Abstract
High cervical spinal cord injuries induce several permanent deficits of vital functions, often leading to the death of the patient. The injury immediately disrupts the bulbospinal pathways innervating phrenic motoneurons that connect to the diaphragm and also causes damages to the sympathetic innervation of the vascular system. The subsequent functional deficits are respiratory failure and cardiovascular dysfunction. In this study, we use a preclinical model of surgical cervical C2 partial section in the rat that mimic these respiratory and cardiovascular impairments. The physiopathology of the injury is assessed by the adaptation of a non‐invasive medical ultrasound echography device (Logic 9, GE, France) to our model.Seven days post‐injury, we observed a live passive displacement of the diaphragm by ultrasound on the injured side in anesthetized animals, corresponding to an absence of hemidiaphragm contraction (−0,37 ± 0,17 mm) compared to contralateral side (3,27 ± 0,44 mm; p<0,01) and to control group (3,79 ± 0,27 mm; p<0,01). These results have been confirmed by in vivo diaphragmatic electromyography, with low electromyographic activity recorded on the ipsilateral side (0,06 ± 0,03 μV.s.s) compared to the contralateral side (0,53 ± 0,08 μV.s.s; p<0,01) and to control group (0,33 ± 0,08 μV.s.s; p = 0,013). We also observed a reduction of the thickness of the rectus abdominis muscle (accessory expiratory muscle) on both sides (injured and non‐injured) at 7 days post‐injury (non‐injured side = 1,78 ± 0,10 mm; injured side = 1,80 ± 0,10 mm) compared to control (2,14 ± 0,08 mm; p = 0,009 and p = 0,013 respectively), suggesting a role for this muscle in active exhalation following the injury.The doppler echocardiography for the cardiovascular evaluation showed a statistical reduction of the left ventricular ejection fraction (LVEF = 59 ± 3%) compared to control (LVEF = 70 ± 2%; p = 0,01), which corresponds to a systolic dysfunction. However, no diastolic dysfunction has been observed. The mean arterial pressure is getting close to non‐injured levels at 7 days post‐injury (68 ± 7 mmHg) compared to control group (84 ± 10 mmHg). These results suggest that the reduction of the sympathetic innervation caused by the spinal cord injury conduct to a cardiovascular dysfunction partly corrected at 7 days post‐injury.Altogether, we demonstrate that medical ultrasound machine could be a reliable non‐invasive method to evaluate chronic respiratory and cardiovascular dysfunction following high cervical spinal cord injury and for studying chronically the evolution of the eventual spontaneous restoration that can occur in this model.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
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