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Essay: Bladder overactivity

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  • Subject area(s): Health essays
  • Reading time: 2 minutes
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  • Published: 7 October 2015*
  • File format: Text
  • Words: 432 (approx)
  • Number of pages: 2 (approx)

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Urinary bladder overactivity E symptoms are observed both in functional and organic morbidities of the bladder. One of clinical circumstances associated with development of symptoms of secondary overactive bladder syndrome (OAB) is hemorrhagic cystitis caused by therapy with drugs belonging to the group of oxazaphosphorins, especially with cyclophosphamide (CP). The drug is still commonly used in therapy of lymphoproliferative conditions, Hodgkin disease and neoplastic diseases (e.g. small-cellular lung cancer or breast cancer), and in therapy of other diseases, including nephrotic syndrome or visceral lupus [1]. However, the use of cyclophosphamide is associated with risk of numerous and multi-systemic adverse effects, including the above mentioned hemorrhagic cystitis with bladder overactivity [2] and myocarditis leading to cardiomyopathy [3]. Pathogenesis of cyclophosphamide-induced hemorrhagic cystitis (CP-HC) is a complex one, associated with systemic biotransformation of oxazaphosphorins and endovesical release of a toxic metabolite ‘ acrolein ‘ secondary initiating release of numerous preformed and de novo synthesized pro-inflammatory mediators, and finally inducing cellular damage. A detailed description of CP-HC pathogenesis is presented in one of our reviews [4].
CP-HC prevention and therapy is based on parallel administration of cytoprotective agents, mainly mesna (a donor of sulfhydryl groups that react with the double bond in acrolein, transforming that oxazaphosphorine metabolite into a less toxic product) [5,6] or amifostine [7]. Other, currently studied cytoprotective agents potentially effective in CP-HC therapy involve phytopharmacological compounds (belonging to groups of flavonoids, vitanoloids, steroidal saponins, vegetable alkaloids and organic sulphur compounds) [4] and prostaglandins analogues [8]. It is generally known that prostaglandins are synthesized locally in the stomach and exert their cytoprotective action towards the gastric mucosal barrier, as well as mucous barrier and mucosal perfusion [9,10]. Prostaglandins are also released by vesical urothelium and demonstrate similar cytoprotective properties [11]. At the same time, there are reports from studies on pathogenesis of idiopathic OAB, suggesting that prostaglandins increase the contractility activity of the detrusor. Therefore, those compounds may be perceived as one of paracrine mediators, that may contribute to bladder overactivity [12].
Considering the above mentioned premises associated with a potential, alleviating effect of prostaglandins administered in CP-HC, our purpose was to determine if those compound were also able to modulate the activity of the autonomic nervous system assessed by spectral heart rate variability (HRV) method, and if those potential changes in autonomic regulation could contribute to their protective properties in course of CP-HC. The assessment was an indirect one, utilizing effects resulting from prostaglandin synthesis inhibition by non-steroid anti-inflammatory drugs (NSAIDs). Moreover, using a non-selective inhibitor of COX-1 and COX-2, or a preferential COX-2 inhibitor, we were trying to determine if the potential effect on ANS activity was demonstrated by constitutive or induced prostaglandins

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