Mehlhorn U, Allen S J, Adams D L, Davis K L, Gogola G R, Warters R D
Department of Anesthesiology, University of Texas-Houston Medical School 77030, USA.
Ann Thorac Surg. 1996 Jul;62(1):143-50. doi: 10.1016/0003-4975(96)00221-4.
Both crystalloid and blood cardioplegia result in cardiac dysfunction associated with myocardial edema. This edema is partially due to the lack of myocardial contraction during cardioplegia, which stops myocardial lymph flow. As an alternative, acceptable surgical conditions have been created in patients undergoing coronary artery bypass operations with esmolol-induced minimal myocardial contraction. We hypothesized that minimal myocardial contraction during circulatory support using either standard cardiopulmonary bypass (CPB) or a biventricular assist device would prevent myocardial edema by maintaining cardiac lymphatic function and thus prevent cardiac dysfunction.
We placed 6 dogs on CPB and 6 dogs on a biventricular assist device and serially measured myocardial lymph flow rate and myocardial water content in both groups and preload recruitable stroke work only in the CPB dogs. In all dogs we minimized heart rate with esmolol for 1 hour during total circulatory support.
Although myocardial lymph flow remained at baseline level during CPB and increased during biventricular assistance, myocardial water accumulation still occurred during circulatory support. However, as edema resolved rapidly after separation from circulatory support, myocardial water content was only slightly increased after CPB and biventricular assistance, and preload recruitable stroke work was normal.
Our data suggest that minimal myocardial contraction during both CPB and biventricular assistance supports myocardial lymphatic function, resulting in minimal myocardial edema formation associated with normal left ventricular performance after circulatory support. The concept of minimal myocardial contraction may be a useful alternative for myocardial protection, especially in high-risk patients with compromised left ventricular function.
晶体和血液心脏停搏液均可导致与心肌水肿相关的心脏功能障碍。这种水肿部分归因于心脏停搏期间心肌收缩缺乏，这会使心肌淋巴液流动停止。作为一种替代方法，在接受冠状动脉搭桥手术的患者中，通过艾司洛尔诱导最小程度的心肌收缩，已创造出可接受的手术条件。我们推测，在使用标准体外循环（CPB）或双心室辅助装置进行循环支持期间，最小程度的心肌收缩可通过维持心脏淋巴功能来预防心肌水肿，从而预防心脏功能障碍。
我们将6只狗置于CPB上，6只狗置于双心室辅助装置上，并连续测量两组的心肌淋巴液流速和心肌含水量，仅在CPB组的狗中测量前负荷可募集搏功。在所有狗中，在全循环支持期间，我们用艾司洛尔将心率降至最低1小时。
虽然在CPB期间心肌淋巴液流速保持在基线水平，在双心室辅助期间增加，但在循环支持期间仍发生了心肌积水。然而，由于在脱离循环支持后水肿迅速消退，CPB和双心室辅助后心肌含水量仅略有增加，且前负荷可募集搏功正常。
我们的数据表明，CPB和双心室辅助期间最小程度的心肌收缩均支持心肌淋巴功能，导致在循环支持后与正常左心室功能相关的最小程度的心肌水肿形成。最小程度心肌收缩的概念可能是心肌保护的一种有用替代方法，尤其是在左心室功能受损的高危患者中。
