Spinal cord blood flow elevation with systemic vasopressor noradrenaline is partly mediated by vasodilation of spinal arteries due to reduced expression of alpha adrenoreceptors

Elevation of mean arterial blood pressure (MAP) has been proposed to raise spinal cord blood flow (SCBF) after traumatic spinal cord injury (TSCI). Current clinical guidelines for cervical TSCI suggest maintaining MAP 85–90 mmHg for 5–7 days using vasopressors, eg, noradrenaline. However, it remains unknown whether these interventions that promote an increased systemic MAP result in improved perfusion in the spinal cord. The local effect of vasopressors on the spinal cord arteries also remains unknown. The aim of this study was to investigate whether the increased systemic MAP results in increased SCBF, and secondly, to examine the mechanism behind noradrenaline (NA) action in spinal cord arteries. An experimental animal study. The study included nine 38–42 kg landrace pigs. In six pigs, MAP was gradually elevated using NA and continuous SCBF was recorded by laser doppler flowmetry. Spinal cord samples from these 6 pigs were excised for isolation of spinal cord arteries that were used for ex-vivo vascular function assessment in isometric myograph. Segments of mesentery from another 3 pigs were used to dissect mesenteric small arteries that were also studied in myograph, as control peripheral arteries. Other spinal cord and mesenteric arterial segments from the same biopsies were dissected and snap-frozen for the following expression analysis. Adrenoceptor's expression in arteries of all included animals was assessed with quantitative PCR. The controlled mixed model found that SCBF was lower at MAP below 50 mmHg and that SCBF increased significantly in the MAP range of 50-100 mmHg (p=.02). Further increase of MAP did not significantly affect SCBF (at MAP range of 100–150 mmHg, p=.15; at 150–200 mmHg, p=.51). However, SCBF significantly increased over the study time-course (at 80 min, p=.002; at 100 min, p