Spinal cord injury induced cardiomyocyte atrophy and impaired cardiac function are severity dependent

Abstract

The principle aim of the present study was to assess how the severity of spinal cord injury (SCI) affects LV mechanics, function, and underlying cardiomyocyte morphology. Here, we utilized different severities of T3 spinal cord contusions (MODERATE, 200Kdyn contusion; SEVERE, 400kdyn contusion; SHAM) and combined standard echocardiography with speckle tracking analyses to investigate in vivo cardiac function and deformation (contractility) after experimental SCI in the Wistar rat. In addition, we investigated changes in the intrinsic structure of cardiac myocytes ex vivo. We demonstrate that SEVERE SCI induces a characteristic decline in left-ventricular chamber size and a reduction in in vivo LV deformation (i.e. radial strain) throughout the entire systolic portion of the cardiac cycle (25.6 ± 3.0 vs. 44.5 ± 8.1 (Pre-injury); P = 0.0029). SEVERE SCI also caused structural changes in cardiomyocytes including decreased length (115.6 μm ± 7.63 vs. 125.8 μm ± 6.75 (SHAM); P = 0.0458), decreased width (7.78 μm ± 0.71 vs. 10.78 μm ± 1.08 (SHAM); P = 0.0015), and an increase in the length/width ratio (14.88 ± 0.66 vs. 11.74 ± 0.89 (SHAM); P = 0.0018), which was significantly correlated with LV flow-generating capacity after SCI (i.e. stroke volume, R² = 0.659; P = 0.0013). MODERATE SCI rodents exhibited no changes in any metric vs. SHAM. This is the first study to demonstrate that the severity of SCI determines the course of changes to the intrinsic structure of cardiomyocytes, which are directly related to contractile function of the LV.

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