The Journal of surgical research · 2006
Intestinal ischemia/reperfusion injury aggravates talc-induced adhesions in rats.
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Murata Pin, Kase Yoshio, Tokita Youhei, Takeda Shuuichi, Sasaki Hiroshi
Аннотация
BACKGROUND: Postoperative intraperitoneal adhesions are the leading cause of intestinal obstruction, but the underlying mechanisms remain incompletely understood. The aim of the current study was to investigate the involvement of intestinal ischemia/reperfusion (I/R) injury in adhesion formation in rats.
MATERIALS AND METHODS: Rats were subjected to either a dusting of talc (15 mg/rat) over the entire small intestine or ischemia induced by clamping the superior mesenteric artery (SMA) for 30 min followed by reperfusion with or without talc dusting. On postoperative days 4, 7, and 14, the scores, lengths, and incidence of adhesions were evaluated. In addition, the contractile force of the jejunal muscle was measured at 0, 24, 48, and 96 h after the treatments using organ bath techniques under bethanechol-stimulated conditions.
RESULTS: Talc induced mild adhesions in rats. Although I/R injury alone did not produce adhesions, it markedly aggravated the talc-induced adhesions, with higher scores and longer adhesions on postoperative days 4, 7, and 14. In addition, I/R injury caused 75-88% suppression of the circular muscle contractile force and 35-52% suppression of the longitudinal muscle contractile force at 24 h after SMA occlusion. However, talc did not affect the contractions.
CONCLUSIONS: Intestinal I/R injury aggravated the talc-induced adhesions, and this consequence might be due to the functional suppression of jejunal muscle contractions. This finding suggests that intestinal ischemia is an important factor in the etiology of postoperative adhesions.
MATERIALS AND METHODS: Rats were subjected to either a dusting of talc (15 mg/rat) over the entire small intestine or ischemia induced by clamping the superior mesenteric artery (SMA) for 30 min followed by reperfusion with or without talc dusting. On postoperative days 4, 7, and 14, the scores, lengths, and incidence of adhesions were evaluated. In addition, the contractile force of the jejunal muscle was measured at 0, 24, 48, and 96 h after the treatments using organ bath techniques under bethanechol-stimulated conditions.
RESULTS: Talc induced mild adhesions in rats. Although I/R injury alone did not produce adhesions, it markedly aggravated the talc-induced adhesions, with higher scores and longer adhesions on postoperative days 4, 7, and 14. In addition, I/R injury caused 75-88% suppression of the circular muscle contractile force and 35-52% suppression of the longitudinal muscle contractile force at 24 h after SMA occlusion. However, talc did not affect the contractions.
CONCLUSIONS: Intestinal I/R injury aggravated the talc-induced adhesions, and this consequence might be due to the functional suppression of jejunal muscle contractions. This finding suggests that intestinal ischemia is an important factor in the etiology of postoperative adhesions.