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链脲佐菌素诱导的糖尿病大鼠结肠和回肠对细胞外和细胞内钙操作的反应发生改变。

The responses to manipulation of extracellular and intracellular calcium are altered in the streptozotocin-diabetic rat colon and ileum.

作者信息

Forrest Abigail, Molleman Areles, Parsons Mike

机构信息

The School of Life Sciences, University of Hertfordshire, CP Snow Building, College Lane, Hatfield, Herts AL10 9AB, United Kingdom.

出版信息

Eur J Pharmacol. 2005 Feb 10;509(1):77-83. doi: 10.1016/j.ejphar.2004.12.029. Epub 2005 Jan 26.

Abstract

Studies were performed to see if alterations in Ca2+ homeostasis underlie the gastrointestinal motility complications seen in many diabetic patients. Experiments were performed on colonic and ileal tissues taken from streptozotocin-induced diabetic and control rats. Diabetes caused alterations in the responses of the tissues to Ca2+ manipulation but these differed between the colon and ileum. In the colon a small but not significant increase in contractile responses to CaCl2 was observed in diabetic tissues, whereas the responses of the ileum were depressed relative to those of the controls. In contrast, responses of the diabetic ileum to the Ca2+ channel agonist Bay K8644 were greater than those of the controls, whilst the agonist failed to contract the colon. Similarly, the Ca2+-ATPase inhibitors, thapsigargin and cyclopiazonic acid, produced contractions which were greater in diabetic ileal tissues. Thus, alterations in the responses of the diabetic gut to Ca2+ manipulation are complex, and also tissue-specific.

摘要

开展了多项研究,以探究钙(Ca2+)稳态的改变是否是许多糖尿病患者出现胃肠动力并发症的原因。对从链脲佐菌素诱导的糖尿病大鼠和对照大鼠获取的结肠和回肠组织进行了实验。糖尿病导致组织对Ca2+ 操控的反应发生改变,但结肠和回肠的情况有所不同。在结肠中,糖尿病组织对氯化钙的收缩反应有小幅增加,但不显著,而回肠的反应相对于对照组则受到抑制。相比之下,糖尿病回肠对Ca2+ 通道激动剂Bay K8644的反应大于对照组,而该激动剂未能使结肠收缩。同样,Ca2+ -ATP酶抑制剂毒胡萝卜素和环匹阿尼酸所引发的收缩在糖尿病回肠组织中更强烈。因此,糖尿病肠道对Ca2+ 操控的反应改变是复杂的,且具有组织特异性。

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