Cerebral Pial Vascular Changes Under Propofol or Sevoflurane Anesthesia During Global Cerebral Ischemia and Reperfusion in Rabbits

Ishiyama, Tadahiko; Shibuya, Kazuhiro; Ichikawa, Manabu; Masamune, Taishi; Kiuchi, Riko; Sessler, Daniel I.; Matsukawa, Takashi

doi:10.1097/ana.0b013e3181cd318b

Cited by 15 publications

(25 citation statements)

References 17 publications

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“…i levels through NMDA receptors and reduce glutamate-induced injury which contributed to neuroprotection, but ketamine and propofol-induced neuroprotection showed opposite dose-dependent relationship in this study. Ketamine, unlike propofol, predominantly inhibits excitatory neurotransmission at glutamatergic synapse, increases cerebral metabolic rate for O 2 (CMRO 2 ), cerebral blood flow (CBF) and intracranial pressure (ICP), but propofol has significant effects on c-aminobutyric acid (GABA A ) receptors and decreases CBF and CMRO 2 , and mitigates ICP [4]. Therefore, it is feasible to assume that each agent enhance its inherent effect on cerebral ischemic injury with concentrations increasing.…”

Section: Discussionmentioning

confidence: 98%

“…Propofol (2,6-diisopropylphenol) and ketamine (phenylcyclohexyl-piperidine) are established nonbarbiturate anesthetic agents, commonly used in the clinical practices. Propofol is considered to be a neuroprotective agent against cerebral ischemia based on the assumption that it has the ability to decrease cerebral blood flow (CBF) in conjunction with a reduction of cerebral metabolic rate for O 2 (CMRO 2 ) and intracranial pressure (ICP) [1][2][3][4]. Recent studies showed that propofol improves neurological outcome and decreases infarct size in animal models of cerebral ischemia [5,6].…”

Section: Introductionmentioning

confidence: 99%

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Inhibition of Neuron-Specific CREB Dephosphorylation is Involved in Propofol and Ketamine-Induced Neuroprotection Against Cerebral Ischemic Injuries of Mice

Luo-wa

Han

et al. 2011

Neurochem Res

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Propofol and ketamine may provide certain degree of neuroprotection, but the underlying mechanism remains unclear to date. The cAMP response element-binding protein (CREB) was proposed that its phosphorylation at Ser133 (P-CREB) constituted a convergence point involved in neuroprotection. The purpose of this study was to determine whether different dosages of propofol and ketamine could provide neuroprotection against permanent middle cerebral artery occlusion (MCAO)-induced ischemic injuries and the involvement of P-CREB. Eighty adult male BALB/c mice that underwent 6 h MCAO were randomly divided into eight groups: Sham-operation; MCAO + saline; MCAO + 25, 50, 100 mg/kg propofol; and MCAO + 25, 50, 100 mg/kg ketamine (intraperitoneal injection 30 min following MCAO). We found that 50, 100 (not 25) mg/kg propofol, and 25 (not 50 and 100) mg/kg ketamine could significantly reduce the infarct volume, edema ratio and neurological deficit (n = 10 per group) as well as inhibit the decrease of P-CREB level in peri-infarct region when compared with that of MCAO + saline group (n = 6 per group). In addition, the results of double-labeled immunofluorescent staining showed that P-CREB co-localized with neuron-specific marker, NeuN, in the peri-infarct region of 50 mg/kg propofol and 25 mg/kg ketamine treated 6 h MCAO mice (n = 4 per group). These results suggested that inhibition of neuron-specific P-CREB dephosphorylation in the peri-infarct region is involved in high dose propofol and low dose ketamine-induced neuroprotection of 6 h MCAO mice.

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Section: Discussionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

Inhibition of Neuron-Specific CREB Dephosphorylation is Involved in Propofol and Ketamine-Induced Neuroprotection Against Cerebral Ischemic Injuries of Mice

Luo-wa

Han

et al. 2011

Neurochem Res

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“…The effect of various chemical substances (Cantu & Hegsted, 1970) on the brain nerve tissue damaged by ischemia as well as various pathological and pathophysiological changes induced by the total cerebral ischemia in rabbits and other laboratory animals are the subject of many studies (Ishiyama et al, 2010). The place of origin of the truncus brachiocephalicus and the a. subclavia sinistra are most commonly used to induce the total cerebral ischemia by ligation (Hossmann 1998;Iwama et al, 2000;Pluta, 1987).…”

Section: Resultsmentioning

confidence: 99%

Variations in Origin of Arteries Supplying the Brain in Rabbit and Their Impact on Total Cerebral Ischemia

Mazensky¹,

Danko²,

Pilipčinec³

et al. 2012

Advances in the Preclinical Study of Ischemic Stroke

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“…are clinical scenarios in which brain ischemia and reperfusion could occur under propofol anesthesia. Global brain ischemia-reperfusion during propofol anesthesia provokes persistent cerebral pial constriction [7]. Cerebral vasoconstriction possibly exacerbates ischemic brain injury [8].…”

Section: Introductionmentioning

confidence: 99%

The effects of Y-27632 on pial microvessels during global brain ischemia and reperfusion in rabbits

et al. 2017

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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.

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Cerebral Pial Vascular Changes Under Propofol or Sevoflurane Anesthesia During Global Cerebral Ischemia and Reperfusion in Rabbits

Cited by 15 publications

References 17 publications

Inhibition of Neuron-Specific CREB Dephosphorylation is Involved in Propofol and Ketamine-Induced Neuroprotection Against Cerebral Ischemic Injuries of Mice

Inhibition of Neuron-Specific CREB Dephosphorylation is Involved in Propofol and Ketamine-Induced Neuroprotection Against Cerebral Ischemic Injuries of Mice

Variations in Origin of Arteries Supplying the Brain in Rabbit and Their Impact on Total Cerebral Ischemia

The effects of Y-27632 on pial microvessels during global brain ischemia and reperfusion in rabbits

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