EARLY ENDOTHELIAL DAMAGE AND LEUKOCYTE ACCUMULATION IN PIGLET BRAINS FOLLOWING CARDIAC-ARREST

This study examined the early microvascular and neuronal consequences of cardiac arrest and resuscitation in piglets. We hypothesized that e arly morphological changes occur after cardiac arrest and reperfusion, and that these findings are partly caused by post-resuscitation hyper tension. Three groups of normothermic piglets (37.5 degrees-38.5 degre es C) were investigated: group I, non-ischemic time controls; group 2, piglets undergoing 8 min of cardiac arrest by ventricular fibrillatio n, 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. Immedi ately following resuscitation, acute hypertension occurred with peak s ystolic pressure equal to 197 +/- 15 mm Hg usually lasting less than 1 0 min. In reacted vibratome sections, isolated foci of extravasated ho rseradish peroxidase were noted throughout the brain within surface co rtical layers and around penetrating vessels in group 2. Stained plast ic sections of leaky sites demonstrated variable degrees of tissue inj ury. While many sections were unremarkable except for luminal red bloo d cells and leukocytes, other specimens contained abnormal neurons, so me appearing irreversibly injured. The number of vessels containing le ukocytes 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 inju ry was only seen in group 2. Endothelial vacuolization was higher in g roups 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 indi cates that these cells may contribute to the genesis of ischemia reper fusion 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 neurona l damage is present as early as 4 h after cardiac arrest in infant pig lets. Hypertension appears to play a role in the production of some of the endothelial changes.