Background To explore postoperative changes in β-adrenergic neurotransmission that participate in pathophysiology of postoperative ileus.
Methods Contractile activity of circular jejunal muscle strips was studied. Groups (n = 6/group) were: naïve controls, sham controls 1 and 7 days after laparotomy, and rats 12 h, 1, 3, and 7 days after laparotomy with standardized small bowel manipulation (postoperative ileus). Dose-responses to the β-agonist isoprenaline (3 × 10−10–10−7 mol L−1) were studied in presence/absence of tetrodotoxin (global neural blockade; 10−6 mol L−1), N6-(1-iminoethyl)-l-lysine (inhibition of inducible nitric oxide synthesis; 10−4 mol L−1), nimesulide (cyclooxygenase-2 inhibition; 10−5 mol L−1), or propranolol (β-blockade; 5 × 10−6 mol L−1). Histochemistry for inflammatory cells and intestinal transit were studied.
Key Results Intramural inflammation and delayed transit (postoperative ileus) occurred only in ileus groups. The inhibitory potential of isoprenaline decreased in all postoperative groups including sham (P < 0.05). Tetrodotoxin enhanced isoprenaline-induced inhibition in ileus and sham groups (P < 0.05). N6-(1-iminoethyl)-l-lysine and nimesulide decreased isoprenaline-induced inhibition in ileus groups 12 h, 1, and 7 days, and in sham controls 7 days postoperatively (P < 0.05). Propranolol prevented isoprenaline effects in all groups (P < 0.05).
Conclusions & Inferences Inhibitory effects of isoprenaline on contractile activity were decreased for 7 days postoperatively. Changes in β-adrenergic neurotransmission do not induce postoperative ileus and appear to be caused by anesthesia and laparotomy rather than bowel manipulation.