APPS November 2002 Meeting Abstract 2424

Bladder distension or minor unheeded injuries in spinally injured people can lead to episodes of high blood pressure. This condition, termed autonomic hyperreflexia, is generally thought to result from the loss of descending reflex inhibition and plasticity within the spinal cord. However, sympathetic nerve traffic is greatly depressed in pathways below a spinal cord lesion and decreased activity of synaptic connections often leads to enhancement of synaptic efficacy. Consistent with this, we have observed an increased responsiveness of isolated tail arteries from spinalized rats to sympathetic nerve stimulation. To determine whether this change can be attributed to decreased activity in the sympathetic nerve supply, we have investigated the effects of decentralizing the sympathetic nerves supplying the tail artery. Both lumbar sympathetic trunks below the L3 ganglia were lesioned under anaesthesia with ketamine (60 mg/kg) and xylazine (10 mg/kg) administered i.p. Two weeks after the operation, the animals were anaesthetised (100 mg/kg pentobarbitone, i.p.) and killed by decapitation. The tail artery was dissected and sections mounted isometrically in wire myographs. Comparisons were made with tissues from sham-operated controls. Concentration response curves to the adrenoceptor agonists, phenylephrine, and clonidine, were shifted to the left but there was no change in maximum force of contraction to these agents. The decentralized tissues were more responsive to activation with high K⁺ solution (60 mM K⁺). Activation of the sympathetic nerves with trains of stimuli at 0.1 - 10 Hz produced contractions of greater force in the decentralized tissues. Furthermore, in decentralized tissues, the sensitivity of the nerve-evoked contractions to the α-adrenoceptor antagonists, prazosin and idazoxan, was reduced. These changes in nerve-evoked responses parallel those observed in tail arteries from spinalized tissues. The findings suggest that the increased responsiveness of tail arteries from spinalized rats can be attributed to decreased activity in their sympathetic nerve supply.