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Titolo:
Autonomic dysreflexia and primary afferent sprouting after clip-compression injury of the rat spinal cord
Autore:
Weaver, LC; Verghese, P; Bruce, JC; Fehlings, MG; Krenz, NR; Marsh, DR;
Indirizzi:
John P Robarts Res Inst, Neurodegenerat Res Grp, London, ON N6A 5K8, Canada John P Robarts Res Inst London ON Canada N6A 5K8 ndon, ON N6A 5K8, Canada Univ Western Ontario, Dept Physiol, London, ON N6A 5K8, Canada Univ Western Ontario London ON Canada N6A 5K8 London, ON N6A 5K8, Canada Univ Western Ontario, Program Neurosci, London, ON N6A 5K8, Canada Univ Western Ontario London ON Canada N6A 5K8 London, ON N6A 5K8, Canada Toronto Western Res Inst, Div Neurosurg & Cellular Mol Biol, Toronto, ON, Canada Toronto Western Res Inst Toronto ON Canada Mol Biol, Toronto, ON, Canada
Titolo Testata:
JOURNAL OF NEUROTRAUMA
fascicolo: 10, volume: 18, anno: 2001,
pagine: 1107 - 1119
SICI:
0897-7151(200110)18:10<1107:ADAPAS>2.0.ZU;2-A
Fonte:
ISI
Lingua:
ENG
Soggetto:
SYMPATHETIC PREGANGLIONIC NEURONS; NERVE GROWTH-FACTOR; SIMPLEX VIRUS TYPE-1; NEUROLOGICAL FUNCTION; GLUTAMATE RECEPTORS; SECONDARY INJURY; IDENTIFICATION; HYPERREFLEXIA; MECHANISMS; PHYSIOLOGY;
Keywords:
cardiovascular control; CGRP; small-diameter afferent neurons; visceral stimulation;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
57
Recensione:
Indirizzi per estratti:
Indirizzo: Weaver, LC John P Robarts Res Inst, Neurodegenerat Res Grp, POB 5015,100 Perth Dr, London, ON N6A 5K8, Canada John P Robarts Res Inst POB 5015,100 Perth Dr London ON Canada N6A 5K8
Citazione:
L.C. Weaver et al., "Autonomic dysreflexia and primary afferent sprouting after clip-compression injury of the rat spinal cord", J NEUROTRAU, 18(10), 2001, pp. 1107-1119

Abstract

Spinal cord injury leads to many forms of autonomic dysfunction including autonomic dysreflexia, a condition involving recurrent episodes of paroxysmal hypertension and associated bradycardia. This hypertension may reach intensities that are life-threatening. We investigated autonomic dysreflexia and the sprouting of central processes of primary afferent neurons (a potential mechanism for autonomic dysreflexia) in a clinically-relevant calibrated clip-compression model of spinal cord injury in the rat. Autonomic dysreflexia was induced by colon distension in the conscious rats 2 weeks after severe (50-g) clip compression injury of the spinal cord at the 4th thoracicsegment. The central arbor of small-diameter primary afferent fibers in laminae III-VII of the spinal cord dorsal horn was also assessed at 2 weeks after cord injury by quantitative morphometry, using calcitonin gene-relatedpeptide as a marker. In response to colon distension, arterial pressure increased by 41 +/- 3 mmHg from a resting value of 109 +/- 4 mmHg, and heart rate decreased by 124 +/- 13 beats/min from a value of 515 +/- 16 beats/min(n = 7). Minimal locomotor function was recovered by these rats: by 2 weeks after injury they attained scores of only 3.1 +/- 1.3 on the Basso, Beattie and Bresnahan scale. Histopathology of the clip-compression lesion site in the cord consisted of extensive central necrosis extending several segments rostral and caudal to the lesion. Quantitative measures of the small-diameter afferent arbors revealed significant increases in area ranging from 20-27% in thoracolumbar segments caudal to the injury (n = 5) in comparisonto sham-injured rats (n = 6). A second study was done to assess the impactof severity of injury on the relationship between the size of the primary afferent arbors and autonomic dysreflexia. At 2 weeks after milder (20-g) clip injury at T4, rats exhibited responses to colon distension that were not those associated with autonomic dysreflexia (n = 5). Arterial pressure increased by only 16 +/- 3 mmHg and heart rate tended to increase (+19 +/- 12beats/min). These rats attained a locomotor score of 7.1 +/- 0.4 by 2 weeks. The lesions at the injury site also contained necrosis and mild cavitation within the gray matter. No change in the small-diameter afferent arbor was detected at 2 weeks after the 20-g clip injury at T4 (n = 6 rats). Thesefindings suggest that after severe but not mild clip compression injury ofthe spinal cord, sprouting of the afferent component of the spinal reflex arc contributes to the development of autonomic dysreflexia. Neither dysreflexia, nor changes in the afferent arbor size occurred after mild cord injury. This clinically relevant clip compression cord injury model, studied more frequently for locomotor function, is excellent for investigating mechanisms for the development of autonomic dysreflexia and strategies for its prevention.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 07/04/20 alle ore 23:18:22