Hydrocephalus Following Experimental Subarachnoid Hemorrhage in Rats with Different Aerobic Capacity |
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Authors: | Yasunori Toyota Hajime Shishido Fenghui Ye Lauren G Koch Steven L Britton Hugh J L Garton Richard F Keep Guohua Xi Ya Hua |
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Affiliation: | 1.Department of Neurosurgery, University of Michigan, Ann Arbor, MI 48109, USA; (Y.T.); (H.S.); (F.Y.); (H.J.L.G.); (R.F.K.); (G.X.);2.Department of Physiology & Pharmacology, University of Toledo College of Medicine & Life Sciences, Toledo, OH 43614, USA;3.Department of Anesthesiology, University of Michigan, Ann Arbor, MI 48109, USA; |
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Abstract: | Low aerobic capacity is considered to be a risk factor for stroke, while the mechanisms underlying the phenomenon are still unclear. The current study looked into the impacts of different aerobic capacities on early brain injury in a subarachnoid hemorrhage (SAH) model using rats bred for high and low aerobic capacity (high-capacity runners, HCR; low-capacity runners, LCR). SAH was modeled with endovascular perforation in HCR and LCR rats. Twenty-four hours after SAH, the rats underwent behavioral testing and MRI, and were then euthanized. The brains were used to investigate ventricular wall damage, blood–brain barrier breakdown, oxidative stress, and hemoglobin scavenging. The LCR rats had worse SAH grades (p < 0.01), ventricular dilatation (p < 0.01), ventricular wall damage (p < 0.01), and behavioral scores (p < 0.01). The periventricular expression of HO-1 and CD163 was significantly increased in LCR rats (p < 0.01 each). CD163-positive cells were co-localized with HO-1-positive cells. The LCR rats had greater early brain injuries than HCR rats. The LCR rats had more serious SAH and extensive ventricular wall damage that evolved more frequently into hydrocephalus. This may reflect changes in iron handling and neuroinflammation. |
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Keywords: | subarachnoid hemorrhage early brain injury hydrocephalus hemeoxgenase-1 CD163 rat |
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