OBJECTIVES: The influence of low dose streptozotocin diabetes on intestinal and vascular injury induced by mesenteric ischaemia/reperfusion (I/R) was studied in rats. The role of reactive oxygen species (ROS) in the exacerbation of ischaemic/postischaemic damage in diabetes was addressed. METHODS: Diabetes was induced by i.p. injection of 3 x 30 mg/kg streptozotocin and after 5 weeks male Wistar rats underwent 60 min ischaemia followed by 30 min reperfusion of the superior mesenteric artery (SMA). The extent of intestinal haemorrhagic injury was assessed macroscopically. Relaxation to acetylcholine of precontracted SMA rings was tested. Chemiluminescence (CL) enhanced by luminol of tissue samples excised from the ileum and SMA was measured. RESULTS: In diabetic rats I/R-induced intestinal injury was significantly more pronounced compared to non-diabetic rats (63.6% potentiation). Decreased endothelial-dependent relaxation of diabetic SMA was not further influenced by I/R. Diabetes itself did not change the CL response of SMA and there was a similar CL increase in the diabetic group with I/R as in the controls. In the intestinal samples CL response was suppressed and I/R only mildly increased CL in the diabetic group. CONCLUSIONS: Diabetes renders the intestinal tissue more vulnerable to the effects of I/R. Endothelial-dependent relaxation of diabetic SMA was not further worsened by I/R. CL responses showed a different involvement of ROS in diabetic intestinal versus vascular tissue.
OBJECTIVES: The influence of low dose streptozotocindiabetes on intestinal and vascular injury induced by mesenteric ischaemia/reperfusion (I/R) was studied in rats. The role of reactive oxygen species (ROS) in the exacerbation of ischaemic/postischaemic damage in diabetes was addressed. METHODS:Diabetes was induced by i.p. injection of 3 x 30 mg/kg streptozotocin and after 5 weeks male Wistar rats underwent 60 min ischaemia followed by 30 min reperfusion of the superior mesenteric artery (SMA). The extent of intestinal haemorrhagic injury was assessed macroscopically. Relaxation to acetylcholine of precontracted SMA rings was tested. Chemiluminescence (CL) enhanced by luminol of tissue samples excised from the ileum and SMA was measured. RESULTS: In diabeticrats I/R-induced intestinal injury was significantly more pronounced compared to non-diabeticrats (63.6% potentiation). Decreased endothelial-dependent relaxation of diabetic SMA was not further influenced by I/R. Diabetes itself did not change the CL response of SMA and there was a similar CL increase in the diabetic group with I/R as in the controls. In the intestinal samples CL response was suppressed and I/R only mildly increased CL in the diabetic group. CONCLUSIONS:Diabetes renders the intestinal tissue more vulnerable to the effects of I/R. Endothelial-dependent relaxation of diabetic SMA was not further worsened by I/R. CL responses showed a different involvement of ROS in diabetic intestinal versus vascular tissue.