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首页> 外文期刊>Pancreas >Tissue kallikrein in severe acute pancreatitis in patients treated with high-dose intraperitoneal aprotinin.
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Tissue kallikrein in severe acute pancreatitis in patients treated with high-dose intraperitoneal aprotinin.

机译：大剂量腹膜内抑肽酶治疗严重急性胰腺炎患者的组织激肽释放酶。

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The activation of the kallikrein-kinin system is thought to be one of the pathophysiologic mechanisms in acute pancreatitis. A radioimmunoassay for human urinary tissue kallikrein was developed and used to measure tissue kallikrein peritoneal exudate and plasma from 48 patients with severe acute pancreatitis. All patients were treated with intraperitoneal lavage. One group (n = 22) received high doses of the protease inhibitor aprotinin (aprotinin group), and the other group, saline (control group). Levels of kallistatin in peritoneal exudates and plasma were measured with an enzyme immunoassay. A large increase in tissue kallikrein was observed in the peritoneal exudate, which declined in both groups after multiple lavages. Complexing of liberated tissue kallikrein with kallistatin was evidenced by gel filtration in both peritoneal exudates and plasma in both groups. The decrease in kallistatin observed in both peritoneal exudate and plasma is therefore regarded as being due not only to repeated lavage, but also to true consumption of the binding protein. Some of the liberated tissue kallikrein in the peritoneal fluid and plasma was complexed to aprotinin. In the control group, six patients were operated on because of pancreatic necrosis, compared with none in the aprotinin group. The levels of tissue kallikrein in the lavage fluid were lower in the control group, but this was the result of the very low tissue kallikrein values in the six patients operated on for pancreatic necrosis. Levels of kallistatin in plasma and peritoneal exudate in these six patients were lower on the day of admission compared with the other patients, and the plasma levels continued to be lower during the first week. Large amounts of tissue kallikrein were found to be released into the peritoneal exudates in acute pancreatitis. Lavages effectively cleared the released tissue kallikrein. The tissue kallikrein was complexed to kallistatin, whereas in the aprotinin group, also to aprotinin both in plasma and in peritoneal fluid. The partitioning of kallikrein between the two inhibitors was the result of the interaction between enzyme and inhibitors and the turnover of the complexes formed. The low admission levels of kallistatin in the six patients operated on because of pancreatic necrosis suggest that kallistatin may act as an early marker of severity in acute pancreatitis.
机译：激肽释放酶激肽系统的激活被认为是急性胰腺炎的病理生理机制之一。开发了一种用于人体泌尿组织激肽释放酶的放射免疫测定法，并用于测量48例重症急性胰腺炎患者的组织激肽释放酶腹膜渗出液和血浆。所有患者均接受腹腔灌洗。一组（n = 22）接受高剂量的蛋白酶抑制剂抑肽酶（抑肽酶组），另一组接受盐水（对照组）。用酶免疫测定法测定腹膜渗出液和血浆中的利司他汀水平。在腹膜渗出液中观察到组织激肽释放酶的大量增加，两组在多次灌洗后均下降。两组腹膜渗出液和血浆中的凝胶过滤均证实了释放的组织激肽释放酶与激肽释放酶的复合。因此，在腹膜渗出液和血浆中观察到的利他汀的减少不仅是由于反复灌洗，而且还因为结合蛋白的真正消耗。腹膜液和血浆中的一些游离组织激肽释放酶与抑肽酶复合。对照组中有6例因胰脏坏死而接受手术治疗，而抑肽酶组则无此手术。对照组的灌洗液中组织激肽释放酶的水平较低，但这是由于六名接受胰腺坏死手术的患者的组织激肽释放酶值非常低的结果。在入院当天，这六名患者的血浆和腹膜渗出液中卡利司汀的水平低于其他患者，并且在第一周血浆水平继续降低。发现在急性胰腺炎中大量组织激肽释放酶释放到腹膜分泌物中。灌洗有效清除了释放的激肽释放酶组织。组织激肽释放酶与激肽释放酶复合，而在抑肽酶组中，血浆和腹膜液中均与抑肽酶复合。激肽释放酶在两种抑制剂之间的分配是酶和抑制剂之间相互作用以及形成的复合物转换的结果。因胰脏坏死而接受手术的6例患者中卡利司汀的入院率较低，这表明卡利司汀可能是急性胰腺炎严重程度的早期指标。

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