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Bladder function was determined\n                      <jats:italic>in\u00a0vivo<\/jats:italic>\n                      by awake cystometry, micturition pattern analysis, and 24\u2010h urine collection. Bladders were harvested for\n                      <jats:italic>in\u00a0vitro<\/jats:italic>\n                      pharmacological investigation by isometric tension recording. Bladders and major pelvic ganglia were investigated by quantitative reverse transcription\u2010polymerase\u00a0chain reaction and histochemistry.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Overflow incontinence was observed at 1\u00a0week after\n                      <jats:styled-content style=\"fixed-case\">BPNI<\/jats:styled-content>\n                      . At 3 and 9\u00a0weeks after\n                      <jats:styled-content style=\"fixed-case\">BPNI<\/jats:styled-content>\n                      , rats showed a bladder phenotype characteristic for\n                      <jats:styled-content style=\"fixed-case\">DU<\/jats:styled-content>\n                      with increased post\u2010void residual urine volumes, reduced voiding efficiencies, and lower maximum pressures. In isolated bladder strips, contractile responses to\n                      <jats:styled-content style=\"fixed-case\">KC<\/jats:styled-content>\n                      l, carbachol, and \u03b1,\u03b2\u2010methylene adenosine 5\u2032\u2010triphosphate (\u03b1,\u03b2\u2010\n                      <jats:styled-content style=\"fixed-case\">mATP<\/jats:styled-content>\n                      ) were preserved. On the other hand, neural\u2010induced contractility was reduced after\n                      <jats:styled-content style=\"fixed-case\">BPNI<\/jats:styled-content>\n                      , in line with reduced expression of protein gene product 9.5 and choline acetyltransferase in the major pelvic ganglion at 1\u00a0week after\n                      <jats:styled-content style=\"fixed-case\">BPNI<\/jats:styled-content>\n                      . The bladder\u2010to\u2010body weight ratio and detrusor thickness increased after\n                      <jats:styled-content style=\"fixed-case\">BPNI<\/jats:styled-content>\n                      , indicating detrusor hypertrophy to compensate for the reduced neural input.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      <jats:styled-content style=\"fixed-case\">BPNI<\/jats:styled-content>\n                      induces a rat model for neurogenic\n                      <jats:styled-content style=\"fixed-case\">DU<\/jats:styled-content>\n                      . In this model, the detrusor maintains its contractility but denervation of the detrusor was observed.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/bju.14649","type":"journal-article","created":{"date-parts":[[2018,12,14]],"date-time":"2018-12-14T08:20:05Z","timestamp":1544775605000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":23,"title":["Functional and molecular characterisation of the bilateral pelvic nerve crush injury rat model for neurogenic detrusor underactivity"],"prefix":"10.1111","volume":"123","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-1197-5044","authenticated-orcid":false,"given":"Karel","family":"Dewulf","sequence":"first","affiliation":[{"name":"Laboratory of Experimental Urology Department of Development and Regeneration KU Leuven Leuven 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