Regional cerebral blood flow following hypothermic circulatory arrest in newborn dogs.

A model of hypothermic circulatory arrest has been developed in newborn dogs which simulates the procedure used for the operative repair of congenital cardiac defects in human infants. Hypothermic circulatory arrest for 1.0 h causes no brain damage, whereas cardiac arrest for 1.75 h results in damage of the cerebral cortex, basal ganglia and to a lesser extent the claustrum and amygdaloid nucleus. In the present study, we determined regional cerebral blood flow (rCBF) during 24 h of recovery from hypothermic circulatory arrest. Newborn nitrous oxide anesthetized and artificially ventilated dogs were cooled to 20 degrees C and subjected to cardiac arrest by the i.v. injection of KCl for either 1.0 or 1.75 h. Thereafter, animals were resuscitated, rewarmed to 37 degrees C, and rCBF measured with [14C]iodoantipyrine at either 2 or 18 h of recovery. Control animals were rendered hypothermic to 20 degrees C without cardiac arrest for 1.0 or 1.75 h prior to rewarming. No alterations in CBF at either 2 or 18 h of recovery were present in any of 16 analyzed structures in animals previously subjected to hypothermic circulatory arrest compared to controls rendered hypothermic alone. A direct linear correlation existed between mean arterial blood pressure and blood flow within frontal, parietal and occipital cortex, occipital white matter, hypothalamus and cerebellar vermis in puppies arrested for 1.75 h and recovered for 2 h, suggesting a loss of CBF autoregulation at this interval. No such association between blood pressure and CBF was apparent at 18 h of recovery.(ABSTRACT TRUNCATED AT 250 WORDS)