title: [The study on the mechanism of brain damage due to high flow and pressure during selective cerebral perfusion].
abstract: It has been reported that the high flow and pressure perfusion produced the brain damage during selective cerebral perfusion. This time we studied the mechanism of this brain damage with mock circulation. We made the mock circulation system of brain with the hard shell reservoir as cranium, and with the triple soft bags as brain tissue, involving into reservoir. We designed the control group that intracranial pressure (ICP) was 0 mmHg at pump off, and the increasing intracranial pressure (IICP) group that ICP was 10 mmHg at pump off. We measured the flow-pressure relationship in the control and IICP group, and then stenosis in outflow. In results, the flow and pressure in both the inflow and outflow side increased significantly (p < 0.001) in control groups, as pump flow increased. The changes of the flow and pressure in IICP group showed a same tendency to the control group. Moreover, both the inflow volume into bag and the outflow volume from bag decreased as pump flow increased stepwisely. The pressure in both inflow and outflow side increased significantly and the volume of the inflow side in IICP group showed a tendency to decrease, compared with the control. The stenosis in the outflow side produced the significant increase in the pressure of both inflow and outflow side, and intracranium, with the same pump flow as the control without stenosis. In conclusion, the high flow perfusion produced the increase of the several pressure in intracranial and extracranial vessels. Moreover, the high flow perfusion produced the decrease of the intracranial blood volume cerebral blood flow. The high flow perfusion does not necessarily contribute to the cerebral tissue perfusion. The stenosis at the side of venous return produced relative high perfusion. This result suggests that the venous return should be taken care of during the selective cerebral perfusion.
authors.affiliation: Second Department of Surgery, Niigata University School of Medicine, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Moro
authors.forename: H
authors.initials: H
authors.lastname: Okazaki
authors.forename: H
authors.initials: H
authors.lastname: Ozeki
authors.forename: M
authors.initials: M
authors.lastname: Sogawa
authors.forename: M
authors.initials: M
authors.lastname: Haga
authors.forename: A
authors.initials: A
authors.lastname: Saito
authors.forename: J
authors.initials: J
authors.lastname: Hayashi
authors.forename: H
authors.initials: H
authors.lastname: Miyamura
authors.forename: S
authors.initials: S
authors.lastname: Eguchi
mesh_terms: D001794:Blood Pressure; D001927:Brain Diseases / Q000209:etiology*; D002560:Cerebrovascular Circulation; D007427:Intracranial Pressure; D008955:Models, Cardiovascular; D010477:Perfusion / Q000009:adverse effects*; D014690:Venous Pressure