The role of angiogenesis after stroke is unclear; if angiogenesis supports long-term recovery of blood flow, then microvessel hyperdensity consequent to angiogenesis should persist in infarcted cortex. Here, we assess the long-term stability of ischemia-induced microvessels after 2-h transient rat middle cerebral artery occlusion (tMCAo) followed by 30, 90, or 165 days of reperfusion. Stereological measures of microvessel density were taken adjacent to and within cortical cysts. Vascular permeability was documented by extravasation of immunoglobulin (IgG) and of fluorescein-dextran. After 30 days reperfusion, a significantly increased microvessel volume density (V V ) was restricted to the inner margin of cystic infarcts as compared with the region external to the infarct or contralateral control cortex (F = 42.675, P < 0.001). The hyperdense ischemic vasculature was abnormally leaky to IgG and fluorescein-dextran. Between 30 and 90 days of reperfusion, this vessel hyperdensity regressed significantly and then regressed further but less drastically between 90 and 165 days. Phagocytic macrophages were restricted to the infarct and dynamic changes in their number correlated with microvessel regression. Additional ED-1 labeled inflammatory cells were widely distributed inside and external to the infarct, even after 165 days of reperfusion. These data show that ischemia evoked angiogenesis results, at least in part, in transient populations of leaky microvessels and phagocytic macrophages. This suggests that a major role of this angiogenesis is for the removal of necrotic brain tissue.

Intradiscal CFA injection led to chronic disk degeneration with allodynia, which was suggested by pain behavior and expression of pain-related mediators. The increment of CGRP, PGE, and iNOS also suggest pain-related signal processing between the IVD and the neural pathway in this animal model. This animal model may be useful for future research related to the pathophysiology and development of novel treatment for spine-related pain.

Background: Investigating atherosclerosis of the coronary artery in ischemic stroke patients is clinically important because comorbidity is relatively common in such patients. We studied the relationship of atherosclerosis of the coronary artery to atherosclerosis of the intracranial cerebral artery and extracranial carotid artery. Further investigation was performed for determining the factors independently associated with coronary artery atherosclerosis in ischemic stroke patients. Methods: We consecutively recruited ischemic stroke patients who had no history of coronary artery disease, and they underwent vascular examination. Patient-based vascular assessment was performed with magnetic resonance angiography of the cerebral arteries and computed tomography coronary angiography. The factors independently associated with coronary artery stenosis (≧50%) were obtained from the conventional vascular risk factors and cerebral arterial stenosis using the logistic regression model. Results: Coronary artery stenosis was observed in 25.4% of the patients and this was associated with age (OR: 1.16, 95% CI: 1.03–1.30) and the presence of stenosis of the extracranial carotid artery (OR: 11.37, 95% CI: 1.88–68.75) after logistic regression analysis. Intracranial arterial stenosis was not independently related to coronary stenosis. Conclusion: Careful concern about coronary artery disease is needed when treating ischemic stroke patients who have atherosclerosis of the extracranial carotid artery.

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