Previous studies have shown that neonatal shaking brain injury (SBI) causes transient microhemorrhages (MHs) in the gray matter of the cerebral cortex and hippocampus. Iron deposits and iron-uptake cells are observed surrounding MHs in this SBI model, suggesting local hypoxic-ischemic conditions. However, whether the shaken pups suffered systemic hypoxic-ischemic conditions has remained uncertain. Further, histopathological correlations of MHs on magnetic resonance imaging (MRI) are still unclear. The present study examined MHs after neonatal SBI using a combination of histochemical and susceptibility-weighted imaging (SWI) analyses. Systemic oxygen saturation analyses indicated no significant difference between shaken and non-shaken pups. MHs on postnatal day 4 (P4) pups showed decreased signal intensity on SWI. Iron histochemistry revealed that these hypointense areas almost completely comprised red blood cells (RBCs). MHs that appeared on P4 gradually disappeared by P7–12 on SWI. These resolved areas contained small numbers of RBCs, numerous iron-positive cells, and punctate regions with iron reaction products. Perivascular iron products were evident after P12. These changes progressed faster in the hippocampus than in cortical areas. These changes in MHs following neonatal SBI may provide new insights into microvascular pathologies and impacts on brain functions as adults.

先前的研究表明，新生儿摇动性脑损伤（SBI）会在大脑皮层和海马的灰质中引起短暂的微出血（MHs）。在此SBI模型中，在MH周围观察到铁沉积物和铁摄取细胞，表明存在局部缺氧缺血性疾病。但是，摇动的幼犬是否患有全身性缺氧缺血性疾病仍不确定。此外，磁共振成像（MRI）上MH的组织病理学相关性仍不清楚。本研究使用组织化学和药敏加权成像（SWI）分析的组合检查了新生儿SBI后的MH。全身血氧饱和度分析表明，摇动和不摇动的幼仔之间没有显着差异。产后第4天（P4）幼崽的MH在SWI上显示信号强度降低。铁组织化学显示，这些低血脂区域几乎完全包含红细胞（RBC）。在P4上出现的MH在SWI上的P7-12逐渐消失了。这些分辨的区域包含少量的红细胞，大量的铁阳性细胞和带有铁反应产物的点状区域。P12后明显出现血管周铁产物。这些变化在海马中的进展快于在皮质区域。新生儿SBI后MH的这些变化可能为微血管病理学及其对成年后脑功能的影响提供新的见解。P12后明显的血管周铁产物。这些变化在海马中的进展快于在皮质区域。新生儿SBI后MH的这些变化可能为微血管病理学及其对成年后脑功能的影响提供新的见解。P12后明显的血管周铁产物。这些变化在海马中的进展快于在皮质区域。新生儿SBI后MH的这些变化可能为微血管病理学及其对成年后脑功能的影响提供新见解。