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在没有残留导管狭窄的情况下,急性胰腺炎不是慢性胰腺炎的病因。

Acute pancreatitis is not a cause of chronic pancreatitis in the absence of residual duct strictures.

作者信息

Sarles H, Camarena-Trabous J, Gomez-Santana C, Choux R, Iovanna J

机构信息

Service d'Hépato-Gastroentérologie, Hôpital Sainte-Marguerite, Marseille, France.

出版信息

Pancreas. 1993 May;8(3):354-7. doi: 10.1097/00006676-199305000-00011.

Abstract

It has been shown that intraductal injections of bile salts into the bile-pancreatic ducts of dogs or rats were immediately followed by acute hemorrhagic pancreatitis and, some months later, by persisting chronic pancreatitis. The study described in this article was designed to test the assumption that these chronic lesions were due to ductal strictures secondary to the toxic effect of bile salts. The bile-pancreatic ducts of 100 rats were injected with 0.2 ml of a solution containing 4 microM Na taurodeoxycholate and 0.2 microM trypsin. The 66 survivors were killed at intervals from 1 day to 2 months following the induction of acute pancreatitis. Four to six sections were done in the first series, and serial 15-micron sections of the entire pancreas were taken from rats surviving 2 months. These showed that from the sixth day on, the largest ducts draining pathological areas were obstructed by fibrosis. Distal to this obstruction, intralobular ducts were dilated and their epithelia flattened or atrophied. Acini were atrophied and replaced by peri- and intralobular fibrosis. Lesions were limited to areas drained by obstructed ducts, with the rest of the parenchyma being normal. We conclude that in experimental animals, as in human beings, chronic lesions that persist after acute pancreatitis are due to duct obstruction, not to acinar necrosis.

摘要

研究表明,向狗或大鼠的胆胰管内注射胆盐后,会立即引发急性出血性胰腺炎,数月后则会出现持续性慢性胰腺炎。本文所述的研究旨在验证这样一种假设,即这些慢性病变是由胆盐毒性作用继发的导管狭窄所致。向100只大鼠的胆胰管内注射0.2毫升含有4微摩尔牛磺脱氧胆酸钠和0.2微摩尔胰蛋白酶的溶液。66只存活的大鼠在急性胰腺炎诱发后的1天至2个月内分批处死。第一组做了4至6个切片,对存活2个月的大鼠的整个胰腺制作了连续的15微米切片。这些切片显示,从第6天起,引流病变区域的最大导管被纤维化阻塞。在该阻塞远端,小叶内导管扩张,其上皮扁平或萎缩。腺泡萎缩,被小叶周围和小叶内纤维化取代。病变局限于阻塞导管引流的区域,其余实质正常。我们得出结论,在实验动物中,如同在人类中一样,急性胰腺炎后持续存在的慢性病变是由于导管阻塞,而非腺泡坏死。

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