In a rat model of stroke, the spatio-temporal distribution of α-smooth muscle actin-positive, (αSMA+) cells was investigated in the infarcted hemisphere (ipsilateral) and compared with the contralateral hemisphere. At day 3 postischemia, αSMA+ cells were concentrated in two main loci within the ipsilateral hemisphere (Area A) in the medial corpus callosum and (Area B) midway through the striatum adjacent to the lateral ventricle. By day 7 and further by day 14, fewer αSMA+ cells remained in Areas A and B but a steady increase in the peri-infarct was observed. αSMA+ cells also expressed glial acidic fibrillary protein [GFAP: αSMA+/GFAP+ (29%); αSMA+/GFAP- (71%) phenotypes] and feline leukemia virus C receptor 2 (FLVCR2), but not ED1(microglia) and established markers of pericytes normally located in vascular wall. αSMA+ cells were also located close to the subventricular zones (SVZ) adjacent to Areas A and B. In conclusion, αSMA+ cells have been identified in a spatial and temporal sequence from the SVZ, at intermediate loci and in the vicinity of the peri-infarct. It is hypothesized that novel populations of αSMA+ precursors of pericytes are born on the SVZ, migrate into the peri-infarct region and are incorporated into new vessels of the peri-infarct regions.

Introduction: Sleep disordered breathing (SDB) in adults is an independent risk factor for coronary artery disease and stroke. Altered platelet reactivity, endothelial dysfunction and inflammation in adults with SDB are known to contribute to the pathogenesis of its cardiovascular complications. Sleep disordered breathing also occurs in children; however little is known about these parameters in non-obese children with SDB. Therefore, this study investigated platelet aggregation, inflammation and endothelial function in children with SDB and healthy matched controls. Methods: Clinical evaluation of SDB was performed on 19 children aged 5-16 years through polysomnography (n = 12 were clinically diagnosed with SDB, n = 7 were controls). Venous blood samples were collected and analysed for measurements of platelet aggregation and inflammation. Platelet aggregation was assessed by the Multiplate analyzer. Inflammation was assessed by intracellular cytokine analysis of T cell by flow cytometry. Plasma asymmetric dimethylarginine (ADMA), a marker of endothelial function, was also quantified. Results: Platelet aggregation was significantly increased in SDB subjects compared to controls (56.7 ± 16.8 aggregation units (AU) vs. 38.3 ± 4.0 AU, p < 0.05). There was a significant increase in inflammation measured by Tcell interferon (IFN)-gamma (SDB 52 ± 4% vs controls 25 ± 3% positive cells, P < 0.005) and tumour necrosis factor (TNF)-alpha (SDB 39 ± 4% vs controls 20 ± 2% positive cells, P < 0.005) in SDB children compared with controls. Children with SDB also exhibited higher ADMA levels (0.43 ± 0.5 vs controls 0.35 ± 0.08 mol/l, p < 0.05). Conclusion: Sleep disordered breathing in children is associated with enhanced platelet aggregation, endothelial dysfunction and inflammatory responses. These parameters may contribute to an increased cardiovascular risk for children with SDB.