Raraty M G, Petersen O H, Sutton R, Neoptolemos J P
Department of Surgery, University of Liverpool, UK.
Baillieres Best Pract Res Clin Gastroenterol. 1999 Jul;13(2):241-51. doi: 10.1053/bega.1999.0022.
Acute pancreatitis is a common, often severe disease with multiple causes. Many of the aetiological factors responsible for triggering acute pancreatitis have been identified but the pathophysiological mechanism by which they do so is still poorly understood. Free calcium ions within the cytosol of the acinar cell ([Ca2+]i) act as a key intracellular second messenger in the processes of stimulus-secretion coupling and may be crucial in the pathogenesis of acute pancreatitis. [Ca2+]i signals have been shown to be disrupted early in experimental pancreatitis, and it is known that an abnormal rise in [Ca2+]i is toxic by a variety of mechanisms. It has been demonstrated that abnormal, prolonged elevations in [Ca2+]i result from caerulein hyperstimulation and ethanol treatment, and it is likely that all the known causes of acute pancreatitis can cause similar disruptions. Elevations in [Ca2+]i have also been shown to be associated with both acinar cell vacuolization and intracellular enzyme activation, both of which are key steps in the pathogenesis of acute pancreatitis. A disturbance of intracellular Ca2+ signalling and the generation of an abnormal elevation in [Ca2+]i appears to be the common factor linking all the known triggers for acute pancreatitis and initiating the further sequence of pathological events leading to clinical disease.
急性胰腺炎是一种常见且往往较为严重的疾病，病因多样。许多引发急性胰腺炎的病因已被确定，但其发病的病理生理机制仍未完全明晰。腺泡细胞胞质内的游离钙离子（[Ca2+]i）在刺激-分泌偶联过程中作为关键的细胞内第二信使，在急性胰腺炎发病机制中可能起着至关重要的作用。在实验性胰腺炎早期已显示[Ca2+]i信号受到干扰，并且已知[Ca2+]i的异常升高通过多种机制具有毒性。已经证明，[Ca2+]i的异常、持续升高是由蛙皮素过度刺激和乙醇处理导致的，并且所有已知的急性胰腺炎病因都可能导致类似的干扰。[Ca2+]i的升高还与腺泡细胞空泡化和细胞内酶激活均有关联，这两者都是急性胰腺炎发病机制中的关键步骤。细胞内钙离子信号的紊乱以及[Ca2+]i的异常升高似乎是连接所有已知急性胰腺炎触发因素并引发导致临床疾病的进一步病理事件序列的共同因素。
