Outcome Model of Asphyxial Cardiac Arrest in Rats

• Published in: Journal of cerebral blood flow and metabolism 1995-11, Vol.15 (6), p.1032-1039
• Main Authors: Katz, Laurence, Ebmeyer, Uwe, Safar, Peter, Radovsky, Ann, Neumar, Robert
• Format: Article
• Language: English
• Subjects: Animals; Asphyxia - complications; Biological and medical sciences; Brain Damage, Chronic - pathology; Brain Ischemia - etiology; Brain Ischemia - pathology; Cardiopulmonary Resuscitation; Disease Models, Animal; Heart Arrest - complications; Heart Arrest - etiology; Heart Arrest - pathology; Male; Medical sciences; Nervous System Diseases - etiology; Neurology; Rats; Rats, Sprague-Dawley; Vascular diseases and vascular malformations of the nervous system
• ISSN: 0271-678X; 1559-7016
• DOI: 10.1038/jcbfm.1995.129

An outcome model with asphyxial cardiac arrest in rats has been developed for quantifying brain damage. Twenty-two rats were randomized into three groups. Control group I was normal, was conscious, and had no asphyxia (n = 6). Sham group II had anesthesia and surgery but no asphyxia (n = 6). All 12 rats in groups I and II survived to 72 h and were functionally and histologically normal. Arrest group III (the model; n = 10) had light anesthesia and apneic asphyxia of 8 min, which led to cessation of circulation at 3–4 min of apnea, resulting in cardiac arrest (no flow) of 4–5 min. All 10 rats had spontaneous circulation restored by standard external cardiopulmonary resuscitation. Nine rats survived controlled ventilation for 1 h and observation to 72 h, while one rat died before extubation. All nine survivors were conscious at 72 h, with neurologic deficit scores (0% = best; 100% = worst) of 7 ± 69? (2–16%). All brain regions at five coronal levels were examined for ischemic neurons. The prevalence of ischemic neurons in five regions was categorically scored. The average total brain histopathologic damage score in group III (n = 9) was 2.1 (p < 0.05 vs. group I or II). A reproducible outcome model of cardiac arrest in rats was documented. It provides a tool for investigating pathophysiological mechanisms of neuronal death caused by a transient global hypoxic–ischemic brain insult.