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特发性巨结肠猫结肠平滑肌功能的改变

Alterations in colonic smooth muscle function in cats with idiopathic megacolon.

作者信息

Washabau R J, Stalis I H

机构信息

Department of Clinical Studies, School of Veterinary Medicine, University of Pennsylvania, Philadelphia 19104-6010, USA.

出版信息

Am J Vet Res. 1996 Apr;57(4):580-7.

PMID:8712528
Abstract

OBJECTIVE

To determine whether colonic smooth muscle dysfunction is involved in the pathogenesis of idiopathic megacolon in cats.

DESIGN

In vitro smooth muscle mechanical measurements.

ANIMALS

Colon from healthy cats and cats with idiopathic megacolon.

PROCEDURE

Colonic smooth muscle strips were suspended in physiologic buffer solution, attached to isometric force transducers, and contracted with acetylcholine (ACh; 10(-9) to 10(-4)M), substance P (SP; 10(-10) to 10(-6)M), cholecystokinin (CCK; 10(-11) to 10(-8)M), potassium chloride (KCl; 10 to 80 mM), or electrical field stimulation (EFS; 25 V, 1 to 30 Hz, 0.5-millisecond duration). Isometric stress responses were compared with those obtained from healthy controls. Colonic smooth muscle strips were also evaluated histologically for neuronal and smooth muscle cell morphology.

RESULTS

Passive isometric stress was not altered, but the active isometric stress responses of megacolon smooth muscle to ACh, SP, CCK, KCl, and EFS were significantly (P < 0.05) diminished, compared with healthy controls. Differences were observed in longitudinal and circular smooth muscle from proximal and distal portions of the colon. Histologic evaluation revealed few abnormalities of smooth muscle cells or of myenteric or submucosal plexus neurons. The contractile response of megacolon smooth muscle to EFS, and the inhibition of this response by tetrodotoxin, suggest that myenteric and submucosal plexus neurons in megacolon smooth muscle are functional.

CONCLUSIONS

Idiopathic megacolon is a generalized dysfunction of colonic smooth muscle in cats. The diminished isometric stress responses to receptor occupancy (ACh, SP, and CCK) and membrane depolarization (KCl) further suggest that the disorder involves disturbance in the activation of smooth muscle myofilaments.

摘要

目的

确定结肠平滑肌功能障碍是否参与猫特发性巨结肠的发病机制。

设计

体外平滑肌力学测量。

动物

健康猫和患有特发性巨结肠的猫的结肠。

步骤

将结肠平滑肌条悬于生理缓冲溶液中,连接到等长力传感器上,并用乙酰胆碱(ACh;10⁻⁹至10⁻⁴M)、P物质(SP;10⁻¹⁰至10⁻⁶M)、胆囊收缩素(CCK;10⁻¹¹至10⁻⁸M)、氯化钾(KCl;10至80 mM)或电场刺激(EFS;25 V,1至30 Hz,0.5毫秒持续时间)使其收缩。将等长应力反应与从健康对照获得的反应进行比较。还对结肠平滑肌条进行组织学评估,以观察神经元和平滑肌细胞形态。

结果

被动等长应力未改变,但与健康对照相比,巨结肠平滑肌对ACh、SP、CCK、KCl和EFS的主动等长应力反应显著(P < 0.05)减弱。在结肠近端和远端的纵行肌和环行肌中观察到差异。组织学评估显示平滑肌细胞或肌间神经丛或黏膜下神经丛神经元几乎没有异常。巨结肠平滑肌对EFS的收缩反应以及河豚毒素对该反应的抑制表明,巨结肠平滑肌中的肌间神经丛和黏膜下神经丛神经元是有功能的。

结论

特发性巨结肠是猫结肠平滑肌的全身性功能障碍。对等长应力反应减弱,对受体占据(ACh、SP和CCK)和膜去极化(KCl)的反应进一步表明,该疾病涉及平滑肌肌丝激活的紊乱。

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