Ketamine Blunts Sympathetic Nerve Activity Responses to a Cold Pressor test

Abstract

Pain evokes increases in blood pressure, heart rate, and central sympathetic outflow, and the perception of pain increases sympathetic nerve activity in an intensity‐dependent manner. That said, the mechanisms underlying the perception of pain and the effects on sympathetic nerve activity are not well established. The purpose of this experiment was to examine the effects of the analgesic ketamine, an NMDA receptor antagonist that reduces pain perception, on pain perception and muscle sympathetic nerve activity (MSNA) during a painful stimulus. In seven healthy participants (2 males; age 30 ± 6 yrs., mass of 83 ± 5 kg) MSNA and pain perception (Visual Analog Scale for Pain) were assessed during a 2‐min cold pressor test with and without intravenous infusion of 20 mg of ketamine, a dose consistent with guidelines from the US Army's Committee on Tactical Combat Casualty Care for pain management on the battlefield. Prior to the cold pressor test, ketamine alone increased heart rate (P=0.020), mean arterial blood pressure (P <0.001), and MSNA from 22 ± 6 burst/min to 32 ± 7 bust/min (P<0.01). During the subsequent cold pressor test, ketamine both decreased pain perception (Visual Analog Scale for Painscore ‐ control: 69 ± 22; ketamine: 22 ± 23, P<0.001) and blunted the peak increase in MSNA (control: Δ22 ± 4 burst/min; ketamine: Δ8 ± 7 burst/min). The increases in blood pressure, heart rate and sympathetic nerve activity elicited by the administration of ketamine suggest that ketamine is acting centrally within the cardiovascular control centers. Furthermore, these data support previous findings demonstrating that sympathetic outflow to a painful stimulus is graded with the pain perception.Support or Funding InformationFunding: Department of Defense – US Army, W81XWH1820012This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.