Lactate accumulation inprimate spinal cord during circulatory arrest

✓ In rhesus monkeys subjected to circulatory arrest, studies were made of the relationship of lactate production in the spinal cord to the duration of circulatory arrest and magnitude of lactate accumulation, and the results were compared to the magnitude of rise in cerebral tissue lactate. Both high and low thoracic laminectomies were performed on each of eight rhesus monkeys. Spinal cord tissue was excised for lactate assay at the upper laminectomy as a control, and a second tissue specimen was excised at the lower laminectomy site at time increments of 30 sec to 30 min after circulatory arrest. Tissue was excised from each site without circulatory arrest in one monkey and showed negligible increase in lactate production, indicating that excision of tissue itself does not result in increased lactate. Nonanoxic samples from seven monkeys averaged 4.60 millimoles (mM)/lactate/kg tissue, with a range of 2.22 to 6.49. Postcirculatory arrest samples from these monkeys averaged 11.10 mM lactate/kg tissue, with a range of 3.62 (at 30 sec) to 14.33 (at 10 min). Anoxic spinal tissue lactate was elevated above controls in each instance, and tissue lactate peaked between 5 to 10 min after circulatory arrest and remained stable with mild fluctuations beyond that time. Thus, the spinal cord responds to circulatory arrest much as cerebral tissue, but with some delay in the accumulation of lactic acid.