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Radical Sphincter-Sparing Resection in Rectal Cancer
Published in Peter Sagar, Andrew G. Hill, Charles H. Knowles, Stefan Post, Willem A. Bemelman, Patricia L. Roberts, Susan Galandiuk, John R.T. Monson, Michael R.B. Keighley, Norman S. Williams, Keighley & Williams’ Surgery of the Anus, Rectum and Colon, 2019
Historically it was considered necessary to clamp and divide these ‘lateral ligaments’ during rectal cancer surgery, and the view of many, including John Goligher, was that ‘if you haven’t made the patient impotent, you probably haven’t cured him of rectal cancer’.53 It is now understood that dividing the ‘lateral ligaments’ is unnecessary as only a few small branches of these nerves and vessels penetrate through the mesorectum and these structures seldom are more than 1mm in diameter.65,92,100 These penetrating structures are often termed ‘T-junctions’ (Figure 33.8).92 Most of the inferior hypogastric plexus forms a distal condensation which curves towards the back of the prostate in men where it forms the neurovascular bundles of Walsh, which descend on the posterolateral aspect of the prostate and taper towards the apex of the prostate (Figure 33.6).99 Here they become the cavernous nerves responsible for male erectile function.92
Physiology of normal sexual function
Published in Jacques Corcos, David Ginsberg, Gilles Karsenty, Textbook of the Neurogenic Bladder, 2015
Pierre Clément, Hélène Gelez, François Giuliano
Parasympathetic fibers to the vagina and the clitoris are conveyed by the pelvic nerve originating from the sacral segments (S2–S4) of the spinal cord from the SPN.10 The neural fibers of the pelvic nerve travel in the pelvic plexus and send branches in the cavernous nerves that originate from the autonomic nerve plexus around the vagina and extend to the proximal urethra and the clitoral body. In rat, preganglionic neurons of the SPN are located almost exclusively (98%) within the L6–S1 spinal cord segment,11 corresponding to the sacral S2–S4 segments in humans.
Male Sexual Function
Published in Anthony R. Mundy, John M. Fitzpatrick, David E. Neal, Nicholas J. R. George, The Scientific Basis of Urology, 2010
Giulio Garaffa, Suks Minhas, David J. Ralph
A parasympathetic input along the cavernous nerves induces relaxation of the cavernosal smooth muscle and ultimately an erection. On the other hand, the stimulation of the hypogastric nerve or of the sympathetic trunk induces contraction of the cavernosal smooth muscle and leads to penile detumescence.
Recent advances in stem cell therapy for erectile dysfunction: a narrative review
Published in Expert Opinion on Biological Therapy, 2023
Bohan Wang, Wenjun Gao, Micha Y. Zheng, Guiting Lin, Tom F Lue
The therapeutic effect of SCT for ED is attributed to paracrine effects that enhance the function of smooth muscle and nerves in the corpus cavernosum [40–42]. This theory is derived from the observation that adipose-derived regenerative cell lysate exhibited similar beneficial effects as intact cells in a rat model of ED caused by cavernous nerve crush injury [43]. Preclinical studies have demonstrated that injected stem cells exert cytoprotective, anti-fibrotic, anti-inflammatory, pro-regenerative, immune-modulating, and antiapoptotic effects [44]. Other mechanisms include neurotrophic effects on the cavernous nerves and activation of host progenitor cells [45]. Moreover, some degree of engraftment and cellular differentiation may also contribute to the favorable outcomes [46]. Overall, stem cell therapy for ED is a promising approach that has shown positive results in preclinical and clinical studies. However, more research is needed to fully understand the mechanism of action and optimize the therapy for maximum efficacy.
An update on emerging drugs for the treatment of erectile dysfunction
Published in Expert Opinion on Emerging Drugs, 2018
U. Milenkovic, J. Campbell, E. Roussel, M. Albersen
Neurons in the spinal cord and peripheral ganglia come together in the sacral nerve center to control erections. They form the parasympathetic neurons that are part of the neurovascular bundle containing the cavernous nerves. These enter the corpora spongiosa and cavernosa to provide the neural basis of erections [30]. Parasympathetic nonadrenergic, noncholinergic release NO in the cavernosal space. Additionally, the cavernosal endothelium itself also releases NO in response to cholinergic nerve stimulation and stretch due to the increased blood flow (vasodilatation). NO is produced by NO synthase (NOS), with specific isoforms depending on the cell type producing it (neuronal (n)NOS and endothelial (e)NOS). NO diffuses into the smooth muscle cells (SMC) and activates intracellular soluble guanylate cyclase (sGC), which in turn incites a cGMP-synthesis. A cGMP-specific protein kinase then inhibits the intracellular flow of calcium, resulting in smooth muscle relaxation, contributing to increased penile blood supply [30]. Rapid filling of the cavernosal space impedes venous leakage through compression of subtunical veins, maintaining rigid erection [31]. The role of cyclic adenosine monophosphate (cAMP), smooth muscle contraction, Rho/RhoA-kinase, potassium channels, and vasoconstriction are discussed in detail elsewhere Sections 3 and 8.
Lower urinary tract symptoms/benign prostatic hyperplasia and erectile dysfunction: from physiology to clinical aspects
Published in The Aging Male, 2018
Aldo E. Calogero, Giovanni Burgio, Rosita A. Condorelli, Rossella Cannarella, Sandro La Vignera
Among iatrogenic factors (caused by medical or surgical treatment), the most common is radical pelvic surgery. The damaged structures are usually nerves (of periprostatic plexus or cavernous nerves); sometimes damage is done to accessory pudendal arteries. A variety of drugs and medications has been studied in association with ED. However, a clear role in determining ED for many medications has been recently debated and results difficult to define. TOMHS compared five anti-hypertensive drugs with a placebo for changes in quality of life (sexual function was assessed by physician interviews). Chlorthalidone (a diuretic drug used in hypertension) had the greatest effect on sexual function two years after treatment, but the placebo achieved almost the same level at four years. Accordingly, chlorthalidone may potentiate ED earlier in those who are likely to develop the condition later in life (see “Epidemiology and risk factors of ED and LUTS/BPH-hypertension and cardiovascular disease” section of this chapter for more) [38].