Arrest of flow through the mesenteric circulation for intervals as short as thirty minutes followed by reperfusion leads to the development of vasospasm which may increase the severity of tissue injury. To test the hypothesis that vasospasm is related to endothelial injury, we examined the ultrastructural changes occurring in the rat superior mesenteric artery (SMA) associated with occlusion <i>in situ</i> for 30, 60, 90 and 120min, followed by reperfusion for 10min. The SMA was perfuse-fixed with Karnovski's fixative at a pressure of 100mmHg before processing for either transmission or scanning electronmicroscopy. After 30 min ischaemia the endoplasmic reticulum of the endothelial cells showed mild dilatation and platelets and leucocytes were adherent to the surface. After 60-90min, endothelial cell swelling became increasingly more severe, and at 120min some cells showed surface blebbing and high amplitude swelling of mitochondria. Following periods of ischaemia of up to 4h, isolated rat SMA preparations perfused with Krebs-Henseleit buffer showed a progressive failure of endothelium-dependent vasodilatation in response to adenosine diphosphate (3x10-<sup>5</sup>M) and acetylcholine (3 x l0-<sup>6</sup>M). This impairment of endothelial function was reversible with prolonged reperfusion. Infusion of isolated rat leucocytes suspended in the perfusate (3 x l0<sup>6</sup> cells/ml) to isolated SMA preparations resulted in a marked increase in leucocyte-induced vasoconstriction after as little as 30min of ischaemia (%ΔR 38.0± 11.2 vs 2.4±0.5, p<0.05). <h3>Conclusion</h3> Despite ultrastructural and functional evidence of relatively mild, reversible injury, endothelial cells of the rat SMA show adhesion of leucocytes <i>in vivo</i> and marked leucocyte-induced vasoconstriction <i>in vitro</i> following reperfusion after as little as thirty minutes of ischaemia.