Acute exercise reduces the response to colon distension in T₅ spinal rats

Abstract

.-Individuals with spinal cord injuries above thoracic level 6 (T 6) experience life-threatening bouts of hypertension, termed autonomic dysreflexia (AD). AD is mediated by peripheral ␣-adrenergic receptor supersensitivity as well as a reorganization of spinal pathways controlling sympathetic preganglionic neurons. A single bout of dynamic exercise may be a safe therapeutic approach to reduce the severity of AD because mild-to-moderate dynamic exercise reduces postexercise ␣-adrenergic receptor responsiveness, lowers postexercise sympathetic nerve activity, and reduces the postexercise response to stress. Therefore, this study was designed to test the hypothesis that mild-to-moderate dynamic exercise attenuates the postexercise response to colon distension (mechanism to elicit AD). To test this hypothesis, six male Wistar rats (406 Ϯ 23 g), 5 wk post-T 5 spinal cord transection, were instrumented with an arterial catheter. After recovery, the response to graded colon distension (10, 30, 50, and 80 mmHg, in random order) was determined before and after a single bout of mild-to-moderate dynamic exercise (9-12 m/min, 0% grade for 40 min). After exercise, the pressor response to graded colon distension was significantly attenuated (preexercise change: 2 Ϯ 1, 9 Ϯ 1, 14 Ϯ 1, and 24 Ϯ 2 vs. postexercise change: 2 Ϯ 1, 2 Ϯ 1, 9 Ϯ 1, and 12 Ϯ 3 mmHg). Thus acute exercise is a safe, therapeutic approach to reduce the severity of AD in paraplegic subjects. autonomic dysreflexia; spinal cord injury AUTONOMIC REGULATION of the cardiovascular system is abnormal and unstable after spinal cord injury. Hypotension occurs immediately after the injury because of loss of tonic supraspinal excitatory drive to spinal sympathetic neurons (3). Subsequently, resting arterial pressure returns toward normal values; however, episodic bouts of hypertension often develop as part of the condition termed autonomic dysreflexia (AD) (24,27). AD occurs in as many as 85% of individuals with lesions above thoracic level 6 (T 6 ) and is characterized by severe hypertension. The paroxysmal hypertension can be caused by stimulation of the skin, distension of the urinary bladder or colon, and muscle spasms (4, 23). If not treated promptly, the hypertension may produce cerebral and subarachnoid hemorrhage, seizures, and renal failure and may lead to death (25). The long-term consequence of repeated episodes of severe hypertension has yet to be determined.Exercise may be a safe therapeutic approach for attenuating the severity of AD by reducing ␣-adrenergic receptor responsiveness. Several investigators have demonstrated that a single bout of mild-to-moderate dynamic exercise significantly attenuated the postexercise response to ␣-adrenergic receptor agonists (14-16, 29, 33). For example, a single bout of dynamic exercise significantly attenuated the postexercise response to ␣-adrenergic receptor activation in the intact conscious rabbit (15), rat (29, 33), and human (14). These data suggest that the ability to increase peripheral vascular resistance aft...

Leg sympathetic response to noxious skin stimuli is similar in high and low level human spinal cord injury

“…Peripheral noradrenaline supersensitivity has been documented in chronic human SCI (Mathias et al, 1976;Arnold et al, 1995), and there is additional evidence for more noradrenaline release per impulse (Gao et al, 2002) as well as an increased number of peripheral receptors post SCI (Velasco et al, 1997). In rats, approximately 50% of the AD pressor response can be attributed to vascular hyper-responsiveness (Collins and DiCarlo, 2002). At present it is difficult to determine the relative contribution of increased sympathetic outflow and peripheral noradrenaline supersensitivity on conductance changes in the current study.…”

Structural neuroplasticity following T5 spinal cord transection: increased cardiac sympathetic innervation density and SPN arborization

“…paraplegia have elevated heart rates (23), increased blood pressure variability (71), episodic bouts of life-threatening hypertension as part of a condition termed autonomic dysreflexia (12,13), and elevated sympathetic activity above the level of the lesion (14,31,48,70). Paraplegia also alters cardiac electrophysiology and the abundance of Ca 2ϩ regulatory proteins in a manner that increases the susceptibility to electrically-induced as well as ischemia and reperfusion-induced ventricular arrhythmias (14,48,49,70,71).…”

Peripheral vascular function in spinal cord injury: a systematic review

“…To our knowledge, only two studies have investigated the effect of exercise on cardiovascular function in animals with SCI. Collins et al 131 reported that acute (1 bout) treadmill exercise reduced the severity of AD induced via colorectal distension. Although those authors attributed this reduction in AD severity to an exerciseinduced reduction in a-adrenoceptor hypersensitivity, no measures of hypersensitivity were included in their experimental design; hence, the mechanistic basis for the acute reduction in AD severity could not be determined.…”