TY - JOUR

T1 - Spinal Cord Disruption Is Associated with a Loss of Cushing-Like Blood Pressure Interactions

AU - Saleem, Saqib

AU - Sarafis, Zoe K

AU - Lee, Amanda H X

AU - Squair, Jordan W

AU - Barak, Otto F

AU - Sober-Williams, Elin

AU - Suraj, Rejitha

AU - Coombs, Geoff B

AU - Mijacika, Tanja

AU - West, Christopher R

AU - Krassioukov, Andrei V

AU - Ainslie, Philip N

AU - Dujic, Zeljko

AU - Tzeng, Yu-Chieh

AU - Phillips, Aaron A

PY - 2019/5/1

Y1 - 2019/5/1

N2 - The capacity of the cerebrovasculature to buffer changes in blood pressure (BP) likely plays an important role in the prevention of stroke, which is three- to fourfold more common after spinal cord injury (SCI). Although the directional relationship between BP and cerebral blood flow (CBF) has traditionally been thought to travel solely from BP to CBF, a Cushing-like mechanism functioning in the inverse direction, in which changes in CBF influence BP, has recently been revealed using Granger causality analysis. Although both CBF buffering of BP and the Cushing-like mechanism are influenced by the sympathetic nervous system, we do not understand the impact of disruption of descending sympathetic pathways within the spinal cord, caused by cervical SCI on these regulatory systems. We hypothesized that people with cervical SCI would have greater BP to CBF transmission, as well as a reduced Cushing-like mechanism. The directional relationships between mean arterial BP (MAP; Finometer® PRO) and middle cerebral artery blood velocity (MCAv; transcranial Doppler) were assessed at rest in 14 cervical SCI subjects and 16 uninjured individuals using Granger causality analysis, while also accounting for end-tidal CO2 tension. Those with SCI exhibited 66% increased forward MAP→MCAv information transmission as compared with the uninjured group (p = 0.0003), indicating reduced cerebrovascular buffering of BP, and did not have a predominant backward Cushing-like MCAv→MAP phenotype. These results indicate that both forward and backward communication between BP and CBF are influenced by SCI, which may be associated with impaired cerebrovascular BP buffering after SCI as well as widespread BP instability.

AB - The capacity of the cerebrovasculature to buffer changes in blood pressure (BP) likely plays an important role in the prevention of stroke, which is three- to fourfold more common after spinal cord injury (SCI). Although the directional relationship between BP and cerebral blood flow (CBF) has traditionally been thought to travel solely from BP to CBF, a Cushing-like mechanism functioning in the inverse direction, in which changes in CBF influence BP, has recently been revealed using Granger causality analysis. Although both CBF buffering of BP and the Cushing-like mechanism are influenced by the sympathetic nervous system, we do not understand the impact of disruption of descending sympathetic pathways within the spinal cord, caused by cervical SCI on these regulatory systems. We hypothesized that people with cervical SCI would have greater BP to CBF transmission, as well as a reduced Cushing-like mechanism. The directional relationships between mean arterial BP (MAP; Finometer® PRO) and middle cerebral artery blood velocity (MCAv; transcranial Doppler) were assessed at rest in 14 cervical SCI subjects and 16 uninjured individuals using Granger causality analysis, while also accounting for end-tidal CO2 tension. Those with SCI exhibited 66% increased forward MAP→MCAv information transmission as compared with the uninjured group (p = 0.0003), indicating reduced cerebrovascular buffering of BP, and did not have a predominant backward Cushing-like MCAv→MAP phenotype. These results indicate that both forward and backward communication between BP and CBF are influenced by SCI, which may be associated with impaired cerebrovascular BP buffering after SCI as well as widespread BP instability.

KW - Blood Flow Velocity/physiology

KW - Blood Pressure/physiology

KW - Cerebrovascular Circulation/physiology

KW - Female

KW - Humans

KW - Male

KW - Spinal Cord Injuries/physiopathology

U2 - 10.1089/neu.2018.5931

DO - 10.1089/neu.2018.5931

M3 - Article

C2 - 30458117

VL - 36

SP - 1487

EP - 1490

JO - Journal of Neurotrauma

JF - Journal of Neurotrauma

SN - 0897-7151

IS - 9

ER -