Abstract
This study determined the effect of pelvic organ decentralization and reinnervation 1 yr later on the contribution of muscarinic and purinergic receptors to ex vivo, nerve-evoked, bladder smooth muscle contractions. Nineteen canines underwent decentralization by bilateral transection of all coccygeal and sacral (S) spinal roots, dorsal roots of lumbar (L)7, and hypogastric nerves. After exclusions, 8 were reinnervated 12 mo postdecentralization with obturator-to-pelvic and sciatic-to-pudendal nerve transfers then euthanized 8-12 mo later. Four served as long-term decentralized only animals. Controls included six sham-operated and three unoperated animals. Detrusor muscle was assessed for contractile responses to potassium chloride (KCl) and electric field stimulation (EFS) before and after purinergic receptor desensitization with α, β-methylene adenosine triphosphate (α,β-mATP), muscarinic receptor antagonism with atropine, or sodium channel blockade with tetrodotoxin. Atropine inhibition of EFS-induced contractions increased in decentralized and reinnervated animals compared with controls. Maximal contractile responses to α,β-mATP did not differ between groups. In strips from decentralized and reinnervated animals, the contractile response to EFS was enhanced at lower frequencies compared with normal controls. The observation of increased blockade of nerve-evoked contractions by muscarinic antagonist with no change in responsiveness to purinergic agonist suggests either decreased ATP release or increased ecto-ATPase activity in detrusor muscle as a consequence of the long-term decentralization. The reduction in the frequency required to produce maximum contraction following decentralization may be due to enhanced nerve sensitivity to EFS or a change in the effectiveness of the neurotransmission.
Highlights
Pathological conditions that disrupt bladder innervation, such as lower motor neuron lesions [1], may alter muscarinic and purinergic components and receptors taking part in detrusor contractility [2,3,4,5,6,7,8]
Parasympathetic nerves are responsible for detrusor contraction by the release of acetylcholine (ACh), the main excitatory neurotransmitter acting on muscarinic receptors [13], and adenosine triphosphate (ATP), a coneurotransmitter acting on purinergic receptors [14]
Some decentralized animals continuously leaked urine and some exhibited unusual postures that were judged to be intermediate between urination and defecation postures with longer duration as reported in the pilot study of this series [17], and those postures were coincident with culture-confirmed bacteriuria, which disappeared with antimicrobial treatment
Summary
Pathological conditions that disrupt bladder innervation, such as lower motor neuron lesions [1], may alter muscarinic and purinergic components and receptors taking part in detrusor contractility [2,3,4,5,6,7,8]. The urinary bladder receives mixed sensory and motor innervation through hypogastric nerves carrying sympathetic axons and pelvic nerves carrying parasympathetic axons. In most species, including humans, intramural ganglia in the bladder wall receive projections from the pelvic plexus ganglia, as well as from hypogastric and pelvic nerves [11, 12]. Parasympathetic nerves are responsible for detrusor contraction by the release of acetylcholine (ACh), the main excitatory neurotransmitter acting on muscarinic receptors [13], and adenosine triphosphate (ATP), a coneurotransmitter acting on purinergic receptors [14]. There is increasing evidence that the autonomic nervous system develops plasticity to compensate for some of the loss of innervation that occurs following trauma, surgery, or diseases through changes
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