Lagerkranser M, Irestedt L, Sollevi A, Andreen M
Anesthesiology. 1984 Jun;60(6):547-52. doi: 10.1097/00000542-198406000-00005.
Central and splanchnic hemodynamic effects during controlled hypotension induced by the administration of the endogenous vasodilator adenosine were studied in ten artificially ventilated dogs under neurolept anesthesia. Adenosine was administered as a continuous infusion in the aorta (n = 3), in the inferior vena cava (n = 3), and after pretreatment with dipyridamole (which inhibits the cellular uptake of adenosine) (n = 4) in a dose sufficient to maintain a mean arterial blood pressure (MABP) level of approximately 50 mmHg. Observations were made before and after 20 min of controlled hypotension. Basal arterial plasma levels of adenosine were in the 10(-7) M range (means = 0.4 microM). The hemodynamic response was similar in all three settings. Adenosine caused a profound decrease in systemic vascular resistance (SVR) (52%, P less than 0.01) and preportal vascular resistance (PPR) (64%, P less than 0.01), while hepatic arterial vascular resistance ( HAR ) increased by 49% (P less than 0.05). Cardiac output increased (22%, P less than 0.05) through increase of stroke volume (77%, P less than 0.01), while heart rate decreased (28%, P less than 0.01). Whole-body oxygen uptake decreased (14%, P less than 0.01). Portal venous blood flow increased by 28% (P less than 0.05), whereas hepatic arterial blood flow decreased by 70% (P less than 0.01). In the preportal tissues, oxygen uptake decreased by 21% (P less than 0.01). In contrast, hepatic oxygen consumption increased (53%, P less than 0.05). Adenosine-induced hypotension was not associated with changes in plasma renin activity or the plasma concentration of norepinephrine. It is concluded that adenosine causes a rapidly induced and easily maintained hypotension and may be a potentially useful agent for controlled hypotension in patients.
在神经安定麻醉下，对10只人工通气的犬研究了内源性血管扩张剂腺苷给药诱导控制性低血压期间的中枢和内脏血流动力学效应。腺苷通过在主动脉（n = 3）、下腔静脉（n = 3）连续输注给药，以及在给予双嘧达莫（抑制腺苷的细胞摄取）预处理后（n = 4）以足以维持平均动脉血压（MABP）水平约50 mmHg的剂量给药。在控制性低血压20分钟前后进行观察。腺苷的基础动脉血浆水平在10（-7）M范围内（均值 = 0.4 microM）。在所有三种情况下血流动力学反应相似。腺苷导致全身血管阻力（SVR）显著降低（52%，P < 0.01）和门静脉前血管阻力（PPR）显著降低（64%，P < 0.01），而肝动脉血管阻力（HAR）增加49%（P < 0.05）。心输出量通过每搏输出量增加（77%，P < 0.01）而增加（22%，P < 0.05），而心率降低（28%，P < 0.01）。全身氧摄取降低（14%，P < 0.01）。门静脉血流量增加28%（P < 0.05），而肝动脉血流量减少70%（P < 0.01）。在门静脉前组织中，氧摄取降低21%（P < 0.01）。相反，肝氧消耗增加（53%，P < 0.05）。腺苷诱导的低血压与血浆肾素活性或去甲肾上腺素血浆浓度的变化无关。结论是腺苷可引起快速诱导且易于维持的低血压，可能是用于患者控制性低血压的潜在有用药物。
