Effect of recombinant human B-type natriuretic peptide on renal hemodynamics in a bioengineering model of acute myocardial infarction with heart failure

Fan Xin-na; Zhang Jing; Cai Li-li; Yang Gui-feng; Fu Xiang-hua

doi:10.3969/j.issn.2095-4344.2014.27.001

Abstract：BACKGROUND:The reduction of renal circulation and perfusion, the decline of renal blood flow, wil al cause renal injury. The heart failure concomitant with renal injury can significantly increase the mortality. But there are arguments about the effect of B-type natriuretic peptide (BNP) on the renal function of patients with heart failure, and little evidence is known about the effect of BNP on the renal hemodynamics. <br> OBJECTIVE:To evaluate the effects of different dosages of recombinant human BNP on renal perfusion in bioengineering models of acute myocardial infarction with heart failure. <br> METHODS:Bioengineering model of York pigs of acute myocardial infarction with heart failure was established with the method of occluding anterior descending branch with bal oon and injecting microthrombus. The models were randomized into recombinant human BNP group and control group (n=6). Clinical dose of recombinant human BNP (bolus of 1.5μg/kg fol owed by a continuous infusion of 0.01μg/(kg.min) for 60 minutes, and then a continuous infusion of 0.02 and 0.03μg/(kg.min) for 60 minutes) was administrated in the BNP group, while equal volume of saline was given in the control group. Renal artery diameter, average peak velocity, mean arterial pressure and transrenal perfusion pressure were recorded at baseline, instantly after the model establishment, 60 minutes after continuous infusion of recombinant human BNP. <br> RESULTS AND CONCLUSION:Compared with baseline information, renal artery diameter maintained unchanged after the models were established, average peak velocity was significantly decreased, renal arterial blood flow was significantly reduced, renal vascular resistance was obviously increased, and transrenal perfusion pressure was obviously decreased. After infusion of 0.01μg/(kg.min) recombinant human BNP, renal arteries began to dilute, renal artery diameter was gradual y increased. The average peak velocity was also increased, but showed no significant differences compared with baseline information. Subsequently average peak velocity was gradual y declined with the increasing dose. Renal vascular resistance was decreased in a dose-dependent relationship after administration of recombinant human BNP. Transrenal perfusion pressure was progressively decreased with the dose ascending, and was significantly lower than the control group after the infusion of 0.03μg/(kg.min) BNP. Renal blood flow was increased gradual y after administration of BNP and reached the highest point after the infusion of 0.02μg/(kg.min) BNP. Recombinant human BNP can increase the renal perfusion in the model of acute myocardial infarction with heart failure, and the highest effect appears at the dosage of 0.02μg/(kg.min).