Jordan D, Shulman S M, Miller E D
Department of Anesthesiology, Columbia University, College of Physicians and Surgeons, New York, New York 10032.
Anesth Analg. 1993 Aug;77(2):281-90. doi: 10.1213/00000539-199308000-00012.
To demonstrate that esmolol, sodium nitroprusside, and isoflurane differ in their abilities to alter adrenal medullary blood flow and other peripheral sympathetic responses to hypotension, 16 mongrel dogs anesthetized with pentobarbital were allocated randomly to one of four test groups and given two hypotensive stimuli, separated by 1 h, to a mean arterial blood pressure of 60 mm Hg for 10 min. The first stimulus, induced by blood loss into a pressurized bottle system, constituted the control for each animal. The second hypotensive stimulus was created by either repeat blood loss (Group 1), esmolol infusion (Group 2), sodium nitroprusside infusion (Group 3), or isoflurane administration (Group 4). Before and 10 min into hypotension, the variables of abdominal organ blood flow, adrenal medullary blood flow, arterial norepinephrine and epinephrine concentrations were measured. In the control animals (Group 1), comparable decreases in abdominal organ blood flow and similar increases in adrenal medullary blood flow, norepinephrine, and epinephrine were elicited by the first and second hypotensive stimulus. Esmolol-induced hypotension (Group 2) abolished the increase in adrenal medullary blood flow and attenuated the increase in epinephrine by 65% (P < 0.03). The decrease in abdominal organ blood flow and the increase in norepinephrine were similar to that observed during baseline hemorrhagic hypotension. In contrast, sodium nitroprusside-induced hypotension (Group 3) abolished abdominal organ vasoconstriction whereas the increases in adrenal medullary blood flow, norepinephrine, and epinephrine were comparable to baseline hemorrhagic hypotension. In fact, abdominal organ blood flow increased 2.5-fold (P < 0.001) during hypotension with SNP. Isoflurane 2%, 1.54 minimum alveolar anesthesia concentration (Group 4), abolished the increases in adrenal medullary blood flow, norepinephrine, and epinephrine observed during baseline hemorrhagic hypotension and attenuated the decrease in abdominal organ blood flow by 70% (P < 0.001). These data demonstrate that esmolol, sodium nitroprusside, and isoflurane differ radically in their ability to alter or blunt peripheral sympathetic responses to hypotension, and suggest that isoflurane is the drug most effective in blunting multiple responses of the peripheral sympathetic system.
为了证明艾司洛尔、硝普钠和异氟烷在改变肾上腺髓质血流以及其他外周交感神经对低血压反应的能力方面存在差异，将16只戊巴比妥麻醉的杂种犬随机分配到四个试验组之一，并给予两种低血压刺激，间隔1小时，使平均动脉血压降至60mmHg并维持10分钟。第一种刺激是通过将血液放入压力瓶系统中诱导产生的，作为每只动物的对照。第二种低血压刺激是通过重复失血（第1组）、静脉输注艾司洛尔（第2组）、静脉输注硝普钠（第3组）或给予异氟烷（第4组）产生的。在低血压发生前和低血压发生10分钟后，测量腹部器官血流、肾上腺髓质血流、动脉去甲肾上腺素和肾上腺素浓度等变量。在对照动物（第1组）中，第一次和第二次低血压刺激引起的腹部器官血流的可比减少以及肾上腺髓质血流、去甲肾上腺素和肾上腺素的类似增加。艾司洛尔诱导的低血压（第2组）消除了肾上腺髓质血流的增加，并使肾上腺素的增加减弱了65%（P<0.03）。腹部器官血流的减少和去甲肾上腺素的增加与基线出血性低血压时观察到的情况相似。相比之下，硝普钠诱导的低血压（第3组）消除了腹部器官血管收缩，而肾上腺髓质血流、去甲肾上腺素和肾上腺素的增加与基线出血性低血压时相当。事实上，使用硝普钠低血压时腹部器官血流增加了2.5倍（P<0.001）。2%异氟烷，1.54最低肺泡麻醉浓度（第4组）消除了基线出血性低血压时观察到的肾上腺髓质血流、去甲肾上腺素和肾上腺素的增加，并使腹部器官血流的减少减弱了70%（P<0.001）。这些数据表明，艾司洛尔、硝普钠和异氟烷在改变或减弱外周交感神经对低血压反应的能力方面存在根本差异，并表明异氟烷是最有效地减弱外周交感神经系统多种反应的药物。
