DOI 10.1227/neu.0000000000004112
Response of Spinal Cord Blood Flow to Hypotensive and Adrenergic Challenges: Doppler Ultrasound of the Porcine Sulcal Artery.
Аннотация
BACKGROUND AND
OBJECTIVES
Management of spinal cord injury includes surgical decompression and pharmacologic elevation of mean arterial pressure (MAP) to augment cord perfusion. However, the relationship between MAP augmentation and spinal cord blood flow remains poorly characterized, and it is unclear whether different adrenergic agents produce differential effects on cord perfusion. Thus, our objective was to directly characterize dynamic spinal cord blood flow responses to controlled MAP perturbations and compare the effects of common vasopressors.
METHODS
We developed a Doppler ultrasonography platform to measure dynamic blood flow signals in the sulcal arteries of uninjured porcine spinal cord. Eight female Yorkshire pigs underwent controlled hypotensive challenges using hemorrhage and hypertensive challenges with 4 adrenergic agonists: phenylephrine (α-agonist), dobutamine (β-agonist), norepinephrine (mixed α/β), and epinephrine (mixed α/β). Mean flow velocity (MFV) and mean power Doppler (MPD) were extracted from spectral Doppler recordings and analyzed in relation to step changes in MAP.
RESULTS
During hypotensive challenges, reductions in MAP were accompanied by decreases in MFV and MPD, with minimal recovery toward baseline. During pharmacologic MAP augmentation, all agents produced increases in MAP, MFV, and MPD. However, dobutamine produced a greater change in blood flow measures when compared with norepinephrine, phenylephrine, and epinephrine.
CONCLUSION
These findings represent the first dynamic measurements of spinal cord blood flow signals in vivo and demonstrate that MAP elevation does not uniformly translate to increased cord perfusion. Pure β-adrenergic stimulation with dobutamine produced a favorable blood flow profile, whereas agents with α-agonist activity may limit effective perfusion through vasoconstriction. This work provides a mechanistic framework for optimizing vasopressor selection in spinal cord injury and lays groundwork for future studies of spinal cord autoregulation.
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