BackgroundGlobal brain ischemia-reperfusion during propofol anesthesia provokes persistent cerebral pial constriction. Constriction is likely mediated by Rho-kinase. Cerebral vasoconstriction possibly exacerbates ischemic brain injury. Because Y-27632 is a potent Rho-kinase inhibitor, it should be necessary to evaluate its effects on cerebral pial vessels during ischemia—reperfusion period. We therefore tested the hypotheses that Y-27632 dilates cerebral pial arterioles after the ischemia-reperfusion injury, and evaluated the time-course of cerebral pial arteriolar status after the ischemia-reperfusion.MethodsJapanese white rabbits were anesthetized with propofol, and a closed cranial window inserted over the left hemisphere. Global brain ischemia was produced by clamping the brachiocephalic, left common carotid, and left subclavian arteries for 15 min. Rabbits were assigned to cranial window perfusion with: (1) artificial cerebrospinal fluid (Control group, n = 7); (2) topical infusion of Y-27632 10−6 mol · L−1 for 30 min before the initiation of global brain ischemia (Pre group, n = 7); (3) topical infusion of Y-27632 10−6 mol · L−1 starting 30 min before ischemia and continuing throughout the study period (Continuous group, n = 7); and, (4) topical infusion of Y-27632 10−6 mol · L−1 starting 10 min after the ischemia and continuing until the end of the study (Post group, n = 7). Cerebral pial arterial and venule diameters were recorded 30 min before ischemia, just before arterial clamping, 10 min after clamping, and 5, 10, 20, 40, 60, 80, 100, and 120 min after unclamping.ResultsMean arterial blood pressure and blood glucose concentration increased significantly after global brain ischemia except in the Continuous group. In the Pre and Continuous groups, topical application of Y-27632 produced dilation of large (mean 18–19%) and small (mean; 25–29%) pial arteries, without apparent effect on venules. Compared with the Control and Pre groups, arterioles were significantly dilated during the reperfusion period in the Continuous and Post groups (mean at 120 min: 5–8% in large arterioles and 11–12% in small arterioles).ConclusionsY-27632 dilated cerebral pial arterioles during reperfusion. Y-27632 may enhance recovery from ischemia by preventing arteriolar vasoconstriction during reperfusion.

SummaryWe measured the effect of Patent Blue dye on oxyhaemoglobin saturations after injection into breast tissue: 40 women had anaesthesia for breast surgery maintained with sevoflurane or propofol (20 randomly allocated to each). Saturations were recorded with a digital pulse oximeter, in arterial blood samples and with a cerebral tissue oximeter before dye injection and 10, 20, 30, 40, 50, 60, 75, 90, 105 and 120 min afterwards. Patent Blue did not decrease arterial blood oxyhaemoglobin saturation, but it did reduce mean (SD) digital and cerebral oxyhaemoglobin saturations by 1.1 (1.1) % and 6.8 (7.0) %, p < 0.0001 for both. The falsely reduced oximeter readings persisted for at least 2 h. The mean (SD) intra-operative digital pulse oxyhaemoglobin readings were lower with sevoflurane than propofol, 97.8 (1.2) % and 98.8 (1.0) %, respectively, p < 0

Japan Primary Registries Network (JPRN); UMIN-CTR ID; UMIN000010640.

BackgroundAlthough sevoflurane and propofol are commonly used anesthetics in rabbits, optimal doses of remain unclear. We thus assessed the optimal hypnotic doses of sevoflurane and propofol, and evaluated the influence of dexmedetomidine on sevoflurane and propofol requirements.MethodsTwenty-eight Japanese white rabbits were randomly assigned to one of four groups (n = 7 each). Rabbits were given either sevoflurane, propofol, sevoflurane + dexmedetomidine, or propofol + dexmedetomidine (injected 30 μg∙kg-1∙hr-1 for 10 min followed by an infusion of 3.5 μg∙kg-1∙hr-1). Hypnotic level was evaluated with Bispectral Index (BIS), a well-validated electroenchalographic measure, with values between 40 and 60 representing optimal hypnosis. BIS measurements were made 10 minutes after the adjustment of target end-tidal sevoflurane concentration in the sevoflurane group and sevoflurane + dexmedetomidine group, and at 10 min after the change of infusion rate in the propofol group and propofol + dexmedetomidine group.ResultsBIS values were linearly related to sevoflurane concentration and propofol infusion rate, with or without dexmedetomidine. Sevoflurane concentration at BIS = 50 was 3.9 ± 0.2% in the sevoflurane group and 2.6 ± 0.3% in the sevoflurane + dexmedetomidine group. The propofol infusion rate to make BIS = 50 was 102 ± 5 mg∙kg-1∙hr-1 in the propofol group, and 90 ± 10 mg∙kg-1∙hr-1 in the propofol + dexmedetomidine group.ConclusionsThe optimal end-tidal concentration of sevoflurane alone was thus 3.9%, and optimal infusion rate for propofol alone was 102 mg∙kg-1∙hr-1. Dexmedetomidine reduced sevoflurane requirement by 33% and propofol requirement by 11%.

Background: Although recent studies using experimental models of ischemic brain injury indicate that systemically-administered β 1 -blockers have potential protective effects on the cerebrovascular system, the precise mechanisms remain unclear. In addition to their cardiovascular effects, water-soluble β 1 -blockers can pass the blood-brain barrier and may exert their vascular action on cerebral microvessels. The aim of this study was to investigate the direct effects of β 1 -blockade on the cerebral microvasculature both in the normal state and ischemia/reperfusion state using the cranial window method. Methods: The closed cranial window method was used to visualize the cerebral microcirculation and changes in the pial arteriole diameter in adult male rabbits. In the first experiment, various concentrations of the selective β 1blocker landiolol were administered into the cranial window to evaluate the dose-response. In the second experiment, the effect of β 1 -blockade on the brain during ischemic/reperfusion injury was investigated. Global brain ischemia/reperfusion was induced by clamping the brachiocephalic, left common carotid, and left subclavian arteries for 15 min. Either landiolol or artificial cerebrospinal fluid was infused 5 min after initiation of ischemia through 120 min after reperfusion. Pial arteriole diameter and hemodynamic and physiological parameters were recorded before ischemia, during ischemia, and 5, 10, 20, 40, 60, 80, 100, and 120 min after reperfusion. Results: In the first experiment, topical administration of landiolol at higher concentrations produced slight pial arteriole dilation (10 − 8 mol/L: 4.3 ± 3.4%, 10 − 6 mol/L: 8.0 ± 5.8%, 10 − 4 mol/L: 7.3 ± 4.0%). In the second experiment, the topical administration of landiolol significantly dilated the pial arteriole diameters during ischemia/reperfusion injury (ischemia: 30.6 ± 38.6%, 5 min: 47.3 ± 42.2%, 10 min: 47.8 ± 34.2%, 20 min: 38.0 ± 39.0%). There were no statistical differences in hemodynamic and physiological parameters between the landiolol and control groups. Conclusions: The blockade of β 1 -adrenergic receptors induced significant vasodilation of pial arterioles during ischemia/reperfusion injury. By contrast, only a slight dilation of the arterioles was observed in the normal state, indicating that ischemic cerebral microvessels are more susceptible to the vasodilatory effect induced by selective blockade of β 1 -adrenergic receptors than normal microvessels.