Open Collections

Taki, Alissa

University of British Columbia

Spinal cord injury (SCI) disrupts supraspinal input to sympathetic pathways that control the heart, leading to altered cardiovascular function. While advances have been made in understanding the impact of SCI on cardiovascular function, its effects on sympathetic ganglia remains largely unclear. The objectives of this study were: 1) to examine the role of the superior cervical ganglia (SCG) and stellate ganglia (StG) in controlling cardiovascular function in rats with and without chronic complete transection SCI at the T3 level (T3-SCI), and 2) to assess anatomical plasticity of the ganglia post-injury. 12 male Wistar rats (6 naïve, 6 T3-SCI at 4 weeks post-injury) underwent surgical instrumentation and parasympathetic blockade for assessment of sympathetic control of cardiovascular function. Through left-ventricular and femoral-arterial pressure catheters, resting cardiovascular function was assessed sequentially at baseline, following superior cervical ganglionectomy (SCGX), and after stellate ganglionectomy (StGX). Excised ganglia were used for immunohistochemical analysis to identify cardiac-projecting neurons in the SCG and StG through markers of neuropeptide Y and calbindin-D28k. Tyrosine hydroxylase was also used as a marker to quantify cell activity in the ganglia. T3-SCI rats demonstrated significantly lower cardiac and hemodynamic indices compared to naïve rats. SCGX did not alter these indices in either group, whereas StGX led to a significant decline in cardiovascular function in naïve rats. In T3-SCI animals, responses to StGX were blunted. Comparisons between naïve animals after StGX and T3-SCI animals at baseline (i.e. intact ganglia) revealed similar cardiovascular function. Furthermore, we found that cardiac-projecting neuronal cell bodies were significantly larger in the SCG and StG of T3-SCI animals. In summary, our findings demonstrate that sympathetic pathways through the StG that modulate the heart are effectively disrupted in chronic T3-SCI, leading to reduced resting cardiovascular function and remodelling of the cardiac-projecting postganglionic neurons post-injury.

Text

2024-11-12

Attribution-NonCommercial-NoDerivatives 4.0 International

http://hdl.handle.net/2429/89658

Experimental Medicine

University of British Columbia

UBCV

http://creativecommons.org/licenses/by-nc-nd/4.0/