AIMS: 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, F., Valeri, A., Dragoni, S., Valoti, M., Sgaragli, G.P. (2007). 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. NEUROUROLOGY AND URODYNAMICS, 26(3), 416-423 [10.1002/nau.20323].

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

Pessina, Federica;Valeri, A.;Dragoni, S.;Valoti, Massimo;Sgaragli, GIAN PIETRO
2007-01-01

Abstract

AIMS: 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, F., Valeri, A., Dragoni, S., Valoti, M., Sgaragli, G.P. (2007). 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. NEUROUROLOGY AND URODYNAMICS, 26(3), 416-423 [10.1002/nau.20323].
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11365/25512
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