Hanouz Jean-Luc, Yvon Alexandra, Flais Frédéric, Rouet René, Ducouret Pierre, Bricard Henri, Gérard Jean-Louis
*Department of Anesthesiology, Centre Hospitalier Universitaire Caen, Caen, France; and †Laboratory of Experimental Anesthesiology and Cellular Physiology, Centre Hospitalier Universitaire Caen, Caen, France.
Anesth Analg. 2003 Nov;97(5):1230-1238. doi: 10.1213/01.ANE.0000086731.87098.99.
We examined the effect of propofol on the main mechanisms involved in ischemia/reperfusion-induced arrhythmias (i.e., spontaneous arrhythmias, conduction blocks, and dispersion of repolarization) in vitro. In a double-chamber bath, guinea pig right ventricular muscle strips were subjected to 30 min of simulated ischemia followed by 30 min of reperfusion (altered zone; AZ) and to standard conditions (normal zone; NZ). Action potential (AP) parameters were recorded in the NZ and AZ. We studied the effects of Intralipid(R) and of propofol at 10(-6), 10(-5), and 2 x 10(-5) M on the occurrence of spontaneous sustained arrhythmias, conduction blocks, and the dispersion of repolarization. In NZ, Intralipid and propofol did not significantly modify the AP parameters. Propofol, but not Intralipid, lessened the ischemia-induced decrease in AP duration (APD) at 90% of repolarization (APD(90)) and attenuated the APD dispersion around the "border zone." Propofol did not modify the occurrence of ischemia-induced arrhythmias. Propofol 10(-6) M, but not Intralipid or propofol at 10(-5) and 2 x 10(-5) M, decreased the occurrence of ischemia-induced conduction blocks. Propofol decreased the occurrence of reperfusion-induced spontaneous sustained arrhythmias. We conclude that, in vitro, propofol attenuated the ischemia-induced APD(90) dispersion around the "border zone" and decreased the occurrence of spontaneous arrhythmias related to myocardial reperfusion injury.
In isolated guinea pig ventricular myocardium propofol, but not Intralipid(R), attenuated the ischemia-induced shortening of action potential and, thus, the dispersion of repolarization and decreased the occurrence of spontaneous ventricular arrhythmia related to reperfusion injury. This result may be important for propofol-based anesthesia in patients at high risk for intraoperative ischemia.
我们在体外研究了丙泊酚对缺血/再灌注诱导的心律失常（即自发性心律失常、传导阻滞和复极离散）所涉及的主要机制的影响。在双腔浴槽中，将豚鼠右心室肌条进行30分钟的模拟缺血，随后进行30分钟的再灌注（改变区；AZ）以及置于标准条件下（正常区；NZ）。在NZ和AZ中记录动作电位（AP）参数。我们研究了10%中链脂肪乳（Intralipid®）以及10⁻⁶、10⁻⁵和2×10⁻⁵ M丙泊酚对自发性持续性心律失常、传导阻滞的发生以及复极离散的影响。在NZ中，10%中链脂肪乳和丙泊酚未显著改变AP参数。丙泊酚而非10%中链脂肪乳减轻了缺血诱导的90%复极化时动作电位时程（APD）的缩短（APD₉₀），并减弱了“边界区”周围的APD离散。丙泊酚未改变缺血诱导的心律失常的发生。10⁻⁶ M丙泊酚而非10%中链脂肪乳或10⁻⁵和2×10⁻⁵ M丙泊酚降低了缺血诱导的传导阻滞的发生。丙泊酚减少了再灌注诱导的自发性持续性心律失常 的发生。我们得出结论，在体外，丙泊酚减弱了缺血诱导的“边界区”周围的APD₉₀离散，并减少了与心肌再灌注损伤相关的自发性心律失常的发生。
在分离的豚鼠心室心肌中，丙泊酚而非10%中链脂肪乳减弱了缺血诱导的动作电位缩短，从而减弱了复极离散，并减少了与再灌注损伤相关的自发性室性心律失常的发生。这一结果对于术中缺血高危患者的丙泊酚麻醉可能具有重要意义。
