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Mild external heating and reduction in spontaneous contractions of the bladder
Author(s) -
Kitney Darryl G.,
Jabr Rita I.,
Vahabi Bahareh,
Fry Christopher H.
Publication year - 2017
Publication title -
bju international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.773
H-Index - 148
eISSN - 1464-410X
pISSN - 1464-4096
DOI - 10.1111/bju.13933
Subject(s) - carbachol , heat shock protein , chemistry , heat shock , hsp70 , poly adp ribose polymerase , endocrinology , biophysics , biology , microbiology and biotechnology , medicine , anatomy , biochemistry , dna , polymerase , stimulation , gene
Objectives To measure the effect of external heating on bladder wall contractile function, histological structure and expression of proteins related to tissue protection and apoptosis. Material and Methods In vitro preparations of bladder wall and ex vivo perfused pig bladders were heated from 37 to 42°C, 46 and 50°C for 15 min. Isolated preparations were heated by radiant energy and perfused bladders were heated by altering perfusate temperature. Spontaneous contractions or pressure variations were recorded, as well as responses to the muscarinic agonist carbachol or motor nerve excitation in vitro during heating. Tissue histology in control and after heating was analysed using haematoxylin and eosin staining and 4′‐6‐diamidino‐2‐phenylindole ( DAPI ) nuclear labelling. The effects of heating on protein expression levels of (i) heat shock proteins HSP 27‐ pS er82 and inducible‐ HSP 70 and (ii) caspase‐3 and its downstream DNA ‐repair substrate poly‐[ ADP ‐ribose] polymerase ( PARP ) were measured. Results Heating to 42°C reduced spontaneous contractions or pressure variations by ~70%; effects were fully reversible. There were no effects on carbachol or nerve‐mediated responses. Tissue histology was unaffected by heating, and expression of heat shock proteins as well as caspase‐3 and PARP were also unaltered. A TRPV 1 antagonist had no effect on the reduction of spontaneous activity. Heating to 46°C had a similar effect on spontaneous activity and also reduced the carbachol contracture. Urothelial structure was damaged, caspase‐3 levels were increased and inducible‐ HSP 70 levels declined. At 50°C evoked contractions were abolished, the urothelium was absent and heat shock proteins and PARP expression was reduced with raised caspase‐3 expression. Conclusions Heating to 42°C caused a profound, reversible and reproducible attenuation of spontaneous activity, with no tissue damage and no initiation of apoptosis pathways. Higher temperatures caused tissue damage and activation of apoptotic mechanisms. Mild heating offers a novel approach to reducing bladder spontaneous activity.