Relationship between sympathetic activity and arterial pressure in conscious spinal rats

Abstract

Spinal cord injury disrupts regulation of arterial pressure, often resulting in episodic hypertension initiated by spinal reflexes. The contribution of spinally generated sympathetic nerve activity (SNA) to control of resting arterial pressure after cord injury is questionable. The mechanisms responsible for the reflex hypertension also are unresolved. One important question concerns whether or not this hypertension is caused by large spinal sympathetic reflexes or by the known increased vascular sensitivity to norepinephrine and limited effectiveness of baroreceptor reflexes that occur after spinal cord injury. We evaluated the relationship between renal SNA and mean arterial pressure (MAP) in basal conditions and during reflex pressor responses induced by colon distension in conscious rats for 1 wk after midthoracic spinal cord transection (SCT). One day after SCT, MAP (69 +/- 6 mmHg) and SNA(6 +/- 2 microV x s) were lower than the MAP (92 +/- 4 mmHg) and SNA (18 +/- 3 microV x s) in the same anesthetized rats before SCT. At 6 days, MAP increased to 94 +/- 6 mmHg, whereas SNA remained low (4 +/- 1 microV x s). One day after SCT, colon distension increased MAP by 28 +/- 4 mmHg and SNA by 35 +/- 6 microV x s; these responses remained unchanged for 6 days. These data suggest that spinally generated SNA makes no apparent contribution to basal MAP. In contrast, afferent stimulation can produce large excitatory spinal sympathetic reflexes that appear adequate to cause substantial increases in arterial pressure.

Complete cervical or thoracic spinal cord transections delay gastric emptying and gastrointestinal transit of liquid in awake rats

“…17 Afterwards, we have observed, in agreement with previous studies, 19 that bladder catheterization is not essential for the daily management of spinal animals, since bladder care can be easily accomplished by expression of urine by abdominal compression three to four times a day. 19 In humans, scarce and con¯icting data about the e ects of SCT on the motility of the upper portions of the GI tract are available: delayed GE of liquids or solids has been reported in SCI patients 8 ± 10,14,16 and subsequently questioned. 11,12 A possible explanation for these discrepancies is the signi®cant variation in age, sex, interval after injury, pattern and injury mechanism in human studies.…”

“…This is in agreement with previous studies in thoracic and cervical spinal rats, which demonstrated that thoracic and cervical spinal transected animals can be studied for prolonged periods of time in healthy conditions. 18,19 In a preliminary study, we have observed that acute cervical spinal cord transection (SCT) decreases GE, intestinal and GI transit of liquid in awake rats. 17 However, the animals were studied only during the ®rst day after SCT and were also submitted to bladder catheterization.…”

“…Bladder emptying was accomplished by manual compression three to four times a day. 19 Animals also received a sc saline injection (5 ml) 6 h after surgery to provide initial hydration. At noon time, we daily weighed the animals submitted to the 7-day study.…”

Orthostatic hypotension following spinal cord injury: understanding clinical pathophysiology

“…6,8,18 Secondly, there is a generalised reduction in sympathetic activity associated with low plasma adrenaline and noradrenaline levels. 6,27,28 This is particularly pronounced in high-level (cervical and high thoracic) complete SCI. Thirdly, there are morphologic alterations that occur within SPN following SCI.…”

“…Factors likely to underlie orthostatic hypotension and symptoms of orthostatic 26 Reduced sympathetic tone below the lesion 6,27,28 Morphologic changes in sympathetic neurons [29][30][31] Plasticity within spinal circuits [31][32][33] Peripheral a-adrenoceptor hyper-responsiveness 34 intolerance in SCI patients are discussed below, and summarised in Table 2.…”