No abstract

To the author's knowledge, an intensive investigation of pulmonary function during the first 2 postoperative days has not previously been reported. Consequently, in this study the effect of regional surgery on respiratory function, monitored every 4 h during the first 2 postoperative days, was analyzed. Hypoxaemia was a constant finding in all patients undergoing general anaesthesia. The degree and duration of hypoxaemia and spirometry changes were related to the site of surgical incision. Clinical signs of atelectasis were commonly observed during the first postoperative day and occurred after the change in PO2 and spirometry. Atelectasis was more common in patients having upper abdominal surgery. The current investigation reveals that the earliest postoperative change indicative of atelectasis is the fall in PO2; that auscultatory changes do not always occur in the presence of postoperative hypoxaemia; that auscultatory signs are not indicative of the extent of the PO2 fall; and that radiology represents a crude method of assessing postoperative atelectasis.

An animal model of organ-specific chemical carcinogenesis has been used to study environmental effects on the incidence of human colorectal adenocarcinoma. Wistar/Furth weanling rats underwent connection of their urinary and fecal streams (ureterosigmoidostomy), connection of their urinary and fecal streams with proximal fecal diversion (rectal bladder), or sham operations. Age-matched, unoperated control and operated animals then received either no carcinogen, 1,2-dimethylhydrazine (DMH) 20 mg/kg body weight, s.c. once weekly for 16 weeks, N-[4-(5-nitro-2-furyl)-2-thiazolylformamide (FANFT) 0.2% of the feed for 16 weeks, or DMH + FANFT concurrently. Thirty-three weeks after carcinogen exposure, surviving animals were killed and examined for bowel and urinary bladder tumors. The incidence of adenocarcinoma of the colon adjacent to the junction between bladder and bowel was significantly higher in animals after ureterosigmoidostomy compared with animals whose fecal stream had been proximally diverted (14/22 vs. 0/34, P less than 0.001). This effect was not dependent upon chemical carcinogen exposure. Nonexposed animals still developed a significantly higher incidence of colon adenocarcinomas adjacent to their bladder-bowel junctions as compared with animals with proximal fecal diversion (5/8 vs. 0/13, P less than 0.01). In unoperated or sham operated animals, adenocarcinomas of the bowel occurred in 33% of DMH-treated animals and transitional cell carcinomas of the urinary bladder in 33% of the FANFT-treated animals. After concurrent exposure to both carcinogens, no increased incidence of bladder tumors was noted when compared with FANFT treatment alone. However, the number of animals with one or more adenocarcinomas of the bowel (22/30 vs. 17/50, P less than 0.001), the mean number of tumors per animal (2.1 +/- 0.2 vs. 1.1 +/- 0.1, P less than 0.01), and the invasiveness of the tumors were all increased after DMH + FANFT as compared with DMH exposure alone. The carcinogenic potential of direct bladder to bowel connection with intact fecal and urinary streams, and the potentiation by FANFT of DMH-induced colon carcinogenesis may have implications in the genesis of human colorectal cancer.

We have investigated the effect of distal small bowel resection on chemically induced tumors of the gastrointestinal tract in Wistar/Furth (W/Fu) rats. Dimethylhydrazine (DMH) (20 mg/kg sc once weekly x 16) was commenced 3 months after rats underwent resection of the distal 30 cm of small bowel (one-third resection) or after sham small bowel resection (controls). Fifty weeks after the start of DMH administration, tumors were found in 15 of 25 animals who underwent small bowel resection compared to 9 of 31 animals in the control group (P less than 0.05). After small bowel resection, 8 of 15 tumors occurred at the site of anastomosis but no anastomotic tumors were seen after sham resection. In addition, tumors were larger and more invasive after small bowel resection. These data indicate that major small bowel resection potentiates DMH induced-intestinal carcinogenesis.