Hydrocephalus Following Experimental Subarachnoid Hemorrhage in Rats with Different Aerobic Capacity

Int J Mol Sci. 2021 Apr 26;22(9):4489. doi: 10.3390/ijms22094489.

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.

Keywords: CD163; early brain injury; hemeoxgenase-1; hydrocephalus; rat; subarachnoid hemorrhage.

MeSH terms

  • Animals
  • Antigens, CD / metabolism
  • Antigens, Differentiation, Myelomonocytic / metabolism
  • Brain / metabolism
  • Disease Models, Animal
  • Heme Oxygenase-1 / metabolism
  • Hydrocephalus / metabolism*
  • Magnetic Resonance Imaging
  • Oxidative Stress*
  • Rats
  • Receptors, Cell Surface / metabolism
  • Running / physiology*
  • Stroke / complications
  • Subarachnoid Hemorrhage / complications*

Substances

  • Antigens, CD
  • Antigens, Differentiation, Myelomonocytic
  • CD163 antigen
  • Receptors, Cell Surface
  • Heme Oxygenase-1