A new model of autonomic dysreflexia induced by gastric distension in the spinal cord-transected rat.
Upper gastrointestinal (GI) motility inhibition after spinal cord injury has been classically considered to result from autonomic dysreflexia (AD). Animal models have been designed in rats to evaluate the presence of AD induced by colonic or bladder distension. However, there are no animal models of AD induced by gastric distension (GD). We examined whether controlled GD could induce AD and compared the pattern of hemodynamic responses induced by GD with colonic distensions (CD) and the interaction between them. Male Wistar rats underwent spinal cord transections performed at the level of C(7)-T(1), T(4)-T(5) and T(9)-T(10) (control) vertebrae and the presence of AD was evaluated after 1 day. In animals with C(7)-T(1) lesions, each CD in a series of 4 consecutive CDs triggered AD while GD only triggered AD after the 2 initial distensions in a series of 4 consecutive GDs. In animals with T(4)-T(5) lesions, in a protocol of 4 consecutive CDs or GDs, AD was triggered only by the 2 initial distensions. In 2 other protocols, consisting of 2 consecutive CDs or GDs followed respectively by 2 GDs or CDs, the effect of 2 GDs was attenuated in animals with C(7)-T(1) and T(4)-T(5) lesions but the hemodynamic changes induced by CDs were not affected by prior GDs. In summary, this is a new model of AD triggered by GD in rats. AD is more intense in animals with C(7)-T(1) lesions than after T(4)-T(5) lesions and AD triggered by GD can be attenuated by prior CDs.
Departamento de Fisiologia e Farmacologia, Universidade Federal do Ceará, Fortaleza, Ceará, Brazil; Service de Neurochirurgie, Centre Hospitalier Universitaire, Caen, France; Departement de Neurosciences, Université Pierre et Marie Curie, Paris, France.
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PRL
Leal
Departamento de Fisiologia e Farmacologia, Universidade Federal do Ceará, Fortaleza, Ceará, Brazil.
P R M
PRM
Cruz
Departamento de Fisiologia e Farmacologia, Universidade Federal do Ceará, Fortaleza, Ceará, Brazil.
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AC
Lopes
Departamento de Fisiologia e Farmacologia, Universidade Federal do Ceará, Fortaleza, Ceará, Brazil.
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RC
Lima
Departamento de Fisiologia e Farmacologia, Universidade Federal do Ceará, Fortaleza, Ceará, Brazil.
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FM
Carvalho
Departamento de Fisiologia e Farmacologia, Universidade Federal do Ceará, Fortaleza, Ceará, Brazil.
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JRV
da Graça
Departamento de Fisiologia e Farmacologia, Universidade Federal do Ceará, Fortaleza, Ceará, Brazil.
A A
AA
Dos Santos
Departamento de Fisiologia e Farmacologia, Universidade Federal do Ceará, Fortaleza, Ceará, Brazil.
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FH
Rola
Departamento de Fisiologia e Farmacologia, Universidade Federal do Ceará, Fortaleza, Ceará, Brazil. Electronic address: gondimfranc@yahoo.com.
F A A
FAA
Gondim
D000818:Animals; D020211:Autonomic Dysreflexia / Q000209:etiology / Q000503:physiopathology*; D001342:Autonomic Nervous System Diseases / Q000209:etiology / Q000503:physiopathology*; D001794:Blood Pressure / Q000502:physiology; D003106:Colon / Q000294:innervation / Q000473:pathology / Q000503:physiopathology; D004195:Disease Models, Animal; D013271:Gastric Dilatation / Q000150:complications / Q000503:physiopathology*; D006439:Hemodynamics / Q000502:physiology; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D013116:Spinal Cord / Q000503:physiopathology / Q000601:surgery; D013119:Spinal Cord Injuries / Q000150:complications / Q000503:physiopathology*; D013997:Time Factors