PubMed Health⌕ Search

Biomedical subjects

F L Bauer

Publications and source records attributed to F L Bauer.

10 recordsLinked to original sources
PubMed1983

Surgical treatment of chronic pancreatitis by distal pancreatectomy.

No consensus exists on the best surgical treatment for chronic pancreatitis. In a retrospective study on 29 patients it was found that pain caused by chronic pancreatitis can be treated effectively by a 95% DP or a 40-80% DP. However, after a 40-80% DP the incidence of endocrine and exocrine pancreatic insufficiency is less frequent than after a 95% DP. Therefore, distal pancreatectomy can be advised as a treatment of pain, caused by chronic pancreatitis. In order to minimize the chance of pancreatic insufficiency resection should be done as conservatively as possible.

Chronic Disease↗
PubMed1980

Contrasting effects of subtotal enteric bypass, enterectomy, and colectomy on azoxymethane-induced intestinal carcinogenesis.

Compensatory hyperplasia after extensive loss of functioning small or large intestine might predispose to the development of neoplasia in the residual adapted bowel. To test this hypothesis, male Fischer rats were randomized to receive 85 to 90% jejunoileal resection or bypass, subtotal colectomy, or no operation (controls). One week later, the first of six weekly s.c. injections of azoxymethane (15 mg/kg/week) was given. At the 36th week postoperatively, mean body weight after enterectomy or colectomy it was 78 to 79% of control. Adaptation after all three operations was characterized by 22 to 84% increments in villous height and crypt depth in the residual functioning ileum (p = 0.05 to 0.001); the depth of colonic crypts was unchanged. Fewer rats developed intestinal tumors after enteric bypass (36%) than after any of the other treatments (80 to 91%) (p = 0.01 to 0.001); the depth of colonic crypts was unchanged. Fewer rats developed intestinal tumors after enteric bypass (36%) than after any of the other treatments (80 to 91%) (p = 0.01 to 0.001). Compared with controls, bypass reduced the number of colonic tumors by 77% (p less than 0.001). Although resection did not affect colonic tumor yield, it tripled the incidence of tumors in the duodenum and jejunum (p = 0.025). Colectomy promoted rectal carcinogenesis (p less than 0.05). Anastomotic tumors were commoner after intestinal resection. the lower frequency of tumors after jejunoileal bypass contrasts with enhanced carcinogenesis after enterectomy or colectomy. Profound reduction in body weight may prevent the promotional effect of adaptive hyperplasia.

Adaptation, Physiological↗
PubMed1979

Enhanced colonic carcinogenesis with azoxymethane in rats after pancreaticobiliary diversion to mid small bowel.

Since biliary excretion of metabolites might determine the pattern of intestinal neoplasms induced by azoxymethane, the number and distribution of tumors were studied in rats after pancreaticobiliary diversion to the mid small bowel. Pancreaticobiliary diversion was performed either immediately before the first of 16 weekly injections of azoxymethane or 10 days after the last. Seven months after pancreaticobiliary diversion, persistent ileal hyperplasia was manifested by higher levels of mucosal RNA and DNA compared with controls (34--102%: P less than 0.001), while there was little residual adaptation in the colon. Qualitative and quantitative analysis of fecal bile acids 6--26 wk after pancreaticobiliary diversion showed few differences. Pancreaticobiliary diversion doubled the incidence of colonic tumors, whether operation preceded (P less than 0.005) or followed (P less than 0.02) the course of azoxymethane. Suture-line tumors were common in the small bowel, particularly in the transposed duodenal stump. Despite intense ileal hyperplasia as a consequence of pancreaticobiliary diversion, the ileum remained resistant to chemical carcinogenesis. The potentiation of colonic neoplasms by pancreaticobiliary diversion probably depends on the stimulation of colonic mucosal proliferation.

Adenocarcinoma↗
PubMed1978

Evidence for an enterotropic hormone: compensatory hyperplasia in defunctioned bowel.

The relative contributions of luminal and systemic factors to the development of compensatory intestinal hyperplasia were assessed by comparing the adaptive response to jejunal resection in functioning and defunctioned ileum. In Thiry--Vella loops of upper ileum, mucosal contents of RNA and DNA increased by 16--21 per cent 2--7 days after jejunectomy (P = 0.05--0.01), but DNA specific activity was unchanged. In lower ileum remaining in continuity with the nutrient stream, nucleic acids were elevated by 27--86 per cent (P less than 0.001) and specific activity by 34--36 per cent (P = 0.05--0.005). Proximal to the site of resection, duodenal hyperplasia was equally rapid but less intense than in the distal bowel. Full adaptation requires both intraluminal nutrients and enterotropic hormones to be present.

Adaptation, Physiological↗
PubMed1978

Proximal enterectomy stimulates distal hyperplasia more than bypass or pancreaticobiliary diversion.

To determine the contribution of intraluminal factors to postresectional intestinal hyperplasia, cell proliferation in the distal intestine of male rats was studied after 50% proximal enterectomy or 50% proximal bypass and also after transposition of the duodenal papilla to the mid small bowel. Within 48 hr all three operations increased RNA and DNA content s in the ileal mucosa 16 to 50% over control values. At 48 hr and 1 week the response distal to resection exceeded that of bypass or pancreaticobiliary diversion; nucleic acid contents, DNA specific activity, villous height, crypt depth, and luminal circumference were greatest 1 week after resection. By 1 month, however, chemical and histological values after resection were equalled or surpassed by those in the other two groups. In excluded jejunum itself, mucosal atrophy lowered RNA and DNA contents to 60% of control levels 1 month postoperatively. Neither pancreaticobiliary diversion nor proximal enteric bypass produces the same rate of distal hyperplasia as proximal resection. Modest colonic hyperplasia may contribute to intestinal adaptation after proximal enterectomy. Adaptive postrescetional cell proliferation appears not to be mediated simply by intraluminal nutrition or enteric secretions; hormonal factors may also be important.

Animals↗
PubMed1978

Contributions of bile and pancreatic juice to cell proliferation in ileal mucosa.

To determine the relative contributions of bile and pancreatic juice to adaptive intestinal hyperplasia, cell proliferation in rat ileal mucosa was studied after supplying bile alone or the combined pancreaticobiliary effluent direct to mid-small bowel. Bile was routed through the choledochus cannulated above the pancreas. Pancreaticobiliary secretions were diverted through a transposed duodenal segment containing the papilla. Diversion of bile into the mid-bowel with and without pancreatic juice caused similar increases in ileal ribonucleic acid (RNA) (16% to 50%) and deoxyribonucleic acid (DNA) (22% to 41%) contents at both 48 hours and 1 week after operation. Specific activity of DNA after injection of tritiated thymidine was greatest after diversion of the combined effluent. After 1 month nucleic acid contents in the upper ileum after pancreaticobiliary diversion were 37% to 59% higher than after transection or biliary diversion (P less than 0.005). Likewise, after biliary diversion villous height and crypt depth were increased only at 1 week, but after diversion of both secretions increases were found at 1 week and 1 month. High luminal concentrations of bile cause transient cell proliferation in ileal mucosa, but the additional presence of pancreatic juice prolongs this adaptive response.

Adaptation, Physiological↗
PubMed1978

Promotion of azoxymethane-induced colonic neoplasia by resection of the proximal small bowel.

Potential enhancement of intestinal neoplasia by compensatory mucosal hyperplasia was tested in rats subjected to 50% proximal small bowel resection (PSBR) 10 days after the last of 16 weekly injections of azoxymethane. Azoxymethane alone increased jejunal contents of RNA and DNA each by 26% at 17 to 18 weeks (p less than 0.01) before there was macroscopic evidence of neoplasia. Three months after PSBR alone, ileal hyperplasia was characterized by increased amounts of RNA (42 to 76%) and DNA (68 to 95%), taller villi, deeper crypts, and luminal dilation (p less than 0.05 to 0.001); however, the colon showed only patchy hyperplasia. When the combined effects of azoxymethane and PSBR were observed 26 to 30 weeks after the first injection, rats with PSBR had an increased number of colonic tumors per animal (2.9 versus 1.6 for controls; p less than 0.02). Despite the intense ileal hyperplasia produced by PSBR, ileal neoplasia did not occur. Enhanced colonic carcinogenesis followed sequential exposure of the mucosa to the carcinogen (azoxymethane) and to the promoting factor (PSBR).

Adaptation, Physiological↗