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

Abstract

21Chronic high-thoracic and cervical spinal cord injury (SCI) results in a complex phenotype of 22 cardiovascular consequences, including impaired left-ventricular contractility. Here, we sought to 23 determine whether such dysfunction manifests immediately post-injury, and if so, whether 24 correcting impaired contractility can improve spinal cord oxygenation (SCO2), blood flow (SCBF) 25 and metabolism. Using a porcine model of SCI, we demonstrate that high-thoracic SCI acutely 26 impairs cardiac contractility and causes substantial reductions in intraparenchymal SCO2 and 27 SCBF within the first hours post-injury. Utilizing the same model, we next show that treating the 28 reduced contractile function with the b-agonist dobutamine is more efficacious at increasing SCO2 29 and SCBF than the current clinical standard of vasopressor therapy, whilst also mitigating 30 increased anaerobic metabolism and hemorrhage in the injured cord. Our data provide compelling 31 evidence that cardio-centric hemodynamic management represents a novel and advantageous 32 alternative to the current clinical standard of vasopressor therapy for acute traumatic SCI. 33

Topological network analysis of patient similarity for precision management of acute blood pressure in spinal cord injury

“…Moreover, the use of some vasopressors might cause more complications in patients 49 while also potentially contributing to intra-spinal hemorrhage . In fact, recent results in acute experimental SCI suggest controlling for hemodynamic dysregulation through a cardiac-focused treatment instead of using standard vasopressors such as norepinephrine 50 .…”

A cross‐species validation of single‐beat metrics of cardiac contractility

“…up to 4 h post‐injury), and level of injury (i.e. T2−3) are sufficient to cause a marked decrement in cardiac contractile function, evidenced by a significant reduction in E es in both rodent and porcine models (Fossey et al., 2022; Poormasjedi‐Meibod et al., 2019; Squair et al., 2018; Wainman et al., 2021; Williams et al., 2020). Moreover, in a recent manuscript, describing a series of experiments in both rodents and individuals with SCI, we reported that SCI induces considerable contractile dysfunction post‐injury that occurs due to the loss of bulbospinal sympathetic control over the heart (Fossey et al., 2022).…”

Acute hyperoxia improves spinal cord oxygenation and circulatory function following cervical spinal cord injury in the rat

“…Second, cervical spinal cord injury also damages the supraspinal vasomotor pathway innervating the sympathetic preganglionic neurons (1,27). Therefore, sympathetic activity might be reduced, causing hypotension and hypoperfusion of the spinal cord (34,35,42). The impaired systemic and central hemodynamics attenuate the oxygen supply to the spinal cord.…”

“…Cervical spinal cord injuries usually cause cardiorespiratory dysfunctions and result in systemic and central hypoxia due to damage to supraspinal respiratory and vasomotor pathways (10,18,19,24,27,38,41,43). In addition, the cervical spinal cord has more extensive microvascular structures than other spinal cord segments (39).…”