-sensitive fluorescent probe (DCFH-DA)method, the renal injury was assessed by periodic acid-Schiff (PAS) and terminaldeoxynucleotidyl transferase mediated nick end labeling (TUNEL) assay.Endothein-1(ET-1) and angiotensin Ⅱ(AngII) was measured with a commerciallyavailable radioimmunoassay kit. Caspase-3and NF-κb were measured by real-timepolymerase chain-reaction.Result: Velocity of renal artery blood flow(VRABF) was lower in AMI+CM groupthan CM group at0minute,8min,15min,4h,24h and x-ray attenuation in cortex washigher in AMI+CM group than CM group at4-hour. The level of serum creatinine(Scr)in AMI+CM group displayed a significantly increase at24-hour compared with CMgroup. The level of ET-1, Ang-II and ROS in CM+AMI group was highest. The histopathologic scores and percentage of tubular cell apoptosis were higher inAMI+CM group at24-hour compared with CM group.Conclusion:The lower of VRABF, and higher level of endothein-1(ET-1) andangiotensinⅡ (AngII) in AMI+CM group caused the severe hypoxia and prolongedretention of contrast media. The higher production of ROS changes played animportant role in more severe renal apoptosis induced by contrast media.