Böttiger B W, Krumnikl J J, Gass P, Schmitz B, Motsch J, Martin E
Department of Anesthesiology, University of Heidelberg, Germany.
Resuscitation. 1997 Feb;34(1):79-87. doi: 10.1016/s0300-9572(96)01029-5.
Experimental data indicate that early microcirculatory reperfusion is disturbed after cardiac arrest. We investigated the influence of prolonged cardiac arrest and basic life support (BLS) procedures on the quality of cerebral microcirculatory reperfusion.
In mechanically ventilated male Wistar rats anesthetized with N2O and halothane, cardiac arrest was induced by electrical fibrillation. Ten animals (group I) were subjected to 17 min of cardiac arrest (no-flow). Nine additional animals (group II) underwent only 12 min of cardiac arrest (no-flow), which was followed by a 5-min phase of BLS (i.e. mechanical ventilation and external cardiac compressions). In both groups, advanced resuscitation procedures including mechanical ventilation, external cardiac massage, 0.2 mg kg-1 epinephrine, 0.5 mmol kg-1 NaHCO3, and defibrillation were started 17 min after induction of cardiac arrest. The perfusion of the cerebral microcirculation was visualized by injection of 0.3 g kg-1 15% fluorescein isothiocyanate (FITC)-albumin 5 min after restoration of spontaneous circulation (ROSC), and the animals were decapitated 2 min later. The left hemispheres were fixed in 4% formalin, and coronal sections of 200 microns thickness at three different standard levels of the rat brain were investigated using fluorescence microscopy. Areas without capillary filling (cerebral 'no-reflow') were identified and calculated.
ROSC could be achieved in five of 10 animals (50%) of group I, and in six of nine animals (67%) of group II (P = n.s.). The severity of cerebral 'no-reflow' was higher in group II compared with group I (6.9 +/- 7.6 vs. 0.7 +/- 0.7% of total sectional areas; P < or = 0.05). Two sham-operated animals showed homogeneous reperfusion.
Wistar rats did not develop a marked cerebral 'no-reflow' phenomenon after circulatory arrest. A relevant degree of cerebral 'no-reflow' occurred, however, in animals subjected to a phase of BLS before circulatory stabilization. Therefore, low-flow states following prolonged cardiocirculatory arrest may aggravate early cerebral microcirculatory reperfusion disorders.
实验数据表明心脏骤停后早期微循环再灌注受到干扰。我们研究了长时间心脏骤停和基础生命支持（BLS）程序对脑微循环再灌注质量的影响。
在使用一氧化二氮和氟烷麻醉的机械通气雄性Wistar大鼠中，通过电颤诱发心脏骤停。10只动物（I组）经历17分钟的心脏骤停（无血流）。另外9只动物（II组）仅经历12分钟的心脏骤停（无血流），随后是5分钟的BLS阶段（即机械通气和体外心脏按压）。在两组中，心脏骤停诱导17分钟后开始包括机械通气、体外心脏按摩、0.2毫克/千克肾上腺素、0.5毫摩尔/千克碳酸氢钠和除颤在内的高级复苏程序。自主循环恢复（ROSC）5分钟后，通过注射0.3克/千克15%异硫氰酸荧光素（FITC）-白蛋白使脑微循环灌注可视化，2分钟后将动物断头。将左半球固定在4%的福尔马林中，使用荧光显微镜在大鼠脑的三个不同标准水平研究200微米厚的冠状切片。识别并计算无毛细血管充盈的区域（脑“无再流”）。
I组10只动物中有5只（50%）实现了ROSC，II组9只动物中有6只（67%）实现了ROSC（P=无显著性差异）。与I组相比，II组脑“无再流”的严重程度更高（分别占总切片面积的6.9±7.6%和0.7±0.7%；P≤0.05）。两只假手术动物显示出均匀的再灌注。
Wistar大鼠在循环骤停后未出现明显的脑“无再流”现象。然而，在循环稳定前经历BLS阶段的动物中出现了相关程度的脑“无再流”。因此，长时间心循环骤停后的低血流状态可能会加重早期脑微循环再灌注障碍。
