Layer P, Goebell H
Abteilung für Gastroenterologie, Universitätsklinikum Essen.
Schweiz Med Wochenschr. 1989 Nov 25;119(47):1655-63.
Calcium homeostasis and exocrine pancreas interact on several levels under both physiologic and pathophysiologic conditions. (1) Calcium ions are important intracellular mediators of cholinergic and hormonal stimulation of the pancreatic acinar cell, and thus play a central role in the stimulus-secretion coupling of ecbolic pancreatic function. (2) The calcium concentration in pancreatic juice is lower than in the interstitial fluid: pancreatic juice calcium is composed of two fractions, one of which is secreted together with enzyme proteins and the other diffuses along paracellular pathways dependent on serum calcium. Disturbed calcium secretion in pancreatic juice can be observed even following slight pancreatic alteration; conversely, disturbed calcium secretion may be of importance in the pathogenesis of chronic calcifying pancreatitis. (3) Hypocalcemia is an important symptom of acute pancreatitis whose pathogenesis has not been fully elucidated. (4) On the other hand, pancreatitis complicates chronic and acute hypercalcemic syndromes though the pathogenic mechanisms is uncertain. Experimental chronic hypercalcemia in animal models causes characteristic pancreatic secretory changes and disturbs the diffusion barrier for calcium. Experimental acute hypercalcemia causes stimulation of pancreatic enzyme secretion and cholecystokinin release. In addition, extracellular calcium has a direct stimulatory effect on pancreatic acinar cells in vitro.
在生理和病理生理条件下,钙稳态与外分泌胰腺在多个层面相互作用。(1)钙离子是胰腺腺泡细胞胆碱能和激素刺激的重要细胞内介质,因此在促胰液分泌功能的刺激-分泌偶联中起核心作用。(2)胰液中的钙浓度低于组织液:胰液钙由两部分组成,一部分与酶蛋白一起分泌,另一部分沿依赖血清钙的细胞旁途径扩散。即使胰腺稍有改变,也可观察到胰液中钙分泌紊乱;相反,钙分泌紊乱可能在慢性钙化性胰腺炎的发病机制中起重要作用。(3)低钙血症是急性胰腺炎的重要症状,其发病机制尚未完全阐明。(4)另一方面,胰腺炎使慢性和急性高钙血症综合征复杂化,但其致病机制尚不确定。动物模型中的实验性慢性高钙血症会导致特征性的胰腺分泌变化,并扰乱钙的扩散屏障。实验性急性高钙血症会刺激胰腺酶分泌和胆囊收缩素释放。此外,细胞外钙在体外对胰腺腺泡细胞有直接刺激作用。