A contraction response of the internal anal sphincter to Botulinum toxin: does low-pressure chronic anal fissure have a different pathophysiology?
Botulinum toxin appears to have an atypical contraction effect on the internal anal sphincter in low-pressure (usually anterior) fissures. This may be accounted for by blockade of acetylcholine released at parasympathetic nerve terminals and the sympathetic ganglion (relaxation). Low pressure fissures may be physiologically different from high-pressure fissures.
We conclude that sumoylation of HIF-1α in RVLM ameliorates brain stem cardiovascular regulatory failure during experimental brain death via upregulation of nitric oxide synthase I/protein kinase G signaling. This information should offer new therapeutic initiatives against this fatal eventuality.