Caceres M J, Schleien C L, Kuluz J W, Gelman B, Dietrich W D
Department of Pediatrics (R-131), University of Miami School of Medicine FL 33101, USA.
Acta Neuropathol. 1995;90(6):582-91. doi: 10.1007/BF00318570.
This study examined the early microvascular and neuronal consequences of cardiac arrest and resuscitation in piglets. We hypothesized that early morphological changes occur after cardiac arrest and reperfusion, and that these findings are partly caused by post-resuscitation hypertension. Three groups of normothermic piglets (37.5 degrees - 38.5 degrees C) were investigated: group 1, non-ischemic time controls; group 2, piglets undergoing 8 min of cardiac arrest by ventricular fibrillation, 6 min of cardiopulmonary resuscitation (CPR) and 4 h of reperfusion; and group 3, non-ischemic hypertensive controls, receiving 6 min of CPR after only 10 s of cardiac arrest followed by 4-h survival. Immediately following resuscitation, acute hypertension occurred with peak systolic pressure equal to 197 +/- 15 mm Hg usually lasting less than 10 min. In reacted vibratome sections, isolated foci of extravasated horseradish peroxidase were noted throughout the brain within surface cortical layers and around penetrating vessels in group 2. Stained plastic sections of leaky sites demonstrated variable degrees of tissue injury. While many sections were unremarkable except for luminal red blood cells and leukocytes, other specimens contained abnormal neurons, some appearing irreversibly injured. The number of vessels containing leukocytes was higher in group 2 than in controls (3.8 +/- 0.6% vs 1.4 +/- 0.4% of vessels, P < 0.05). Evidence for irreversible neuronal injury was only seen in group 2. Endothelial vacuolization was higher in groups 2 and 3 than in group 1 (P < 0.05). Ultrastructural examination of leaky sites identified mononuclear and polymorphonuclear leukocytes adhering to the endothelium of venules and capillaries only in group 2. The early appearance of luminal leukocytes in ischemic animals indicates that these cells may contribute to the genesis of ischemia reperfusion injury in this model. In both groups 2 and 3 endothelial cells demonstrated vacuolation and luminal discontinuities with evidence of perivascular astrocytic swelling. Widespread microvascular and neuronal damage is present as early as 4 h after cardiac arrest in infant piglets. Hypertension appears to play a role in the production of some of the endothelial changes.
本研究检测了仔猪心脏骤停及复苏后的早期微血管和神经元变化。我们假设心脏骤停和再灌注后会出现早期形态学改变，且这些发现部分是由复苏后高血压所致。对三组体温正常的仔猪（37.5摄氏度 - 38.5摄氏度）进行了研究：第1组为非缺血时间对照组；第2组为经历8分钟室颤性心脏骤停、6分钟心肺复苏（CPR）及4小时再灌注的仔猪；第3组为非缺血性高血压对照组，仅经历10秒心脏骤停后接受6分钟CPR并存活4小时。复苏后立即出现急性高血压，收缩压峰值等于197±15毫米汞柱，通常持续不到10分钟。在反应性振动切片中，第2组仔猪大脑表层皮质层内及穿透血管周围可见散在的辣根过氧化物酶外渗灶。渗漏部位的塑料染色切片显示出不同程度的组织损伤。虽然许多切片除管腔内红细胞和白细胞外无明显异常，但其他标本含有异常神经元，有些呈现不可逆损伤。第2组含白细胞的血管数量高于对照组（血管的3.8±0.6% 对1.4±0.4%，P < 0.05）。仅在第2组中发现不可逆神经元损伤的证据。第2组和第3组的内皮细胞空泡化程度高于第1组（P < 0.05）。对渗漏部位的超微结构检查发现，仅在第2组中单核和多形核白细胞黏附于小静脉和毛细血管内皮。缺血动物管腔内白细胞的早期出现表明这些细胞可能促成该模型中缺血再灌注损伤的发生。在第2组和第3组中，内皮细胞均表现为空泡化和管腔连续性中断，伴有血管周围星形胶质细胞肿胀的证据。早在仔猪心脏骤停后4小时就出现了广泛的微血管和神经元损伤。高血压似乎在某些内皮变化的产生中起作用。
