Meissner A, Weber T P, Van Aken H, Zbieranek K, Rolf N
Klinik und Poliklinik für Anästhesiologie und operative Intensivmedizin der Westfälischen Wilhelms-Universität Münster, Germany.
Anesth Analg. 1998 Nov;87(5):1009-14.
Clonidine, an alpha2-adrenergic agonist, has been widely used in anesthesia because of its sedative, analgesic, sympatholytic, and specific hemodynamic effects. The use of clonidine in myocardial ischemia is controversial because of its bradycardic and hypotensive effects. In the present study, we tested the hypothesis that clonidine improves recovery from myocardial stunning in conscious dogs. Seven dogs were chronically instrumented to allow measurement of left atrial pressure (LAP), aortic blood pressure (ABP), left ventricular pressure (LVP), maximal rate of increase of LVP (LVdP/dtmax), and myocardial wall thickening fraction (WTF). The myocardial blood flow was measured using colored microspheres. To compensate for any potential interaction between the two ischemic episodes, experiments were performed on separate days in a cross-over fashion (four animals underwent Condition 1, and three underwent Condition 2 as their first experiment). The ischemic episodes involved 1) 10 min of ischemia of the left anterior descending (LAD) coronary artery without any intervention, and 2) 10 min of LAD ischemia 30 min after 10 microg/kg iv clonidine. WTF was measured before the induction of ischemia or the application of clonidine (baseline) and at predetermined time points until complete recovery of myocardial function. WTF recovered faster during the first 2 h of reperfusion when clonidine was administered. The increase in plasma epinephrine was attenuated by clonidine during ischemia, but there was no change during reperfusion. The increase of plasma norepinephrine levels was attenuated during ischemia and reperfusion. The hemodynamic effects of clonidine did not depress myocardial perfusion or impair myocardial function.
In this study, we investigated the effects of IV clonidine on myocardial stunning in chronically instrumented dogs. Clonidine improved the recovery from myocardial stunning and attenuated increases in catecholamine plasma levels.
可乐定是一种α2肾上腺素能激动剂，因其具有镇静、镇痛、交感神经阻滞和特定的血流动力学效应，已在麻醉中广泛应用。由于其减慢心率和降低血压的作用，可乐定在心肌缺血中的应用存在争议。在本研究中，我们检验了可乐定可改善清醒犬心肌顿抑恢复的假说。七只犬被长期植入仪器，以测量左心房压力（LAP）、主动脉血压（ABP）、左心室压力（LVP）、左心室压力最大上升速率（LVdP/dtmax）和心肌壁增厚分数（WTF）。使用彩色微球测量心肌血流量。为补偿两次缺血发作之间的任何潜在相互作用，实验在不同日期以交叉方式进行（四只动物先进行条件1实验，三只动物先进行条件2实验）。缺血发作包括：1）左前降支（LAD）冠状动脉10分钟缺血，无任何干预；2）静脉注射10μg/kg可乐定30分钟后，LAD缺血10分钟。在缺血诱导或可乐定应用前（基线）以及在预定时间点直至心肌功能完全恢复时测量WTF。给予可乐定时，再灌注的前2小时内WTF恢复更快。缺血期间可乐定可减弱血浆肾上腺素的升高，但再灌注期间无变化。缺血和再灌注期间血浆去甲肾上腺素水平的升高均减弱。可乐定的血流动力学效应未降低心肌灌注或损害心肌功能。
在本研究中，我们研究了静脉注射可乐定对长期植入仪器犬心肌顿抑的影响。可乐定改善了心肌顿抑的恢复，并减弱了儿茶酚胺血浆水平的升高。
