Nielsen S H, Magid E, Spannow J, Christensen S, Lam H R, Petersen J S
Department of Clinical Biochemistry, Sundby Hospital, Copenhagen, Denmark.
Acta Physiol Scand. 1997 Aug;160(4):301-10. doi: 10.1046/j.1365-201X.1997.00162.x.
Renal function was measured by clearance technique before and after acute myocardial infarction (MI) induced by left coronary artery ligation in male Sprague-Dawley rats. The animals were anaesthetized with halothane-nitrous oxide, paralysed with pancuronium and artificially ventilated. All parameters were stable throughout the experiment in sham-operated time control animals (n = 8). After MI, rats developed left ventricular dysfunction with increased left ventricular end-diastolic pressure and decreased mean arterial pressure. MI produced antidiuresis and antinatriuresis without changes in glomerular filtration rate (GFR), lithium clearance or renal albumin excretion (n = 8). The antidiuretic and antinatriuretic responses to MI were similar in rats with chronic bilateral renal denervation (n = 5). Three additional rats with chronic bilateral renal denervation had cardiac arrest and were resuscitated with cardiac massage, i.v. lidocaine and intracardiac adrenaline administration. These animals showed a transient increase in urine flow rate, sodium and albumin excretion with maximum 30-60 min after resuscitation, while GFR and lithium clearance were normal. Since cardiac ischaemia and sympathetic stimulation are strong stimuli for the release of atrial natriuretic peptide (ANP), we examined if ANP (0.25, 0.50, and 1.00 microg kg(-1) min(-1), n = 8 per dose) affects urinary albumin excretion. ANP increased dose-dependently the urine/plasma concentration ratio of albumin relative to inulin, which suggests that ANP increases the glomerular permeability for albumin. We conclude that MI causes stimulation of renal tubular sodium and water reabsorption by a mechanism which is independent of intact renal innervation. MI does not produce any change in renal albumin excretion in rats, but transient albuminuria may be observed in rats following cardiac arrest and/or manoeuvres used in cardiac resuscitation. Since ANP produces albuminuria, we speculate that ANP may be an important mediator of albuminuria in states with elevated plasma concentrations of ANP.
通过清除技术测量雄性斯普拉格 - 道利大鼠左冠状动脉结扎诱导急性心肌梗死（MI）前后的肾功能。动物用氟烷 - 氧化亚氮麻醉，泮库溴铵麻痹并人工通气。在假手术时间对照动物（n = 8）的整个实验过程中，所有参数均稳定。MI后，大鼠出现左心室功能障碍，左心室舒张末期压力升高，平均动脉压降低。MI导致抗利尿和抗利钠作用，而肾小球滤过率（GFR）、锂清除率或肾白蛋白排泄无变化（n = 8）。慢性双侧肾去神经大鼠（n = 5）对MI的抗利尿和抗利钠反应相似。另外三只慢性双侧肾去神经大鼠发生心脏骤停，通过心脏按摩、静脉注射利多卡因和心内注射肾上腺素进行复苏。这些动物在复苏后30 - 60分钟内尿流率、钠和白蛋白排泄出现短暂增加，而GFR和锂清除率正常。由于心脏缺血和交感神经刺激是心房利钠肽（ANP）释放的强烈刺激因素，我们研究了ANP（0.25、0.50和1.00微克·千克⁻¹·分钟⁻¹，每组剂量n = 8）是否影响尿白蛋白排泄。ANP剂量依赖性地增加了白蛋白相对于菊粉的尿/血浆浓度比，这表明ANP增加了肾小球对白蛋白的通透性。我们得出结论，MI通过一种独立于完整肾神经支配的机制刺激肾小管钠和水的重吸收。MI在大鼠中不会引起肾白蛋白排泄的任何变化，但在心脏骤停和/或心脏复苏中使用的操作后，大鼠可能会出现短暂的蛋白尿。由于ANP会产生蛋白尿，我们推测ANP可能是血浆ANP浓度升高状态下蛋白尿的重要介质。
