RECOVERY OF CEREBRAL BLOOD-FLOW AND ENERGY-STATE IN PIGLETS AFTER HYPOTHERMIC CIRCULATORY ARREST VERSUS RECOVERY AFTER LOW-FLOW BYPASS

A miniature piglet model that replicates clinical hypothermic (14-degr ees-C nasopharyngeal) circulatory arrest and low-flow (50 ml/kg per mi nute) bypass was used to study carotid blood flow with electromagnetic flow probe, cerebral blood flow by microsphere injection, cerebral me tabolic rate by arteriovenous oxygen and glucose extractions, lactate production by cerebral arteriovenous difference, and cerebral edema. D ata from five animals that underwent circulatory arrest and five anima ls that underwent low-flow bypass (aged 28.8 +/- 0.4 [mean +/- standar d error of the mean] days) were analyzed. The duration of circulatory arrest and low-flow bypass was 1 hour. In a parallel study with the sa me animal model, phosphorus 31 magnetic resonance spectroscopy was use d to assess cerebral phosphocreatine, nucleoside triphosphate (adenosi ne triphosphate), and intracellular pH. Five animals (aged 31.8 +/- 1. 1 days) underwent- circulatory arrest, and five underwent low-flow byp ass. A brief phase of hyperemic carotid blood flow was seen immediatel y after the onset of reperfusion in the circulatory arrest group but n ot in the low-flow group. In the circulatory arrest and low-flow bypas s groups, cerebral blood flow (percentage of baseline 71.2% +/- 8.3% a nd 69.1% +/- 5.8%, respectively cerebral oxygen consumption (45.6% +/- 10.0%, 44.5% +/- 7.6%), and cerebral glucose consumption (31.5% +/- 3 0.7%, 83.5% +/- 24.2%) remained depressed after 45 minutes of reperfus ion and rewarming to normothermia. However, after 3 more hours of puls atile normothermic reperfusion, cerebral oxygen consumption and cerebr al glucose consumption had returned to baseline. Phosphocreatine, aden osine triphosphate, and pH were maintained at or above baseline levels throughout low-flow bypass and throughout 3 hours of normothermic rep erfusion. In contrast, both phosphocreatine and adenosine triphosphate became undetectable 32 +/- 3.7 minutes after onset of circulatory arr est. During and early after circulatory arrest, pH decreased to a mini mum of 6.506 +/- 0.129 at 40 minutes after reperfusion. After 3 hours of normothermic reperfusion, phosphocreatine and adenosine triphosphat e recovered to 98.6% +/- 9.0% and 90.1% +/- 13.5% of baseline, respect ively, and pH was 7.087 +/- 0.051, similar to baseline (7.1755 +/- 0.0 41). In the low-flow bypass group, the disparity between the depressed level of cerebral oxygen consumption and normal high-energy phosphate levels may reflect incomplete cerebral rewarming or decreased energy consumption. In the circulatory arrest group, the parallel recovery of oxygen consumption and high-energy phosphates eventually achieving ba seline levels suggests that the degree of hypothermia used provides ad equate protection for acute cerebral recovery after 1 hour of circulat ory arrest. Clinically observed cognitive deficits observed after 1 ho ur of hypothermic circulatory arrest may therefore be related to delay ed mechanisms of injury, such as excitotoxicity, and may be amenable t o postarrest therapeutic interventions.