Effects of afferent neural stimulation on critical oxygen delivery: a hemodynamic explanation

Abstract

Injury and activation of somatic afferent nerve fibers may alter critical oxygen delivery (DO2C), the point at which oxygen consumption becomes dependent upon delivery, and hence reduce tolerance to hypovolemia. The present study investigated the mechanism of this. Anesthetized mongrel dogs were divided into two groups: control (n = 6) and those subject to brachial nerve stimulation (BNS; n = 5). Whole body oxygen delivery (DO2I) and consumption were initially similar in both groups. DO2I was reduced by cardiac tamponade to determine DO2C. DO2C was significantly higher in BNS compared with control (11.5: 11.0-16.7 vs. 7.5: 6.9-9.5 ml.min-1.kg-1; median: Q1 - Q3), whereas critical oxygen extraction ratios were lower (54.8: 39.7-61.2 vs. 78.3: 53.5-92.4%). At approximately DO2C, normalized femoral blood flow was lower than renal flow in control (renal-femoral difference 17.4: 8.7-40.0%) but not in BNS (-7.8: -14.8 to +11.8%). These results indicate that activation of somatic afferent nerve fibers elevates DO2C. This could be due to an impairment in peripheral oxygen extraction as a consequence of a redistribution of blood flow away from metabolically active vital organs toward relatively inactive skeletal muscle.