輸液可以預防脊髓麻醉後低血壓引致之腎臟功能不良

Fluid Administration Prevents Renal Dysfunction during Hypotension under Spinal Anesthesia in a Rat Model

背景：低血壓常造成腎臟功能受損，尤其降低分布到腎臟皮質之血流。輸液治療常被用來防止高位脊髓麻醉伴隨的低血壓；本實驗的目的為研究事先給予輸液，在高位脊髓麻醉下對血壓、心率、腎臟血流及其分布和腎功能的影響。方法：以大白鼠為實驗動物，控制組在脊髓麻醉之前給予每公斤每小時5毫升之輸液、實驗組給予三倍輸液速度；以0.5％ bupivacaine經預先置入的脊髓導管實施高位脊髓麻醉(>T4)，連續記錄其血壓、心率及腎皮質微血流量（CMBF ；經雷射都卜勒）；並以每半小時為單位記錄脊髓麻醉後腎絲球過濾率(GFR)、腎血漿流量(ERPF)、尿流量(UFR)和電解質分泌量，研究腎功能的變化。結果：脊髓麻醉後5至10分鐘可見明顯的低血壓，輸液並不能預防低血壓的發生，兩組之血壓在脊髓麻醉30分鐘後和基礎值並無差別；控制組之GFR和ERPF在脊髓麻醉30分鐘內明顯減少而後恢復；CMBF及UFR則在60分鐘後才恢復。實驗組只有GFR在30分鐘內下降；ERPF、CMBF及UFR均維持甚或有增加。結論：高位脊髓麻醉雖然阻斷了腎交感神經，在其後的低血壓發生時仍會導致短暫的腎臟功能不良，腎皮質血流量及尿流量受影響的時間比GFR、ERPF更久；增加輸液速度並不能防止低血壓的產生，卻可以預防低血壓引致之腎臟功能變化。

Background: Severe hypotension deteriorates renal functions and renal hemodynamics especially renal cortical blood flow. Systemic hypotension following high level spinal anesthesia may impair renal functions in spite of the blockade of renal sympathetic nerves that may help prevent vasoconstriction. Fluid loading is clinically applied for preventing hypotension but the effects on the changes of renal functions have not been studied. This study was designed to investigate the effects of fluid loading on systemic hemodynamics, renal hemodynamics and functions especially the blood distribution to renal cortex. Methods: A rat model was used in our study. Intravenous normal saline infusion was started in both control group (5 ml/kg/h, 8 rats) and fluid loading group (15 ml/kg/h, 8 rats) 30 min before spinal anesthesia. A high level (above T4) spinal anesthesia was conducted via a preset intrathecal catheter with 0.5% hyperbaric bupivacaine. Blood pressure, heart rate and renal cortical microvascular blood flow (CMBF) were measured via a laser Doppler probe firmly contacted on renal cortex and recorded continuously after spinal anesthesia. Renal functions including glomerular filtration rates (GFR, by inulin clearance), effective renal plasma flow (ERPF, by P-aminohippurate clearance), urine flow rate (UFR) and electrolytes excretion were measured every 30 min after spinal anesthesia. Results: Severe hypotension was notable within 5-10 min after intrathecal anesthesia and recovered within 30 min in both groups but the difference was not significant between groups. In the control group, GFR and ERPF decreased significantly in the first 30 min by 51.9 ± 19.8% and 44.3 ± 13.7% respectively (P < 0.05) and recovered after 60 min. Also the deteriorations of UFR and CMBF were significantly longer (over 60 min). In fluid loading group, ERPF, UFR and CMBF could maintain throughout the experiment but only GFR was affected in the first 30 min. Conclusions: Fluid administration did not prevent hypotension following high level spinal anesthesia but might have beneficial effects on renal hemodynamics especially on the renal cortical circulation and urine flow rate.