Autonomic control of the heart and renal vascular bed during autonomic dysreflexia in high spinal cord injury.

Autonomic function and hemodynamics were studied in nine spinal cord injured (SCI) subjects, at rest and during peripheral afferent stimulation, bladder percussion. Nine able-bodied subjects were studied for comparison during unstimulated conditions. Spontaneous baroreceptor reflex sensitivity was calculated from recordings of ECG and intraarterial blood pressure. An index of sympathetic activity was provided by measuring total body noradrenaline (NA) spillover by isotope dilution technique. Renal vascular resistance was calculated from PAH-clearance.SCI subjects had lower total body NA spillover (1011 +/- 193 vs 2261 +/- 328 pmol/min, P < 0.01), but similar baroreceptor reflex sensitivity and hemodynamics compared to able-bodied subjects at rest. In SCI group, during bladder percussion, mean arterial pressure increased (79 +/- 5 vs 113 +/- 8 mm Hg, P < 0.01), whereas heart rate was reduced during the first minute of the manoeuvre (62 +/- 2 vs 56 +/- 2 bpm, P < 0.05). Baroreceptor reflex sensitivity remained unchanged. Total body NA spillover and renal vascular resistance increased by 332 % (from 1004 +/- 218 pmol/min, P < 0.05) and 55 % (from 0.078 +/- 0.011 mmHg/ml/min, P < 0.05), respectively.SCI subjects demonstrated lower total body sympathetic outflow but normal baroreceptor reflex sensitivity at rest, suggesting a balanced autonomic output to the heart. Bladder percussion caused a substantial increase in renal vascular resistance and blood pressure, which was partly due to marked generalised sympathetic activation. This activation was counterbalanced by an increased vagal activity as evidenced by reduction of the heart rate.