CAJ | 학술논문

背景：肾循环灌注减少、肾血流降低会造成肾损伤，心力衰竭患者合并肾损伤会明显增加死亡率。但B型钠尿肽对于心力衰竭患者肾功能的影响目前存在较大争论，关于B型钠尿肽对心力衰竭肾灌注的研究很少。 　　目的：评价不同剂量重组人B型钠尿肽对急性心肌梗死伴心力衰竭生物工程模型肾循环的血流动力学效应。 　　方法：应用前降支球囊闭塞结合微血栓悬液灌注构建急性心肌梗死伴心力衰竭约克猪模型共12头，随机分入重组人B型钠尿肽组和对照组(n=6)。重组人B型钠尿肽组给予重组人B型钠尿肽1.5μg/kg，2 min内匀速静推后，以0.010μg/(kg?min)静脉泵入60 min，然后依次加量至0.020μg/(kg?min)、0.030μg/(kg?min)静脉泵入各60 min。对照组依照相同给药方法给予生理盐水。在球囊闭塞前、成模后即刻、不同剂量重组人B型钠尿肽给药后60 min，行肾动脉造影，比较肾动脉管径的变化。多普勒导丝测定肾动脉平均峰值速率。计算平均动脉压和跨肾灌注压。 　　结果与结论：造模成功后与基线比较，肾动脉管径无变化，肾动脉平均峰值速率明显下降，肾动脉血流量显著降低，肾动脉血管阻力明显升高，跨肾灌注压明显降低。给予重组人B型钠尿肽0.010μg/(kg?min)后可见肾动脉扩张，并随剂量增加，肾动脉直径继续增加。肾动脉平均峰值速率增高，但较基线差异无显著性意义，此后，随剂量增加，肾动脉平均峰值速率逐渐下降。给药后肾动脉血管阻力逐渐下降，呈剂量依赖性。跨肾灌注压随着药物剂量的升高进行性下降，至0.030μg/(kg?min)泵入时显著低于对照组。给予重组人B型钠尿肽后肾动脉血流量逐渐升高，最高点出现在0.020μg/(kg?min)。结果可见急性心肌梗死伴心力衰竭模型应用重组人B型钠尿肽可增加肾灌注，0.020μg/(kg?min)效果最强。揹景：腎循環灌註減少、腎血流降低會造成腎損傷，心力衰竭患者閤併腎損傷會明顯增加死亡率。但B型鈉尿肽對于心力衰竭患者腎功能的影響目前存在較大爭論，關于B型鈉尿肽對心力衰竭腎灌註的研究很少。 　　目的：評價不同劑量重組人B型鈉尿肽對急性心肌梗死伴心力衰竭生物工程模型腎循環的血流動力學效應。 　　方法：應用前降支毬囊閉塞結閤微血栓懸液灌註構建急性心肌梗死伴心力衰竭約剋豬模型共12頭，隨機分入重組人B型鈉尿肽組和對照組(n=6)。重組人B型鈉尿肽組給予重組人B型鈉尿肽1.5μg/kg，2 min內勻速靜推後，以0.010μg/(kg?min)靜脈泵入60 min，然後依次加量至0.020μg/(kg?min)、0.030μg/(kg?min)靜脈泵入各60 min。對照組依照相同給藥方法給予生理鹽水。在毬囊閉塞前、成模後即刻、不同劑量重組人B型鈉尿肽給藥後60 min，行腎動脈造影，比較腎動脈管徑的變化。多普勒導絲測定腎動脈平均峰值速率。計算平均動脈壓和跨腎灌註壓。 　　結果與結論：造模成功後與基線比較，腎動脈管徑無變化，腎動脈平均峰值速率明顯下降，腎動脈血流量顯著降低，腎動脈血管阻力明顯升高，跨腎灌註壓明顯降低。給予重組人B型鈉尿肽0.010μg/(kg?min)後可見腎動脈擴張，併隨劑量增加，腎動脈直徑繼續增加。腎動脈平均峰值速率增高，但較基線差異無顯著性意義，此後，隨劑量增加，腎動脈平均峰值速率逐漸下降。給藥後腎動脈血管阻力逐漸下降，呈劑量依賴性。跨腎灌註壓隨著藥物劑量的升高進行性下降，至0.030μg/(kg?min)泵入時顯著低于對照組。給予重組人B型鈉尿肽後腎動脈血流量逐漸升高，最高點齣現在0.020μg/(kg?min)。結果可見急性心肌梗死伴心力衰竭模型應用重組人B型鈉尿肽可增加腎灌註，0.020μg/(kg?min)效果最彊。
배경：신순배관주감소、신혈류강저회조성신손상，심력쇠갈환자합병신손상회명현증가사망솔。단B형납뇨태대우심력쇠갈환자신공능적영향목전존재교대쟁론，관우B형납뇨태대심력쇠갈신관주적연구흔소。 　　목적：평개불동제량중조인B형납뇨태대급성심기경사반심력쇠갈생물공정모형신순배적혈류동역학효응。 　　방법：응용전강지구낭폐새결합미혈전현액관주구건급성심기경사반심력쇠갈약극저모형공12두，수궤분입중조인B형납뇨태조화대조조(n=6)。중조인B형납뇨태조급여중조인B형납뇨태1.5μg/kg，2 min내균속정추후，이0.010μg/(kg?min)정맥빙입60 min，연후의차가량지0.020μg/(kg?min)、0.030μg/(kg?min)정맥빙입각60 min。대조조의조상동급약방법급여생리염수。재구낭폐새전、성모후즉각、불동제량중조인B형납뇨태급약후60 min，행신동맥조영，비교신동맥관경적변화。다보륵도사측정신동맥평균봉치속솔。계산평균동맥압화과신관주압。 　　결과여결론：조모성공후여기선비교，신동맥관경무변화，신동맥평균봉치속솔명현하강，신동맥혈류량현저강저，신동맥혈관조력명현승고，과신관주압명현강저。급여중조인B형납뇨태0.010μg/(kg?min)후가견신동맥확장，병수제량증가，신동맥직경계속증가。신동맥평균봉치속솔증고，단교기선차이무현저성의의，차후，수제량증가，신동맥평균봉치속솔축점하강。급약후신동맥혈관조력축점하강，정제량의뢰성。과신관주압수착약물제량적승고진행성하강，지0.030μg/(kg?min)빙입시현저저우대조조。급여중조인B형납뇨태후신동맥혈류량축점승고，최고점출현재0.020μg/(kg?min)。결과가견급성심기경사반심력쇠갈모형응용중조인B형납뇨태가증가신관주，0.020μg/(kg?min)효과최강。
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. 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. 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. 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).