It is well recognized that reperfusion causes tissue damage in excess
of that produced by ischemia alone. The present study was designed to
test this and to evaluate the role of the calcium antagonist, diltiaze
m (400 mu g/kg body weight administered intravenously over 95 min), in
ischemia-reperfusion injury of the intestine. Intestinal ischemia was
produced by occlusion of the superior mesenteric artery (SMA) with in
terruption of the collateral flow for 30 min. Reperfusion was establis
hed by declamping the SMA for 1 h, and mucosal injury was assessed usi
ng a grading scale from 0 to 5. The severity of mucosal damage increas
ed significantly after Ih of reperfusion, from a mean grade of 2.1 in
the ischemia group to 3.8 in the ischemia-reperfusion group (p < 0.01)
. Diltiazem was effective in the amelioration of histologic changes of
reperfusion injury and reduced the degree of mucosal injury from a me
an grade of 3.8 in the ischemia-reperfusion group to 2.5 in the diltia
zem group (p < 0.05). This study strongly suggests that calcium ions a
re involved in the pathogenesis of ischemia-reperfusion injury and tha
t diltiazem attenuates this injury by preventing the intracellular cal
cium influx that occurs during reperfusion.