2000 Fiscal Year Final Research Report Summary
Effect of inhalatonal anesthetic on cerebral microcirculation : rheological analyses with intravital fluorescence microscopy
| Project/Area Number |
11671498
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Anesthesiology/Resuscitation studies
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| Research Institution | Tottori University (2000)
Shimane Medical University (1999) |
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Principal Investigator |
NAKAJIMA Toshito Tottori University, Faculty of Medicine, Lecturer, 医学部・附属病院, 講師 (00284050)
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| Co-Investigator(Kenkyū-buntansha) |
NIIMI Hideyuki Natinal Cardiovascular Venter, Cascular Physiology, Director, 脈管生理部, 部長(研究職) (50026134)
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| Project Period (FY) |
1999 – 2000
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| Keywords | intravital fluorescence microscopy / pial microcirculation / halothane / microvasodilation / pressure-autoregulation / shear-stress / cell-free layer / flow-dependent factors |
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| Research Abstract |
Halothane has been shown to increase cerebral blood flow, inducing the impairment of cerebral autoregulation. These may result from microvasodilation, but very few study has been done from the level of microcirculation. These investigations were undertaken to examine microcirculatory hemodynamic changes in the pial microvasculature of cat parietal cortex during halothane anesthesia, based on intravital microscopic observation. In addition, microvasodilatory responses were analyzed with some rheological factors such as shear stress, wall tension, and cell-free layer.
The present analysis in vivo data showed :
(1)When a vasodilatory(on autoregulatory)response is intact in single microvessels, the flowrate might be increased or maintained in spite of decreases in MAP and RBC-velocity. In contrast. if the microvasodilation is suppressed, it appears to be insufficient in vasodilatory response to reduced blood pressure. Autoregulation of cerebral microcirculation was impaired by inhaled halothane, resulting, in part, from microvasculan insufficiency in vasodilatory response to reduced arterial pressure.
(2)Two factors may be attributed to such a microvasodilation "during halothane inhalation", that is, (a) myogenic response to hypotension and(b)direct neurogenic effect of halothane. However, the vasodilation with the percentage reversal increase in the shear rate "after the discontinuation of halothane inhalation" may exclusively refer to flow-velocity dependent vasodilation. The impairment of pressure-autoregulation("pressure sensitive" myogenic mechanism)by halothane anesthesia may be related to intensified flow-dependent("shear stress sensitive")mechanism.
(3)The cell-free layer thickness increased with a decrease in the PSR or wall shear stress. The thinning of cell free layer occurs with increasing shear rate which may have rheological importance in manipulating flow shear stress experienced by inner vascular wall.
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