Affiliations: Departament of Anesthesiology, National Cardiovascular Center, Suita, Osaka 565‐8565, Japan | Department of Vascular Physiology, National Cardiovascular Center, Suita, Osaka 565‐8565, Japan | Clinical Research Institute, China–Japan Friendship Hospital, Beijing 100029, China
Note: [] Corresponding author: H. Niimi, Department of Vascular Physiology, National Cardiovascular Center Research Institute, Suita, Osaka 565‐8565, Japan. E‐mail: niimi@ri.ncvc.go.jp.
Abstract: Cerebral microcirculatory changes in rat with a cardiopulmonary bypass (CPB) at normothermia was investigated in relation to cerebrovascular disorders caused by surgical operation with CPB. The mean arterial pressure was changed from 50 to 200 mmHg by changing the pump flow‐rate. A non‐pulsatile flow model was developed by stopping the cardiac beat using a fibrillator. The pial microcirculation was visualized using fluorescence‐labeled red cells and dextran, and was directly observed under a fluorescence videomicroscope during CPB. Based on the recorded videoimages, the arteriolar diameter and red cell velocity were measured, in which single arterioles with approximately 40 μm diameter were selected among the pial arterioles. It was shown that when the arterial pressure was changed: (1) arteriolar vasodilation or constriction appeared during pulsatile flow but it disappeared during non‐pulsatile flow, and (2) the arteriolar red cell velocity increased or decreased linearly during non‐pulsatile flow as well as pulsatile flow. The flow‐rate was almost constant at a large range of the mean arterial pressure from 60 to 160 mmHg during pulsatile flow (autoregulation), but it increased or decreased during non‐pulsatile flow with an increase or decrease in mean arterial pressure, respectively. It was suggested that pulsativity might be responsible for cerebral autoregulation.
