Cortical microcirculatory disturbance in the super acute phase of subarachnoid hemorrhage - In vivo analysis using two-photon laser scanning microscopy

• Published in: Journal of the neurological sciences 2016-09, Vol.368, p.326-333
• Main Authors: Ishikawa, Mami, Kajimura, Mayumi, Morikawa, Takayuki, Tsukada, Kosuke, Tsuji, Toshiyuki, Kusaka, Gen, Tanaka, Yuichi, Suematsu, Makoto
• Format: Article
• Language: English
• Subjects: Analysis of Variance; Animals; Astrocytes - metabolism; Cerebral Cortex - blood supply; Cerebral Cortex - diagnostic imaging; Cerebral Cortex - pathology; Cerebrovascular Circulation - physiology; Disease Models, Animal; Green Fluorescent Proteins - genetics; Green Fluorescent Proteins - metabolism; Imaging, Three-Dimensional; Ischemia; Male; Mice; Mice, Transgenic; Microcirculation; Microscopy, Confocal; Neurology; Neurovascular function; Subarachnoid hemorrhage; Subarachnoid Hemorrhage - diagnostic imaging; Subarachnoid Hemorrhage - pathology; Time Factors; Vasodilation
• ISSN: 0022-510X; 1878-5883
• DOI: 10.1016/j.jns.2016.06.067

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 60 min 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 60 min 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.