Gender-related neuronal and smooth muscle damage of guinea pig isolated urinary bladder from anoxia-glucopenia and reperfusion injury and its relationship to glycogen content.
OBJECTIVE
To investigate the effects of anoxia and glucopenia (A-G) on both male and female guinea pig urinary bladder.


METHODS
In whole bladders superfused with oxygenated Krebs' solution, intrinsic nerves underwent electrical field stimulation (EFS) and smooth muscle stimulated with carbachol, ATP, and high potassium. The effect of 1, 2, or 3 hr A-G on the contractile response and the ensuing recovery in Krebs' solution, was monitored. Glycogen content in male and female urinary bladders was also measured.


RESULTS
Under different stimuli male urinary bladder proved to contract more efficiently than female organ. After 1 hr A-G the EFS response of male urinary bladder was virtually abolished and returned to 60% of control response in the recovery phase; in female bladder the EFS responses fully recovered during the reperfusion phase. Full recovery of the response to carbachol, ATP, and high potassium stimulations was observed in both genders. A-G had to be extended to 2 hr to cause smooth muscle impairment (higher in male than in female) and a neuronal impairment in female urinary bladders. When 2-deoxyglucose (2-DG), an inhibitor of glycolysis, was added during 1 hr A-G, both neuronal and smooth muscle damages were significantly enhanced in male, as well as, though to a lesser extent, in female bladder. A significantly higher glycogen content was observed in female as compared to male bladders, which was inversely related with the duration of exposure to A-G.


CONCLUSIONS
The higher resistance of female urinary bladder to A-G/reperfusion, can be partly ascribed to the higher glycogen content.
Pessina
Federica
F
Dipartimento di Scienze Biomediche, Università di Siena, Siena, Italy. pessinafed@unisi.it
Valeri
Aurora
A
Dragoni
Stefania
S
Valoti
Massimo
M
Sgaragli
Giampietro
G
D000255:Adenosine Triphosphate / Q000494:pharmacology; D000818:Animals; D002217:Carbachol / Q000494:pharmacology; D018679:Cholinergic Agonists / Q000494:pharmacology; D003847:Deoxyglucose / Q000493:pharmacokinetics; D005260:Female; D005947:Glucose / Q000494:pharmacology; D006003:Glycogen / Q000378:metabolism*; D006168:Guinea Pigs; D000860:Hypoxia / Q000378:metabolism / Q000473:pathology; D066298:In Vitro Techniques; D008297:Male; D009119:Muscle Contraction / Q000187:drug effects / Q000502:physiology; D009130:Muscle, Smooth / Q000294:innervation / Q000378:metabolism / Q000473:pathology; D017933:Peripheral Nervous System / Q000187:drug effects / Q000378:metabolism / Q000473:pathology*; D011189:Potassium Chloride / Q000494:pharmacology; D015427:Reperfusion Injury / Q000378:metabolism / Q000473:pathology*; D012727:Sex Characteristics; D001743:Urinary Bladder / Q000294:innervation / Q000378:metabolism / Q000473:pathology*
D018679:Cholinergic Agonists; D011189:Potassium Chloride; D000255:Adenosine Triphosphate; D002217:Carbachol; D006003:Glycogen; D003847:Deoxyglucose; D005947:Glucose