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Abstract：
It has been proposed that diuretics can improve renal tissue oxygenation through inhibition of tubular sodium reabsorption and reduced metabolic demand. However, the impact of clinically used diuretic drugs on the renal cortical and medullary microcirculation is unclear. Therefore, we examined the effects of three commonly used diuretics, at clinically relevant doses, on renal cortical and medullary perfusion and oxygenation in non-anaesthetised healthy sheep. Merino ewes received acetazolamide (250 mg; n = 9), furosemide (20 mg; n = 10) or amiloride (10 mg; n = 7) intravenously. Systemic and renal haemodynamics, renal cortical and medullary tissue perfusion and P O 2 ${P_{{{\\mathrm{O}}_{\\mathrm{2}}}}}$ , and renal function were then monitored for up to 8 h post-treatment. The peak diuretic response occurred 2 h (99.4 ± 14.8 mL/h) after acetazolamide, at which stage cortical and medullary tissue perfusion and P O 2 ${P_{{{\\mathrm{O}}_{\\mathrm{2}}}}}$ were not significantly different from their baseline levels. The peak diuretic response to furosemide occurred at 1 h (196.5 ± 12.3 mL/h) post-treatment but there were no significant changes in cortical and medullary tissue oxygenation during this period. However, cortical tissue P O 2 ${P_{{{\\mathrm{O}}_{\\mathrm{2}}}}}$ fell from 40.1 ± 3.8 mmHg at baseline to 17.2 ± 4.4 mmHg at 3 h and to 20.5 ± 5.3 mmHg at 6 h after furosemide administration. Amiloride did not produce a diuretic response and was not associated with significant changes in cortical or medullary tissue oxygenation. In conclusion, clinically relevant doses of diuretic agents did not improve regional renal tissue oxygenation in healthy animals during the 8 h experimentation period. On the contrary, rebound renal cortical hypoxia may develop after dissipation of furosemide-induced diuresis.
摘要：
已经提出利尿剂可以通过抑制肾小管钠重吸收和减少代谢需求来改善肾组织氧合。然而,临床使用的利尿药对肾皮质和髓质微循环的影响尚不清楚.因此,我们检查了三种常用利尿剂的效果，在临床相关剂量下，非麻醉健康绵羊的肾皮质和髓质灌注和氧合。美利诺母羊接受乙酰唑胺（250毫克；n=9），呋塞米（20mg;n=10）或阿米洛利（10mg;n=7）静脉注射。全身和肾脏血流动力学，肾皮质和髓质组织灌注和PO2${P_{{\\mathrm{O}}_{\\mathrm{2}}}}$，然后在治疗后8小时内监测肾功能。利尿剂反应高峰出现在乙酰唑胺后2h（99.4±14.8mL/h），在该阶段皮质和髓质组织灌注和PO2${P_{{\\mathrm{O}}_{\\mathrm{2}}}}$与基线水平无显著差异。对呋塞米的利尿剂反应峰值出现在治疗后1小时（196.5±12.3mL/h），但在此期间皮质和髓质组织氧合没有显着变化。然而,皮质组织PO2${P_{{{\\mathrm{O}}_{\\mathrm{2}}}}$从基线时的40.1±3.8mmHg下降到3小时时的17.2±4.4mmHg和6小时后的20.5±5.3mmHg。阿米洛利不产生利尿反应，并且与皮质或髓质组织氧合的显着变化无关。总之,在8h实验期间，临床相关剂量的利尿剂并未改善健康动物的局部肾组织氧合。相反,呋塞米引起的利尿消散后，可能会出现反跳性肾皮质缺氧。
