TY - JOUR
T1 - Sympathetic responses to central hypovolemia
T2 - New insights from microneurographic recordings
AU - Ryan, Kathy L.
AU - Rickards, Caroline A.
AU - Hinojosa-Laborde, Carmen
AU - Cooke, William H.
AU - Convertino, Victor A.
PY - 2012
Y1 - 2012
N2 - Hemorrhage remains a major cause of mortality following traumatic injury in both military and civilian settings. Lower body negative pressure (LBNP) has been used as an experimental model to study the compensatory phase of hemorrhage in conscious humans, as it elicits central hypovolemia like that induced by hemorrhage. One physiological compensatory mechanism that changes during the course of central hypovolemia induced by both LBNP and hemorrhage is a baroreflex-mediated increase in muscle sympathetic nerve activity (MSNA), as assessed with microneurography. The purpose of this review is to describe recent results obtained using microneurography in our laboratory as well as those of others that have revealed new insights into mechanisms underlying compensatory increases in MSNA during progressive reductions in central blood volume and how MSNA is altered at the point of hemodynamic decompensation. We will also review recent work that has compared direct MSNA recordings with noninvasive surrogates of MSNA to determine the appropriateness of using such surrogates in assessing the clinical status of hemorrhaging patients.
AB - Hemorrhage remains a major cause of mortality following traumatic injury in both military and civilian settings. Lower body negative pressure (LBNP) has been used as an experimental model to study the compensatory phase of hemorrhage in conscious humans, as it elicits central hypovolemia like that induced by hemorrhage. One physiological compensatory mechanism that changes during the course of central hypovolemia induced by both LBNP and hemorrhage is a baroreflex-mediated increase in muscle sympathetic nerve activity (MSNA), as assessed with microneurography. The purpose of this review is to describe recent results obtained using microneurography in our laboratory as well as those of others that have revealed new insights into mechanisms underlying compensatory increases in MSNA during progressive reductions in central blood volume and how MSNA is altered at the point of hemodynamic decompensation. We will also review recent work that has compared direct MSNA recordings with noninvasive surrogates of MSNA to determine the appropriateness of using such surrogates in assessing the clinical status of hemorrhaging patients.
KW - Baroreflex function
KW - Central hypovolemia
KW - Hemorrhage
KW - LBNP
KW - MSNA
KW - Sympathetic activity
UR - http://www.scopus.com/inward/record.url?scp=84866297460&partnerID=8YFLogxK
U2 - 10.3389/fphys.2012.00110
DO - 10.3389/fphys.2012.00110
M3 - Article
C2 - 22557974
AN - SCOPUS:84866297460
SN - 1664-042X
VL - 3 APR
JO - Frontiers in Physiology
JF - Frontiers in Physiology
M1 - Article 110
ER -