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Activation-dependent descending reflex evacuation of anal canal in a rat model

机译:大鼠模型中依赖于激活的肛管降反射排空

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The evacuative motor responses of the anal canal and recto-anal reflexes during defecation were studied in an isolated rat recto-anal model preparation using (i) partitioned organ bath, (ii) electrical stimulation, (iii) balloon distension and (iv) morphological techniques. Electrical field stimulation applied to the anal canal or to the distal part of the rectum elicited tetrodotoxin (10 -7 M)-sensitive frequency-dependent local or descending contractions of the anal canal and the local responses were bigger in amplitude (14.9 ± 1.35 mN) than the descending contractions (5.3 ± 0.7 mN at frequency of 5 Hz, p < 0.05). The balloon-induced distension of the distal rectum evoked descending responses of the anal canal consisting of a short contraction (1.50 ± 0.18 mN) followed by deep relaxation (3.12 ± 0.34 mN). In the presence of atropine (3 x 10~(-7) M) the electrically-elicited (5 Hz) local or descending contractions of the anal canal were suppressed and a relaxation revealed. The initial contraction component of the distension-induced response was decreased while the relaxation was not changed. During atropine treatment, spantide (10~(-7) M) lowered even more the contractile component of the anal canal response. NG-nitro-L-arginine (5 x 10~(-4) M) enhanced the contraction, prevented the atropine-dependent relaxation of the electrically-elicited response and inhibited the distension-induced relaxation. L-Arginine (5 x 10~(-4) M) suppressed the contraction and extended the relaxation. ChAT-, substance P- and NADPH-diaphorase-positive perikarya and nerve fibers were observed in myenteric ganglia of the anal canal. The results suggest activation-dependent descending reflex motority of the anal canal involving electrical stimulation-displayed cholinergic and tachykininergic and distensionmanifested nitrergic neuro-muscular communications.
机译:在隔离的大鼠直肠肛门模型制备中,使用(i)分隔器官浴,(ii)电刺激,(iii)球囊扩张和(iv)形态学研究了排便过程中肛管和直肠肛门反射的排空运动反应技术。施加于肛门管或直肠远端的电场刺激会引起河豚毒素(10 -7 M)敏感的频率依赖性的肛门管局部或下行收缩,且局部反应的幅度较大(14.9±1.35 mN) )比下降的收缩幅度(频率为5 Hz时为5.3±0.7 mN,p <0.05)。球囊引起的远端直肠扩张引起肛门管的下降反应,包括短时收缩(1.50±0.18 mN),然后深部松弛(3.12±0.34 mN)。在阿托品(3 x 10〜(-7)M)存在的情况下,电刺激的(5 Hz)肛管局部或下降收缩受到抑制,并显示出松弛。扩张引起的反应的初始收缩成分减少,而松弛没有改变。在阿托品治疗期间,司必肽(10〜(-7)M)进一步降低了肛管反应的收缩成分。 NG-硝基-L-精氨酸(5 x 10〜(-4)M)增强了收缩,阻止了由阿托品引起的电刺激反应的松弛,并抑制了由扩张引起的松弛。 L-精氨酸(5 x 10〜(-4)M)抑制了收缩并延长了松弛时间。在肛门管的肌层神经节中观察到ChAT-,P-物质和NADPH-黄递酶阳性的周核和神经纤维。结果表明,肛管激活依赖性降反射运动涉及电刺激显示胆碱能,速激肽能和扩张表现出的硝化神经-肌肉通讯。

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