Effect of norepinephrine on spinal cord blood flow and parenchymal hemorrhage size in acute-phase experimental spinal cord injury

Abstract

Purpose In the acute phase of spinal cord injury (SCI), ischemia and parenchymal hemorrhage are believed to worsen the primary lesions induced by mechanical trauma. To minimize ischemia, keeping the mean arterial blood pressure above 85 mmHg for at least 1 week is recommended, and norepinephrine is frequently administered to achieve this goal. However, no experimental study has assessed the effect of norepinephrine on spinal cord blood flow (SCBF) and parenchymal hemorrhage size. We have assessed the effect of norepinephrine on SCBF and parenchymal hemorrhage size within the first hour after experimental SCI. Methods A total of 38 animals were included in four groups according to whether SCI was induced and norepinephrine injected. SCI was induced at level Th10 by dropping a 10-g weight from a height of 10 cm. Each experiment lasted 60 min. Norepinephrine was started 15 min after the trauma. SCBF was measured in the ischemic penumbra zone surrounding the trauma epicenter using contrast-enhanced ultrasonography. Hemorrhage size was measured repeatedly on parasagittal B-mode ultrasonography slices.Results SCI was associated with significant decreases in SCBF (P = 0.0002). Norepinephrine infusion did not significantly modify SCBF. Parenchymal hemorrhage size was significantly greater in the animals given norepinephrine (P = 0.0002). Conclusion In the rat, after a severe SCI at the Th10 level, injection of norepinephrine 15 min after SCI does not modify SCBF and increases the size of the parenchymal hemorrhage.Keywords Spinal cord injury Á Spinal cord blood flow Á Norepinephrine Á Contrast-enhanced ultrasonography A. Dubory and E. Laemmel have equally contributed to this work. E. Vicaut and J. Duranteau have equally contributed to this work.

Cardio-centric hemodynamic management improves spinal cord oxygenation and mitigates hemorrhage in acute spinal cord injury

“…Within the spinal cord microenvironment, DOB+ appeared to alleviate spinal cord ischemia more effectively than NE by optimizing cord oxygenation, blood flow and metabolic indices. In contrast, NE did not modify SCBF and worsened hemorrhaging, mirroring observations from Soubeyrand et al 4 in a feline model. Several studies have linked NE with central gray matter hemorrhaging in experimental models 5,6 , which is thought to result from unfavourable blood flow redistribution in the cord microenvironment 3 .…”

“…Hemodynamic management is one of the only neuroprotective strategies available to clinicians, and current guidelines suggest that mean arterial pressure (MAP) be maintained between 85-90 mmHg with intravenous fluids and vasopressors such as norepinephrine (NE), with the aim of offsetting systemic hypotension and maintaining adequate spinal cord perfusion 2 . Though this “one-size-fits-all” strategy can improve spinal cord blood flow (SCBF), vasopressor management with NE has been shown to produce potentially harmful SCBF profiles in some acute SCI patients 3 and has been shown by multiple investigators to exacerbate intraparenchymal hemorrhage 4–6 . In the setting of acute SCI, clinical studies have shown strong associations between increased cord hemorrhaging and worsened neurological outcomes (i.e.…”

Exploration of surgical blood pressure management and expected motor recovery in individuals with traumatic spinal cord injury

“…Animal models demonstrate that normotension should be maintained and that induced hypertension avoided given the evidence suggesting increased risk of spinal cord hemorrhage [32]. Subsequent animal models of the risk of hypertension demonstrated that norepinephrine did not improve spinal cord perfusion but was associated with increased size of parenchymal hemorrhage [33]. Kepler et al and Inoue et al found either decreased motor function with MAP > 85 mmHg or no correlation between MAP > 85 mmHg and motor recovery [34,35].…”

Structural trace of adaptation in motive nuclei of spinal cord of rats in hypokinesia and after physical loading in the recovery period

“…Зміни концентрації та конформації цих компонентів визначають виникнення значних морфофункціональних зрушень у рухових нейроцитах СМ за ДГК. Крім того, звертається увага на наявність у цих просторах медіаторів, нейрогормонів, гормонів периферичних ендокринних залоз та інших біологічно активних речовин (Nepomnjashсhih and Bakarev, 2009;Soubeyrand et al, 2014), які активізують процеси перебудови нейроцитів при ДГК.…”