Impact of acute high thoracic spinal cord injury on in vivo vascular function in rats

Cardiovascular dysfunction is a major cause of morbidity and mortality following high-thoracic spinal cord injury (SCI), yet the acute impact of SCI on integrated neurovascular control remains poorly defined. In the current study, we aimed to investigate the acute effects of complete T3 transection (T3-SCI) on in vivo hemodynamic function, superior mesenteric artery (SMA) autoregulation, sympathetic baroreflex sensitivity (sBRS), and sympathetic vascular transduction (SVT) in anesthetized rats. Nineteen male Wistar rats were randomized into naïve control (n = 10) or T3-SCI (n = 9) experimental groups. Rats were anesthetized with intravenous urethane, and arterial blood pressure (ABP), SMA blood flow (Q_SMA), and splanchnic sympathetic nerve activity (sSNA) were simultaneously recorded. SMA autoregulation was evaluated using controlled venous blood withdrawal and reinfusion. sBRS was assessed via graded phenylephrine infusion, and SVT was quantified by analyzing mean arterial pressure (MAP), Q_SMA, and SMA conductance (C_SMA) responses to sSNA bursts. We found that T3-SCI exhibited lower resting sSNA, MAP, heart rate (HR), and diastolic Q_SMA compared to naïve (all P < 0.03). Despite this, dynamic SMA autoregulation remained intact in T3-SCI, as evidenced by preserved lower limit of autoregulation and autoregulation index. However, sBRS was completely abolished in T3-SCI rats, which, unlike naïve rats, did not suppress sSNA in response to PE-induced increases in ABP. Furthermore, signatures of SVT were markedly attenuated in T3-SCI. This study demonstrates that while dynamic SMA autoregulation is acutely preserved in T3-SCI, loss of supraspinal sympathetic control results in immediate and significant impairments in splanchnic/mesenteric sympathetic arterial tone, SVT and baroreflex function.