Amelioration of Brain Damage After 12 Minutes' Cardiac Arrest in Dogs

Abstract

To determine the efficacy of cerebral microcirculation promoting therapy in postischemic brain failure, 11 dogs awakening from methohexital sodium anesthesia were subjected to 12 minutes of reversible circulatory arrest by ventricular fibrillation. Physiological variables were controlled for six hours after resuscitation, and the dogs were observed for seven days. Six dogs without the special postresuscitative therapy did not awaken, and either died within 36 hours or remained comatose for seven days. In five dogs, a combination of the following measures was applied: (1) mean arterial pressure was raised to 150 to 180 mm Hg with norepinephrine for six hours; (2) heparinization; (3) rapid intra-aortic injection of dextran 40 (10 ml/kg body weight); and (4) normovelemic hemodilution with dextran 40 to a hematocrit reading of 25% to 30%. All five treated dogs awakened within 24 hours and appeared normal on the seventh day. Therapy enhanced constriction of pupils and normalization of the electroencephalogram (P less than .05). Postischemic neurological deficit is at least partially due to impaired reperfusion and can be ameliorated or prevented by blood flowing-promoting therapy.

Relationship of blood pressure and flow during CPR to chest compression amplitude: Evidence for an effective compression threshold

“…One should be especially cautious in drawing conclusions from this study regarding the risk/benefit ratio of CPR with more forceful compressions, because the animals were pretreated with heparin, which alters the pathologic lesions of traumatic over compression and may have some influence on the outcome of resuscitation [10].…”

Un niveau réduit d’hématocrite aggrave les lésions cérébrales après un arrêt circulatoire hypothermique prolongé chez le rat

“…Coronal sections of six rats were prepared for immunohistochemistry analysis, performed using an avidin-biotin peroxidase method as described previously. 15 Briefly, sections were washed in 0.1 mol·L -1 PBS, incubated in 0.1 mol·L -1 PBS containing 1% bovine albumin and 0.2% Triton-X-100 for 30 min, and subsequently incubated overnight with specific first antibody (C-Fos, Sigma, St. Louis, USA; 1:10000 dilution; Bcl-2, Sigma, 1:1000 dilution; Bax, Sigma, 1:5000 dilution). The next day, the brain sections were incubated with appropriate secondary IgG (1:200 dilution) for one hour, and with avidin-biotin peroxidase for one hour in a humidified chamber.…”

An experimental circulatory arrest model in the rat to evaluate calcium antagonists in cerebral resuscitation

“…Animal models previously described in cerebral resuscitation studies employ dogs or monkeys as subjects [3][4][5]. The canine model developed by Safar et al [3] is created by inducing 12 minutes of unsupported ventricular fibrillation, from which as many as 67% (23/ 34) of the dogs are never resuscitated and therefore do not enter into the cerebral resuscitation phase of the study.…”