Reperfusion injury following cerebral ischemia: pathophysiology, MR imaging, and potential therapies

INTRODUCTION: Restoration of blood flow following ischemic stroke can be achieved by means of thrombolysis or mechanical recanalization. However, for some patients, reperfusion may exacerbate the injury initially caused by ischemia, producing a so-called “cerebral reperfusion injury”. Multiple pathological processes are involved in this injury, including leukocyte infiltration, platelet and complement activation, postischemic hyperperfusion, and breakdown of the blood–brain barrier. METHODS/RESULTS AND CONCLUSIONS: Magnetic resonance imaging (MRI) can provide extensive information on this process of injury, and may have a role in the future in stratifying patients’ risk for reperfusion injury following recanalization. Moreover, different MRI modalities can be used to investigate the various mechanisms of reperfusion injury. Antileukocyte antibodies, brain cooling and conditioned blood reperfusion are potential therapeutic strategies for lessening or eliminating reperfusion injury, and interventionalists may play a role in the future in using some of these therapies in combination with thrombolysis or embolectomy. The present review summarizes the mechanisms of reperfusion injury and focuses on the way each of those mechanisms can be evaluated by different MRI modalities. The potential therapeutic strategies are also discussed

A prolonged interval between deep intestinal ischemia and anastomotic construction does not impair wound strength in the rat.

Contains fulltext : 51827.pdf (publisher's version ) (Closed access)INTRODUCTION: Transient intestinal ischemia can reduce anastomotic strength, which poses an increased risk of complications. The objective of this study is to establish if a prolonged interval between profound ischemia and construction of an anastomosis affects anastomotic strength. METHODS: Male Wistar rats were used: in experimental groups, profound mesenteric ischemia was induced by clamping both superior mesenteric artery and more distal arteries in the ileal mesentery. Resection and anastomosis in ileum and colon were performed immediately (IR0) or 24 h after releasing the clamps (IR24). In controls (C0 and C24), arteries were not clamped. After 5 days, anastomotic bursting pressure (BP), breaking strength (BS), and hydroxyproline were measured, and histological analysis was performed. RESULTS: Mortality and anastomotic dehiscence rates were significantly higher in IR0 compared to C0. In ileum, the BS was 34% lower (p<0.05) in IR0 compared to C0, while there were no significant differences in BS or BP between the IR24 and C24 groups. In colon anastomoses, although no differences in BS and BP were found, bursting site was at the anastomosis in 82% in group IR0 vs 30% in group C0, reflecting reduced anastomotic strength in the former. Again, after 24 h, there were no differences between IR and C group. Hydroxyproline and histology were not different between groups. CONCLUSIONS: Extending the interval between transient deep intestinal ischemia and construction of an anastomosis does not impair wound strength