Bladder urine oxygen tension for assessing renal medullary oxygenation in rabbits: experimental and modeling studies.
Bladder urine oxygen tension for assessing renal medullary oxygenation in rabbits: experimental and modeling studies.
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用于评估兔肾髓质氧合的膀胱尿氧分压：实验和模型研究。
DOI：
10.1152/ajpregu.00195.2016
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发表时间：
2016
期刊：
影响因子：
--
通讯作者：
Evans,RogerG
中科院分区：
文献类型：
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作者：
Sgouralis,Ioannis;Kett,MichelleM;Ow,ConniePC;Abdelkader,Amany;Layton,AnitaT;Gardiner,BruceS;Smith,DavidW;Lankadeva,YugeeshR;Evans,RogerG
如果膀胱中尿液的氧张力 (Po2) 随髓质 Po2 变化，则可用于监测急性肾损伤的风险。因此，我们研究了这种关系，并表征了麻醉兔子输尿管和膀胱壁上的氧气扩散。然后开发了一个计算模型来根据膀胱尿 Po2 预测髓质 Po2。静脉输注[Phe2,Ile3,Orn8]-加压素和输注NG-硝基-L-精氨酸均降低尿Po2和髓质Po2(8-17%)，但对肾血流量和尿流量具有相反的影响。这些刺激期间膀胱尿 Po2 的变化与髓质 Po2 的变化密切相关（兔内 Po2 = 0.87-0.90）。注入靠近肾脏的输尿管的盐水的 Po2 差异可以在膀胱中检测到，尽管在输尿管流量较小时这种差异会减弱。氧气穿过膀胱壁的扩散非常缓慢，因此计算模型中没有考虑这一点。该模型根据已知的膀胱尿 Po2、尿流量和动脉 Po2 值预测盆腔输尿管中的 Po2（推测反映髓质 Po2）。模拟表明，在麻醉兔尿流量的生理范围内（单个肾脏为 0.1-0.5 毫升/分钟），膀胱尿 Po2 的变化可以解释盆腔尿/髓质 Po2 变化的 10-50%。因此，可以从尿 Po2 的变化推断髓质 Po2 的变化，因此尿 Po2 可能可用作急性肾损伤风险的实时生物标志物。
Oxygen tension (Po2) of urine in the bladder could be used to monitor risk of acute kidney injury if it varies with medullary Po2. Therefore, we examined this relationship and characterized oxygen diffusion across walls of the ureter and bladder in anesthetized rabbits. A computational model was then developed to predict medullary Po2from bladder urine Po2. Both intravenous infusion of [Phe2,Ile3,Orn8]-vasopressin and infusion ofNG-nitro-l-arginine reduced urinary Po2and medullary Po2(8–17%), yet had opposite effects on renal blood flow and urine flow. Changes in bladder urine Po2during these stimuli correlated strongly with changes in medullary Po2(within-rabbitr2= 0.87–0.90). Differences in the Po2of saline infused into the ureter close to the kidney could be detected in the bladder, although this was diminished at lesser ureteric flow. Diffusion of oxygen across the wall of the bladder was very slow, so it was not considered in the computational model. The model predicts Po2in the pelvic ureter (presumed to reflect medullary Po2) from known values of bladder urine Po2, urine flow, and arterial Po2. Simulations suggest that, across a physiological range of urine flow in anesthetized rabbits (0.1–0.5 ml/min for a single kidney), a change in bladder urine Po2explains 10–50% of the change in pelvic urine/medullary Po2. Thus, it is possible to infer changes in medullary Po2from changes in urinary Po2, so urinary Po2may have utility as a real-time biomarker of risk of acute kidney injury.