Longhurst Penelope A, Levendusky Mark C, Bezuijen Martina W
Department of Basic and Pharmaceutical Sciences, Albany College of Pharmacy, New York 12208, USA.
J Urol. 2004 Feb;171(2 Pt 1):933-7. doi: 10.1097/01.ju.0000093561.95283.df.
We investigated the effects of the combination of bladder outlet obstruction and diabetes mellitus on in vitro rat bladder body strip function.
Longitudinal strips were removed from ventral and dorsal detrusor of age matched control, 2-week diabetic, 2-week obstructed and 2-week obstructed diabetic rats. Contractile responses to electrical field stimulation, carbachol, adenosine triphosphate, KCl and phenylephrine, and relaxations in response to norepinephrine and isoproterenol were measured.
Bladders from diabetic, obstructed and obstructed diabetic rats were 1.6-fold, 2.6-fold and 3.6-fold heavier than those from controls. Responses of bladder strips from diabetics to all stimuli were similar to those of controls. Strips from obstructed rats were significantly less responsive to norepinephrine than those from controls or diabetics and strips from obstructed diabetics were significantly less responsive to norepinephrine and isoproterenol than those from all other groups. Strips from obstructed diabetics had significantly decreased responses to field stimulation, while responses to carbachol were decreased to a lesser extent. Responses of strips from obstructed rats to field stimulation were also decreased compared with controls but were significantly greater than those of the obstructed diabetic group. Responses to adenosine triphosphate, KCl and phenylephrine were similar in all groups.
The combination of outlet obstruction and diabetes mellitus causes significant increases in bladder mass compared with either diabetes or obstruction alone. Bladder strips from obstructed diabetics show characteristics of denervation accompanied by alterations in beta-adrenergic function, suggesting that the coexistence of outlet obstruction and diabetes increases the rate of development of bladder decompensation.
我们研究了膀胱出口梗阻与糖尿病联合作用对体外大鼠膀胱体条功能的影响。
从年龄匹配的对照大鼠、糖尿病2周大鼠、梗阻2周大鼠以及梗阻合并糖尿病2周大鼠的腹侧和背侧逼尿肌取下纵向肌条。测量电场刺激、卡巴胆碱、三磷酸腺苷、氯化钾和去氧肾上腺素引起的收缩反应，以及去甲肾上腺素和异丙肾上腺素引起的舒张反应。
糖尿病大鼠、梗阻大鼠以及梗阻合并糖尿病大鼠的膀胱重量分别是对照大鼠的1.6倍、2.6倍和3.6倍。糖尿病大鼠膀胱条对所有刺激的反应与对照大鼠相似。梗阻大鼠的肌条对去甲肾上腺素的反应明显低于对照大鼠或糖尿病大鼠，梗阻合并糖尿病大鼠的肌条对去甲肾上腺素和异丙肾上腺素的反应明显低于其他所有组。梗阻合并糖尿病大鼠的肌条对电场刺激的反应显著降低，而对卡巴胆碱的反应降低程度较小。梗阻大鼠肌条对电场刺激的反应与对照大鼠相比也降低，但明显大于梗阻合并糖尿病组。所有组对三磷酸腺苷、氯化钾和去氧肾上腺素的反应相似。
与单独的糖尿病或梗阻相比，膀胱出口梗阻与糖尿病联合作用导致膀胱重量显著增加。梗阻合并糖尿病大鼠的膀胱条表现出失神经特征，同时伴有β-肾上腺素能功能改变，提示膀胱出口梗阻与糖尿病并存会增加膀胱失代偿的发展速度。
