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Background@# Cerebral blood flow (CBF) has direct effects on neuronal function and neurocognitive disorders. Oxidative stress from abdominal aortic surgery is important in the pathophysiology of CBF impairment. We investigated the effect of edaravone on the pial arteriolar diameter changes induced by abdominal aortic surgery and the involvement of the endothelium in the changes. @*Methods@# The closed cranial window technique was used in rabbits to measure changes in pial arteriolar diameter after the unclamping of abdominal aortic cross-clamping with an intravenous free radical scavenger, edaravone (control group [n = 6], edaravone 10 μg/kg/min [n = 6], 100 μg/kg/min [n = 6]). Pial vasodilatory responses to topical application of acetylcholine (ACh) into the cranial window were investigated before abdominal aortic cross-clamping and after unclamping with intravenous administration of edaravone (control group [n = 6], edaravone 100 μg/kg/min [n = 6]). @*Results@# Aortic unclamping-induced vasoconstriction was significantly attenuated by continuous infusion of edaravone at 100 μg/kg/min. Topical ACh after unclamping did not produce any changes in pial arteriolar responses in comparison to before aortic cross-clamping in the control or edaravone groups. The changes in the response to topical ACh after unclamping in the saline and edaravone groups did not differ significantly. @*Conclusions@#Free radicals during abdominal aortic surgery might have contracted cerebral blood vessels independently of endothelial function in rabbits. Suppression of free radicals attenuated the sustained pial arteriolar vasoconstriction after aortic unclamping. Thus, the free radical scavenger might have some brain protective effect that maintains CBF independently of endothelial function.
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BACKGROUND@#Hypercapnia causes dilation of cerebral vessels and increases cerebral blood flow, resulting in increased intracranial pressure. Sevoflurane is reported to preserve cerebrovascular carbon dioxide reactivity. However, the contribution of inhaled anesthetics to vasodilatory responses to hypercapnia has not been clarified. Moreover, the cerebrovascular response to desflurane under hypercapnia has not been reported. We examined the effects of sevoflurane and desflurane on vasodilatory responses to hypercapnia in rats.@*METHODS@#A closed cranial window preparation was used to measure the changes in pial vessel diameters. To evaluate the cerebrovascular response to hypercapnia and/or inhaled anesthetics, the pial vessel diameters were measured in the following states: without inhaled anesthetics at normocapnia (control values) and hypercapnia, with inhaled end-tidal minimal alveolar concentration (MAC) of 0.5 or 1.0 of either sevoflurane or desflurane at normocapnia, and an MAC of 1.0 of sevoflurane or desflurane at hypercapnia.@*RESULTS@#Under normocapnia, 1.0 MAC, but not 0.5 MAC, of sevoflurane or desflurane dilated the pial arterioles and venules. In addition, under both 1.0 MAC of sevoflurane and 1.0 MAC of desflurane, hypercapnia significantly dilated the pial arterioles and venules in comparison to their diameters without inhaled anesthetics. The degrees of vasodilation were similar for desflurane and sevoflurane under both normocapnia and hypercapnia.@*CONCLUSIONS@#Desflurane induces cerebrovascular responses similar to those of sevoflurane. Desflurane can be used as safely as sevoflurane in neurosurgical anesthesia.
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BACKGROUND: Hypercapnia causes dilation of cerebral vessels and increases cerebral blood flow, resulting in increased intracranial pressure. Sevoflurane is reported to preserve cerebrovascular carbon dioxide reactivity. However, the contribution of inhaled anesthetics to vasodilatory responses to hypercapnia has not been clarified. Moreover, the cerebrovascular response to desflurane under hypercapnia has not been reported. We examined the effects of sevoflurane and desflurane on vasodilatory responses to hypercapnia in rats. METHODS: A closed cranial window preparation was used to measure the changes in pial vessel diameters. To evaluate the cerebrovascular response to hypercapnia and/or inhaled anesthetics, the pial vessel diameters were measured in the following states: without inhaled anesthetics at normocapnia (control values) and hypercapnia, with inhaled end-tidal minimal alveolar concentration (MAC) of 0.5 or 1.0 of either sevoflurane or desflurane at normocapnia, and an MAC of 1.0 of sevoflurane or desflurane at hypercapnia. RESULTS: Under normocapnia, 1.0 MAC, but not 0.5 MAC, of sevoflurane or desflurane dilated the pial arterioles and venules. In addition, under both 1.0 MAC of sevoflurane and 1.0 MAC of desflurane, hypercapnia significantly dilated the pial arterioles and venules in comparison to their diameters without inhaled anesthetics. The degrees of vasodilation were similar for desflurane and sevoflurane under both normocapnia and hypercapnia. CONCLUSIONS: Desflurane induces cerebrovascular responses similar to those of sevoflurane. Desflurane can be used as safely as sevoflurane in neurosurgical anesthesia.
Assuntos
Animais , Ratos , Anestesia , Anestésicos , Arteríolas , Dióxido de Carbono , Circulação Cerebrovascular , Hipercapnia , Pressão Intracraniana , Vasodilatação , VênulasRESUMO
No abstract available.
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OBJECTIVES: Sarcopenia and osteoporosis affects activities of daily living and quality of elderly people. However, little is known about its impact on elderly locomotor diseases, such as osteoporotic vertebral fracture (OVF). There is no report investigating the influence of both sarcopenia and osteoporosis on outcomes of OVF. This study aimed to evaluate the clinical outcomes of OVF in elderly patients from sarcopenic perspectives. METHODS: This prospective study was conducted with 396 patients, aged 65 years or more, hospitalized for the treatment of OVF (mean age, 81.9 ± 7.1 years; 111 males, 285 females). The primary outcome was the Japanese Orthopaedic Association (JOA) score for lumbar disease (at first visit, hospital discharge, and 1 year after treatment) and Barthel index (at the same time and before hospitalization). The second outcome was living place after discharge. Susceptibility to sarcopenia and osteoporosis were evaluated and clinical results of conservative treatment were compared. RESULTS: Sarcopenia significantly affected Barthel index at first visit and discharge. Sarcopenia patients had significantly higher rate for discharge to nursing home and living in nursing home after 1 year than patients without sarcopenia. Osteoporosis significantly affected the JOA score at the first visit and the Barthel index before hospitalization, at the first visit, discharge, and after 1 year. Osteoporosis did not affect the living place at discharge and after 1 year. CONCLUSIONS: Sarcopenia and osteoporosis affected outcomes of conservative treatment for OVF; moreover, sarcopenia affected the living place of OVF patients at discharge and after 1 year.