Extended latency of the cortical component of the somatosensory-evoked potential accompanying moderate increases in cerebral blood flow during systemic hypoxia in cats

Abstract

In 24 adult cats, the somatosensory-evoked potential (SEP) and cerebral blood flow (CBF) were measured under paralyzed, anesthetized conditions during exposure to two different ventilatory regimens. Group I cats (ventilated from 20 to 2% oxygen) responded ith a significant increase in white matter blood flow from 25.0 ± 7.8 to 43.8 ±10.5 ml/100 g/min recorded at 7% O 2. Gray matter blood flows in these animals increased but not to significant levels above the control blood flow measured at 20%. No significant changes in blood flow were observed in group II animals ventilated over the range of 25–30% oxygen as gray matter rose slightly (but not significantly) with hypoxia and white matter flows remained at levels of 25–30 ml/100g/min. The latency of the cortical component of the SEP was related to the degree of hypoxia. For both groups, significan textension in the latency to the occurrence of the cortical component of the SEP (normalized to the % of control SEP) occurred in each case ( P < 0.05). An inverse, linear relationship existed between the latency to the appearance of cortical component (ms) and the percentage oxygen concentration of the ventilatory mixture. No significant changes in thalamocortical conduction times were found, which indicates that hypoxia may have generalized effects on the synaptic pathways supporting the conduction of the SEP. The variation in blood flow and the latency of the cortical component observed between groups I and II may reflect the oxygen concentration used at the beginning of the experiment (25 vs 20%) and the gradations between them vs 3 and 2%. No systemic hypercapnia nor acidiosis was found within the mid-range oxygen concentrations which could account for the variations in flow and the evoked response. The results show that the SEP may be a reliable indicator of hypoxia as blood flows increase during transient cerebral hyperfusion probably resulting from vasodilation.