Lowenstein E, Foëx P, Francis C M, Davies W L, Yusuf S, Ryder W A
Anesthesiology. 1981 Oct;55(4):349-59. doi: 10.1097/00000542-198110000-00004.
The effects of increasing inspired halothane concentration (0.5, 1.0, 1.5, 2.0 per cent) upon left ventricular myocardium supplied by a critically narrowed coronary artery and a normal coronary artery were studied in 11 open-chested dogs. Regional ventricular function was measured by continuous recording of ventricular segment length using pairs of implanted miniature ultrasonic length detectors in the left anterior descending coronary artery (LAD) and left circumflex coronary artery (LC) territories before and during critical stenosis of the LAD by a micrometer-controlled snare. Critical narrowing was documented by ischemic regional ventricular function (i.e., post-systolic shortening; systolic lengthening) limited to the LAD territory when FIO2 = 0 for 90 seconds. Hemodynamic variables (aortic, left atrial and left ventricular pressure, and heart rate) were measured, ECG lead II was recorded, and the first derivative of left ventricular pressure (LV dP/dt) and coronary perfusion pressure derived for each halothane concentration before and during LAD narrowing. Increasing halothane was associated with equivalent progressive depression of global ventricular function before and during LAD constriction. Prior to LAD constriction, no ischemic changes in regional function occurred. Regional ventricular function was normal during 0.5 percent halothane in the presence of LAD constriction. With increasing halothane during LAD constriction, ischemic regional ventricular function was observed in the LAD territory in eight of eleven hearts, whereas regional ventricular function remained normal in the LC territory. The epicardial ECG was recorded in three dogs and was insensitive as an indicator of ischemia, becoming abnormal only after severe ischemic changes were established. In these studies, in which heart rate remained constant, arterial blood pressure and LV dP/dt decreased, and left ventricular end-diastolic pressure increased, decrease in blood flow and oxygen delivery due to a lower perfusion pressure distal to the coronary artery narrowing appears to be primarily responsible for the observations. The authors hypothesize that clinically unapparent episodes of regional myocardial ischemia distal to narrowed coronary arteries may be an important cause of perioperative myocardial infarction.
在11只开胸犬身上研究了增加吸入氟烷浓度（0.5%、1.0%、1.5%、2.0%）对由严重狭窄冠状动脉和正常冠状动脉供血的左心室心肌的影响。通过在左前降支冠状动脉（LAD）和左旋支冠状动脉（LC）区域使用成对植入的微型超声长度探测器连续记录心室节段长度来测量局部心室功能，在LAD通过微米控制圈套器进行临界狭窄之前和期间进行测量。当FIO2在90秒内为0时，缺血性局部心室功能（即收缩后缩短；收缩期延长）仅限于LAD区域，以此记录临界狭窄情况。测量血流动力学变量（主动脉、左心房和左心室压力以及心率），记录心电图II导联，并在LAD狭窄之前和期间针对每种氟烷浓度得出左心室压力的一阶导数（LV dP/dt）和冠状动脉灌注压力。增加氟烷与LAD收缩之前和期间整体心室功能的同等程度逐渐降低相关。在LAD收缩之前，局部功能未发生缺血性改变。在LAD收缩且氟烷浓度为0.5%时，局部心室功能正常。在LAD收缩期间随着氟烷浓度增加，11只心脏中的8只在LAD区域观察到缺血性局部心室功能，而LC区域的局部心室功能保持正常。在三只犬身上记录了心外膜心电图，其作为缺血指标不敏感，仅在严重缺血改变确立后才变得异常。在这些心率保持恒定的研究中，动脉血压和LV dP/dt降低，左心室舒张末期压力升高，冠状动脉狭窄远端灌注压力降低导致的血流和氧输送减少似乎是这些观察结果的主要原因。作者推测，冠状动脉狭窄远端临床上不明显的局部心肌缺血发作可能是围手术期心肌梗死的一个重要原因。
