Zäll S, Edén E, Winsö I, Volkmann R, Sollevi A, Ricksten S E
Department of Anesthesia and Intensive Care, Sahlgren's Hospital, University of Gothenburg, Sweden.
Anesth Analg. 1990 Dec;71(6):631-6.
Adenosine, a potent vasodilator both in animals and in humans, has been used to produce controlled hypotension in patients, especially during cerebral aneurysm surgery. However, in animals adenosine by intrarenal infusion decreases renal blood flow (RBF), glomerular filtration rate (GFR), urine flow, and causes an inhibition of renin secretion. In this study we evaluated the effect of adenosine on RBF in patients (n = 15) scheduled for cerebral aneurysm surgery who had been anesthetized with a modified neurolept-anesthesia during controlled hyperventilation. Perioperative hypotension was achieved with infusion of adenosine (252.8 +/- 55.8 micrograms.kg-1.min-1) (n = 8) or sodium nitroprusside (2.5 +/- 0.8 micrograms.kg-1.min-1) (n = 7). Mean arterial pressure was lowered by 25%-30%, to approximately 60-70 mm Hg, in both groups. Glomerular filtration rate and RBF were measured using standard renal clearance methods for 51Cr-ethylenediaminetetraacetic acid and paraaminohippuric acid. Urine and blood samples were collected during normotension before and after a bolus dose of hypertonic mannitol, during hypotension, and during normotension after clipping of the aneurysm. Adenosine induced a marked decrease in GFR (-91%) and RBF (-92%), and a pronounced increase in renal vascular resistance. Sodium nitroprusside caused a significantly (P less than 0.01) less pronounced decrease in GFR (-24%) and RBF (-36%), but did not affect renal vascular resistance. After discontinuation of the hypotensive agents, GFR returned to baseline levels in both groups. Renal blood flow, however, increased above baseline after discontinuation of adenosine (+93%) but not after sodium nitroprusside. Sodium nitroprusside increased renin secretion, which was not seen with adenosine. Four patients in the adenosine group developed reversible atrioventricular conduction disturbances.(ABSTRACT TRUNCATED AT 250 WORDS)
腺苷在动物和人类体内均为强效血管扩张剂,已被用于使患者产生控制性低血压,尤其是在脑动脉瘤手术期间。然而,在动物实验中,经肾内输注腺苷会降低肾血流量(RBF)、肾小球滤过率(GFR)、尿流量,并抑制肾素分泌。在本研究中,我们评估了腺苷对计划进行脑动脉瘤手术的患者(n = 15)肾血流量的影响,这些患者在控制性过度通气期间接受了改良神经安定麻醉。通过输注腺苷(252.8±55.8微克·千克⁻¹·分钟⁻¹)(n = 8)或硝普钠(2.5±0.8微克·千克⁻¹·分钟⁻¹)(n = 7)实现围手术期低血压。两组患者的平均动脉压均降低了25% - 30%,降至约60 - 70毫米汞柱。使用标准肾清除方法,通过51铬 - 乙二胺四乙酸和对氨基马尿酸来测量肾小球滤过率和肾血流量。在给予大剂量高渗甘露醇之前和之后的正常血压期间、低血压期间以及动脉瘤夹闭后的正常血压期间收集尿液和血液样本。腺苷导致肾小球滤过率显著降低(-91%)和肾血流量显著降低(-92%),并使肾血管阻力显著增加。硝普钠导致肾小球滤过率(-24%)和肾血流量(-36%)的降低明显不那么显著(P < 0.01),但不影响肾血管阻力。停用降压药物后,两组患者的肾小球滤过率均恢复至基线水平。然而,停用腺苷后肾血流量高于基线水平(+93%),而停用硝普钠后则没有。硝普钠增加肾素分泌,而腺苷则未出现这种情况。腺苷组有4名患者出现可逆性房室传导障碍。(摘要截选至250字)