プロポフォール鎮静下のブタにおけるデクスメデトミジンの鎮静効果、血行動態の評価

This study examined the sedative effect of, and hemodynamic response to dexmedetomidine administration in propofol-sedated swine. Sixteen swine were subjects. After anesthetic induction and preparation, the propofol infusion rate was adjusted to maintain a bispectral index (BIS) value between 55 and 65 (i.e., baseline). With the propofol infusion rate fixed at the baseline rate, dexmedetomidine was infused continuously at a rate of 0.2, 0.4, and 0.7 μg・kg -1・h-1 for one hour at each rate. The BIS value and hemodynamic parameters were recorded at each step. Dexmedetomidine decreased the BIS value, mean arterial blood pressure, heart rate, cardiac output, and mixed venous oxygen saturation in a dose-dependent manner. The systemic vascular resistance (SVR) did not change, but the pulmonary vascular resistance (PVR) increased. Oxygen delivery (DO2) and oxygen consumption (VO2) decreased. A small dose of dexmedetomidine (0.2 μg・kg-1・h-1) greatly enhanced the sedative effects of propofol with only small changes in hemodynamics and systemic oxygen balance, suggesting it may be useful in reducing the propofol dose requirement. However, dexmedetomidine 0.4 μg・kg-1・h-1 suppressed cardiac contractility, and 0.7 μg・kg-1・h-1 induced hemodynamic instability and further systemic oxygen imbalance while the additional sedative effect was limited. A lower dose of dexmedetomidine may be recommended when using it in combination with propofol

Tau imaging detects distinctive distribution of tau pathology in ALS/PDC on the Kii Peninsula

OBJECTIVE: To characterize the distribution of tau pathology in patients with amyotrophic lateral sclerosis/parkinsonism dementia complex on the Kii Peninsula (Kii ALS/PDC) by tau PET using [11C]PBB3 as ligand.METHODS: This is a cross-sectional study of 5 patients with ALS/PDC and one asymptomatic participant with a dense family history of ALS/PDC from the Kii Peninsula who took part in this study. All were men, and their age was 76 ± 8 (mean ± SD) years. Thirteen healthy men (69 ± 6 years) participated as healthy controls (HCs). Dynamic PET scans were performed following injection of [11C]PBB3, and parametric PET images were generated by voxel-by-voxel calculation of binding potential (BP* ND) using a multilinear reference tissue model. [11C] Pittsburgh compound B (PiB) PET, MRI, and cognitive tests were also performed.RESULTS: A voxel-based comparison of [11C]PBB3 BP* ND illustrated PET-detectable tau deposition in the cerebral cortex and white matter, and pontine basis including the corticospinal tract in Kii ALS/PDC patients compared with HCs (uncorrected p < 0.05). Group-wise volume of interest analysis of [11C]PBB3 BP* ND images showed increased BP* ND in the hippocampus and in frontal and parietal white matters of Kii ALS/PDC patients relative to HCs (p < 0.05, Holm-Sidak multiple comparisons test). BP* ND in frontal, temporal, and parietal gray matters correlated with Mini-Mental State Examination scores in Kii ALS/PDC patients (p < 0.05). All Kii ALS/PDC patients were negative for [11C]PiB (β-amyloid) except one with marginal positivity.CONCLUSION: [11C]PBB3 PET visualized the characteristic topography of tau pathology in Kii ALS/PDC, corresponding to clinical phenotypes of this disease

Data from: Tau imaging detects distinctive distribution of tau pathology in ALS/PDC on the Kii Peninsula

OBJECTIVE: To characterize the distribution of tau pathology in patients with amyotrophic lateral sclerosis/parkinsonism-dementia complex on the Kii Peninsula (Kii ALS/PDC) by tau PET using [11C]PBB3 as ligand. METHODS: This is a cross-sectional study of five patients with ALS/PDC and one asymptomatic participant with a dense family history of ALS/PDC from the Kii Peninsula who took part in this study. All were men, and their age was 76 ± 8 (mean ± SD) years. Thirteen healthy men (69 ± 6 years) participated as healthy controls (HCs). Dynamic PET scans were performed following injection of [11C]PBB3, and parametric PET images were generated by voxel-by-voxel calculation of binding potential (BPND) using a multilinear reference tissue model. [11C]PiB PET, MRI, and cognitive tests were also performed. RESULTS: A voxel-based comparison of [11C]PBB3 BPND illustrated PET-detectable tau deposition in the cerebral cortex and white matter, and pontine basis including the corticospinal tract in Kii ALS/PDC patients compared with HCs (uncorrected p < 0.05). Group-wise VOI analysis of [11C]PBB3 BPND images showed increased BPND in the hippocampus and in frontal and parietal white matters of Kii ALS/PDC patients relative to HCs (p < 0.05, Holm-Sidak multiple comparisons test). BPND in frontal, temporal, and parietal gray matters correlated with Mini-Mental State Examination scores in Kii ALS/PDC subjects (p < 0.05). All Kii ALS/PDC patients were negative for [11C]PiB (amyloid β) except one with marginal positivity. CONCLUSION: [11C]PBB3 PET visualized the characteristic topography of tau pathology in Kii ALS/PDC, corresponding to clinical phenotypes of this disease