*Department of Anesthesiology, Jinling Hospital, School of Medicine, Nanjing University, Nanjing, P. R. China; †Department of Anesthesiology, First Affiliated Hospital of Nanjing Medical University, Nanjing, P. R. China; and ‡Department of Anesthesiology, Shands Hospital, School of Medicine, University of Florida, Gainesville, FL.
J Cardiovasc Pharmacol. 2013 Sep;62(3):325-8. doi: 10.1097/FJC.0b013e3182a1e118.
Epinephrine was recently shown to induce a hypotension episode. Activation of β₂-adrenoceptors with smooth muscle relaxation may be the underlying mechanism. This study investigated the effects of ICI 118551, a β₂-adrenoceptors antagonist, on epinephrine-induced blood pressure reduction via different administration routes in rats.
A total of 144 Sprague Dawley rats were equally randomized into 3 groups (intranasal, intravenous, and intra-arterial administration), each with 4 subgroups: saline + saline, ICI 118551 + saline, saline + epinephrine, and ICI 118551 + epinephrine. All rats were anesthetized while spontaneously breathing. Epinephrine was administered at doses of 5 μg/kg via nose, 0.25 μg/kg via femoral vein, and 0.1 μg/kg via aorta. Mean arterial pressure and heart rate were monitored.
Mean arterial pressure decreased in all 3 saline + epinephrine subgroups after administration (P < 0.05), whereas it did not in other subgroups. Heart rate had no significant change in all subgroups.
Epinephrine-induced blood pressure reduction can be prevented by ICI 118551 in rats, suggesting that the activation of β₂-adrenoceptors contributes to blood pressure reduction.
肾上腺素最近被证明会引起低血压发作。β₂-肾上腺素受体的激活可能导致平滑肌松弛，这是其潜在的作用机制。本研究通过在大鼠中经不同途径给予 ICI 118551（β₂-肾上腺素受体拮抗剂），探讨其对肾上腺素诱导的血压降低的影响。
共 144 只 Sprague Dawley 大鼠被平均随机分为 3 组（鼻内、静脉内和动脉内给药），每组又分为 4 个亚组：盐水+盐水、ICI 118551+盐水、盐水+肾上腺素和 ICI 118551+肾上腺素。所有大鼠均在自主呼吸下麻醉。通过鼻腔给予 5 μg/kg 肾上腺素，通过股静脉给予 0.25 μg/kg 肾上腺素，通过主动脉给予 0.1 μg/kg 肾上腺素。监测平均动脉压和心率。
所有 3 个盐水+肾上腺素亚组给药后平均动脉压均降低（P < 0.05），而其他亚组则没有。所有亚组的心率均无明显变化。
ICI 118551 可预防肾上腺素诱导的大鼠血压降低，提示β₂-肾上腺素受体的激活参与了血压降低。
