Reperfusion edema

Nishio et al., 2002 Cats MCAo 1 h, with reperfusion 30.5 and 36.5, intraischemia plus 3 h, with slow or rapid rewarming Somatosensory evoked potentials (SEPs), edema at 5 h reperfusion Edema reduced in hypothermia with slow re warming, recovery of SEPs enhanced with slow rewarming... 

Treatment of Cryptosporidium parvum infection of the GI tract in immunocompromised patients Poshschemic pulmonary reperfusion edema Hepahhs B infection Gaucher s disease... 

Kundu S, Herman SJ, Winton TL (1998) Reperfusion edema after lung transplantation radiographic manifestations. Radiology 206 75-80... 

As discussed above, due to the influence of reperfusion, vasogenic edema develops differently in... 

Kollmar et al., 2002 SD rats MCAo 2 h, with 5 h 33 only during reperfusion CBF, infarct volume, edema at 5 h reperfusion pH-stat reduced infarct volume and edema, increased CBF... 

Kollmar et al., 2002 Wistar rats MCAo 2 h, with reperfusion 33 and 37, started 1 h after reperfusion MRI, neurological function, edema, infarct volume, 1-5 d postischemia Increased survival, improved neurological function, reduced edema, reduced infarct volume... 

The effect of hypothermia on CBF may also be dependent on acid-base management during hypothermic treatment (51,52). Following 2 h of normothermic MCAO and 5 h of hypothermic (33°C) reperfusion, Kollmar et al. (52) showed that pH-stat management significantly decreased cerebral infarct volume and edema, probably by increasing CBF. 

Approximately 25% of patients with TIA have cerebral infarction with transient signs in which DWI positivity corresponds to cytotoxic edema this progresses to permanent parenchymal injury and increased tissue water content visible as a lesion on T2-weighted MRI. Approximately 20% of patients have early DWI abnormality but no evidence of later T2-weighted abnormality. This suggests reversibility of the initial DWI abnormality if blood flow is restored early enough to prevent permanent parenchymal injury, as seen in patients with stroke in whom the DWI-detected lesion may regress with reperfusion. 

It was observed that rats with a transient MCA occlusion have a larger brain infarction when recombinant human IL-1 P is injected into the lateral ventricle immediately after reperfusion [7,41]. Similar results have been obtained in rats with a permanent MCA occlusion [7,42]. The intraventricular injection of recombinant human IL-1 p also enhances the formation of brain edema and increases both the number of neutrophils in ischemic areas and neutrophil-endothelial cell adhesion. The most widely recognized functions of IL-1 appear to be the induction of endothelial cell adhesion molecule expression and the promotion of neutrophil tissue infiltration [7,41]. These observations suggest that IL-1 may play a deleterious role in cerebral ischemia. Studies showing a reduction in infarct size after the administration of IL-1 antagonists or inhibitors provide further evidence of the importance of IL-1 in cerebral ischemia [41,43-49]. The possible harmful mechanisms induced or activated by IL-1 include fever, increased heart rate and arterial blood pressure, enhancement of N-methyl-D-aspartate-mediated injury, proliferation of microglia, release of arachidonic acid, and stimulation of NO synthesis [7,50]. 

Measurement of hemodynamic parameters by catheterization. Acute or chronic effects of ischemia/reperfusion or ischemia alone can be studied. The contribution of blood components and neurohormonal changes is considered. Experimental model close to clinical conditions but many confounding factors may be involved when investigating mechanisms. Arrthythmias, hypotension or pulmonary edema can occur during the experimental procedure. 

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