Mami Ishikawa1, Mayumi Kajimura2, Takayuki Morikawa3, Kosuke Tsukada4, Toshiyuki Tsuji2, Gen Kusaka5, Yuichi Tanaka5, Makoto Suematsu2. 1. Department of Neurosurgery, Saitama Medical Center, Jichi Medical University, Japan; Department of Biochemistry School of Medicine, Keio University, Japan. Electronic address: m.ishikawa@jichi.ac.jp. 2. Department of Biochemistry School of Medicine, Keio University, Japan. 3. Department of Biochemistry School of Medicine, Keio University, Japan; Department of Stem Cell Biology, Research Institute, National Center for Global Health and Medicine, Japan. 4. Graduate School of Science and Technology, Keio University, Japan. 5. Department of Neurosurgery, Saitama Medical Center, Jichi Medical University, Japan.
Abstract
OBJECTIVE: Subarachnoid hemorrhage (SAH) causes cerebral ischemia and drastically worsens the clinical status at onset. However, the arterial flow is surprisingly well maintained on the cerebral surface. We investigated cortical microcirculatory changes in the super acute phase of SAH using two-photon laser scanning microscopy (TPLSM). METHODS: SAH was induced at the skull base in 10 mice using a prone endovascular perforation model. Before SAH, and 1, 2, 5, 10, 20, 30 and 60min after SAH, the cortical microcirculation was observed with TPLSM through a cranial window. Diameters of penetrating and precapillary arterioles were measured and red blood cell (RBC) velocities in precapillary arterioles were analyzed using a line-scan method after administration of Q-dot 655 nanocrystals. RESULTS: One minute after SAH, RBC velocity and flow in precapillary arterioles drastically decreased to <20% of the pre-SAH values, while penetrating and precapillary arterioles dilated significantly. Subsequently, the arterioles either dilated or constricted inconsistently for 60min with continual decreases in RBC velocity and flow in the arterioles, suggesting neurovascular dysfunction. CONCLUSION: SAH caused sudden worsening of the cortical arteriolar velocity and flow at onset. The neurovascular unit cannot function sufficiently to maintain cortical microcirculatory flow in the super acute phase of SAH.
OBJECTIVE:Subarachnoid hemorrhage (SAH) causes cerebral ischemia and drastically worsens the clinical status at onset. However, the arterial flow is surprisingly well maintained on the cerebral surface. We investigated cortical microcirculatory changes in the super acute phase of SAH using two-photon laser scanning microscopy (TPLSM). METHODS:SAH was induced at the skull base in 10 mice using a prone endovascular perforation model. Before SAH, and 1, 2, 5, 10, 20, 30 and 60min after SAH, the cortical microcirculation was observed with TPLSM through a cranial window. Diameters of penetrating and precapillary arterioles were measured and red blood cell (RBC) velocities in precapillary arterioles were analyzed using a line-scan method after administration of Q-dot 655 nanocrystals. RESULTS: One minute after SAH, RBC velocity and flow in precapillary arterioles drastically decreased to <20% of the pre-SAH values, while penetrating and precapillary arterioles dilated significantly. Subsequently, the arterioles either dilated or constricted inconsistently for 60min with continual decreases in RBC velocity and flow in the arterioles, suggesting neurovascular dysfunction. CONCLUSION:SAH caused sudden worsening of the cortical arteriolar velocity and flow at onset. The neurovascular unit cannot function sufficiently to maintain cortical microcirculatory flow in the super acute phase of SAH.