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刺激大鼠胰腺外分泌并不需要胰腺充血。潜在的胆碱能作用。

Stimulated pancreatic exocrine secretion does not require pancreatic hyperemia in rats. Potential cholinergic role.

作者信息

Conter R L, Washington J L, Kauffman G L

机构信息

Department of Surgery, Milton S. Hershey Medical Center, Pennsylvania State University, Hershey 17033.

出版信息

Dig Dis Sci. 1993 Jul;38(7):1270-7. doi: 10.1007/BF01296078.

Abstract

Although blood flow and cholinergic tone influence gastric and salivary gland secretion, their role in pancreatic secretion is poorly defined. The purpose of the present study was: (1) to test the hypothesis that an increase in pancreatic blood flow accompanies stimulated pancreatic exocrine secretion, and (2) to examine the effects of cholinergic agents on basal and stimulated blood flow using hydrogen gas clearance. Stimulated pancreatic exocrine secretion (secretin 0.4, 0.8, 1.6 micrograms/kg/hr) resulted in a significant (P < 0.005) increase in secretory volume; however, pancreatic blood flow was not significantly changed, and a negative correlation between blood flow and secretion was observed. A pharmacologic dose of secretin (5.0 micrograms/kg/hr) resulted in a significant (P < 0.05) increase in pancreatic blood flow, which was inhibited by atropine (5.0 micrograms/kg/hr) infusion. Although 2-deoxyglucose caused a significant decrease (P < 0.03) in basal pancreatic blood flow, atropine had no effect on basal blood flow levels. These observations suggest that: (1) under physiologic conditions, secretin- or 2-deoxyglucose-stimulated pancreatic secretion does not require pancreatic hyperemia; (2) a pharmacologic dose of secretin does produce pancreatic hyperemia, perhaps through a local cholinergic mechanism; (3) peripheral cholinergic tone does not contribute significantly to basal pancreatic blood flow; and (4) basal pancreatic blood flow may be influenced by central mechanisms.

摘要

尽管血流和胆碱能张力会影响胃和唾液腺的分泌,但它们在胰腺分泌中的作用却不太明确。本研究的目的是:(1)检验胰腺外分泌受刺激时胰腺血流增加的假说;(2)使用氢气清除法研究胆碱能药物对基础血流和受刺激血流的影响。刺激胰腺外分泌(促胰液素0.4、0.8、1.6微克/千克/小时)导致分泌量显著增加(P<0.005);然而,胰腺血流没有显著变化,且观察到血流与分泌之间呈负相关。药理剂量的促胰液素(5.0微克/千克/小时)导致胰腺血流显著增加(P<0.05),这一增加被注入阿托品(5.0微克/千克/小时)所抑制。尽管2-脱氧葡萄糖使基础胰腺血流显著降低(P<0.03),但阿托品对基础血流水平没有影响。这些观察结果表明:(1)在生理条件下,促胰液素或2-脱氧葡萄糖刺激的胰腺分泌不需要胰腺充血;(2)药理剂量的促胰液素确实会导致胰腺充血,可能是通过局部胆碱能机制;(3)外周胆碱能张力对基础胰腺血流的贡献不大;(4)基础胰腺血流可能受中枢机制影响。

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