Table 1.
Experimental groups.
Fig 1.
A. To create the cecal hinge, the abraded cecum was stitched in two places (arrows) to appose a 1 cm X 2 cm area where the peritoneum had been removed. B. Quantification of the primary adhesion. The free cecum was cut from the adhesion area, the contents removed, and the edges trimmed. The adhesion was outlined and the area recorded. C. Completed strictureplasty surgery. D. The intestinal segment 7 days following strictureplasty was instrumented and inflated until suture failure. The sutures can be seen beneath the fatpad adhesion that encased the suture line. E. Sample trace of intraluminal pressure. The first dip (arrow) was associated with mesothelial splitting at a different site from the suture line. This sample withstood a pressure of 179 mmHg.
Fig 2.
Representative postoperative adhesions seen in the cecal hinge model.
Images A-C were taken from the same rat in the 4-day treatment group. A. Greater omentum to cecum (C, in all panels), the extent indicated by a bracket. B. Left adnexal fatpad (*) is adherent to the cecum. In this rat there was no primary adhesion, which can be appreciated by the fold in the tissue between the abdominal wall and the cecum. C. Cohesive adhesion between the small intestine and the cecum (arrow). D. Band-like adhesion between the mesentery of the small intestine and the cecum.
Fig 3.
Modeled manual therapy attenuated or prevented primary postoperative adhesions.
A. Areas of primary adhesions (means ± SEM; * p < 0.05). B. The proportion of rats with primary adhesion formation was lower than untreated rats (Fischer’s exact test, * = p < 0.0001). Numbers per group are indicated within bars.
Fig 4.
Ratings of necropsy videos (not including primary adhesion).
There were no differences between treated and untreated groups in rated parameters of non-primary postoperative adhesions (n = 7 per group; means ± SEM). There were numerous differences over time, representing the natural biology of postoperative adhesions (Table 2).
Table 2.
Statistical results for video ratings (Fig 4).
Fig 5.
Effects of surgery and buprenorphine on fecal pellet discharge.
A. Surgery and 1 dose of buprenorphine immediately after surgery (beginning of Epoch 1) led to reduced fecal pellet discharge 20 to 24 hours after administration. B. Surgery and 3 doses of buprenorphine immediately after surgery (beginning of Epoch 1) led to reduced fecal pellet discharge from 12 to 24 hours after administration. The observed differences between doses were not statistically significant, and there was no effect of treatment under either condition. Shaded area represents 7:00 PM– 7:00 AM. Baseline data in both panels are from rats from the 3-dose group, taken the week before surgeries. n = 14/group at each Epoch, means ± SEM.
Fig 6.
Relative expression of M1 or M2 markers by intraperitoneal macrophages.
Intraperitoneal macrophages were isolated by peritoneal lavage at postoperative days specified in the X-axes. Cells were stained with anti-CD11b to positively identify monocyte lineage cells and anti-HIS48 to exclude neutrophils. Expression levels of the indicated markers (A) arginase, (B) CD163, (C) CD86, (D) iNOS are depicted as fold changes normalized to expression by intraperitoneal macrophages isolated from naïve rats. n = 7/group, means ± SEM. * p<0.05 post hoc test.
Fig 7.
Ratings of necropsy videos 7 days following adhesiolysis.
There were no differences between treated (n = 15) and untreated (n = 12) rats in adhesion parameters following adhesiolysis (means ± SEM). These results are comparable to those reported in Fig 4.
Fig 8.
Strictureplasty burst strengths.
While the variability of the burst strengths was greater following treatment (untreated n = 6, treated n = 7, means ± SEM), the means were not.