Some histopathologic aspects of cerebral injury in dogs subjected to profound hypothermia and circulatory arrest

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Abstract
A group of mongrel dogs was subjected to profound hypothermia with and without circulatory arrest using Drew''s method. Except for 3 normothermic perfusion controls, all dogs were cooled to esophageal temperatures of 6 to 12. 5[degree] C. and perfused or subjected to circulatory arrest for 30 to 60 min., exclusive of time for cooling and rewarming. Circulatory arrest was established in 9 dogs, divided into groups of 3, for 30 min., 45 min., and 60 min., respectively. The initial esophageal temperatures in the circulatory arrest dogs ranged from 6 to 8[degree] C. Survival time varied from one hour to 96hr. and, in most animals, from 24 to 96 hr. The brains in all animals, except of control dog, were fixed in situ by Cammermeyer''s method and removed after 4 hr, sectioned, and studied by a number of standard histological staining techniques. The brain of a control dog (normothermic) was removed immediately on death and fixed in formol saline. It was confirmed that Cammermeyer''s method of fixation prevents fixation artifacts that occur by removal of the unfixed brain. In dogs subjected to profound hypothermia, but without circulatory arrest, and perfused for 60 min., reversible neuronal swelling and milk edema of white matter occurred, but only the edema persisted after 72 hr. of survival. In the dogs in which circulatory arrest was induced for a variable period of time under profound hypothermia, significant irreversible cerebral neuronal damage was avoided if circulatory arrest was not maintained over thirty minutes. Some dogs withstood 45 min. of circulatory arrest quite well. The cerebral edema found after 45 min. of profound hypothermia and circulatory arrest did not show reversibility after 96 hr. of survival. It was accompanied by astroglial reactions. Neuronal swelling and pyknosis persisted after circulatory arrest over 45 min. Severe damage occurred in the Purkinje cells of the cerebellum and in the caudate nucleus. Damage to nerve cells of the cerebral cortex was present but widely scattered. Proliferation of vascular endothelium seen in the caudate nucleus, after 60 min. of profound hypothermia and circulatory arrest, appeared to be a reaction to hypothermia and probably induced local ischemia.

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