Anesthetic effects on susceptibility to cortical spreading depression

Kudo, Chiho; Toyama, Motomichi; Sato, Aiji; Hanamoto, Hiroshi; Morimoto, Yoshinari; Sugimura, Mitsutaka; Niwa, Hitoshi

doi:10.1016/j.neuropharm.2012.10.018

Cited by 46 publications

(41 citation statements)

References 16 publications

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“…SD-induced peak hyperemia (component II) is often smaller, and the initial hypoperfusion (component I) is more prominent, when resting CBF and vessel calibers are elevated (e.g., acetazolamide, inhalational anesthesia, dimethyl sulfoxide) than when they are reduced (e.g., barbiturate or propofol anesthesia, indomethacin, hypocapnia, or post-SD oligemia after a preceding SD) (71,95,257,394,460). Although anesthetics can alter SD susceptibility (74,191,200,240,241,375,404,443,466), they do not appear to have a consistent direct effect on the hemodynamic response (443); both absent and potent peak hyperemic responses have been reported in unanesthetized animals in different studies (95,424,443). Nevertheless, anesthesia can indirectly influence the hemodynamic response by changing resting CBF (128) or systemic blood pressure (see below).…”

Section: Potential Sources Of Heterogeneity In the Cbf Response To Sdmentioning

confidence: 99%

Spreading Depression, Spreading Depolarizations, and the Cerebral Vasculature

Ayata

Lauritzen

2015

Physiological Reviews

458

600

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Spreading depression (SD) is a transient wave of near-complete neuronal and glial depolarization associated with massive transmembrane ionic and water shifts. It is evolutionarily conserved in the central nervous systems of a wide variety of species from locust to human. The depolarization spreads slowly at a rate of only millimeters per minute by way of grey matter contiguity, irrespective of functional or vascular divisions, and lasts up to a minute in otherwise normal tissue. As such, SD is a radically different breed of electrophysiological activity compared with everyday neural activity, such as action potentials and synaptic transmission. Seventy years after its discovery by Leão, the mechanisms of SD and its profound metabolic and hemodynamic effects are still debated. What we did learn of consequence, however, is that SD plays a central role in the pathophysiology of a number of diseases including migraine, ischemic stroke, intracranial hemorrhage, and traumatic brain injury. An intriguing overlap among them is that they are all neurovascular disorders. Therefore, the interplay between neurons and vascular elements is critical for our understanding of the impact of this homeostatic breakdown in patients. The challenges of translating experimental data into human pathophysiology notwithstanding, this review provides a detailed account of bidirectional interactions between brain parenchyma and the cerebral vasculature during SD and puts this in the context of neurovascular diseases.

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Section: Potential Sources Of Heterogeneity In the Cbf Response To Sdmentioning

confidence: 99%

Spreading Depression, Spreading Depolarizations, and the Cerebral Vasculature

Ayata

Lauritzen

2015

Physiological Reviews

458

600

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“…SD frequency is anesthetic dependent. In experimental preparations, pentobarbital, urethane and propofol do not substantively suppress SD frequency [62], whereas inhalational anesthetics (e.g., isoflurane, halothane, N 2 O) and dexmedetomidine do [63, 62, 64-66]. In humans, ketamine, N 2 O, and isoflurane suppress peri-infarct SD frequency compared with propofol, opioids or midazolam [67, 68].…”

Section: Ischemic Depolarizationsmentioning

confidence: 99%

Anesthesia in Experimental Stroke Research

Hoffmann

Sheng

Ayata

et al. 2016

Transl. Stroke Res.

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Anesthetics have enabled major advances in development of experimental models of human stroke. Yet their profound pharmacologic effects on neural function can confound the interpretation of experimental stroke research. Anesthetics have drug and dose-specific effects on cerebral blood flow and metabolism, neurovascular coupling, autoregulation, ischemic depolarizations, excitotoxicity, inflammation, neural networks, and numerous molecular pathways relevant for stroke outcome. Both pre- and post-conditioning properties have been described. Anesthetics also modulate systemic arterial blood pressure, lung ventilation, and thermoregulation, all of which may interact with the ischemic insult as well as the therapeutic interventions. These confounds present a dilemma. Here, we provide an overview of the anesthetic mechanisms of action and molecular and physiologic effects on factors relevant to stroke outcomes that can guide the choice and optimization of the anesthetic regimen in experimental stroke.

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“…Specifically, intraperitoneal propofol hemisuccinate (PHS), a water-soluble prodrug of propofol, administered 15 min prior to KCl–induced CSD on the cortex of mice, decreased the number of CSD deflections at doses of 120 and 200 mg/kg without any effect on CSD amplitude [202]. In contrast, Kudo et al failed to demonstrate any inhibitory effect of propofol on the frequency of KCl-induced CSD in rats [203]. This result may have been due to the fact that a water-insoluble formulation of propofol widely administered as a anesthetic in clinical setting was used.…”

Section: Reviewmentioning

confidence: 99%

Cortical spreading depression as a target for anti-migraine agents

et al. 2013

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Spreading depression (SD) is a slowly propagating wave of neuronal and glial depolarization lasting a few minutes, that can develop within the cerebral cortex or other brain areas after electrical, mechanical or chemical depolarizing stimulations. Cortical SD (CSD) is considered the neurophysiological correlate of migraine aura. It is characterized by massive increases in both extracellular K+ and glutamate, as well as rises in intracellular Na+ and Ca2+. These ionic shifts produce slow direct current (DC) potential shifts that can be recorded extracellularly. Moreover, CSD is associated with changes in cortical parenchymal blood flow.CSD has been shown to be a common therapeutic target for currently prescribed migraine prophylactic drugs. Yet, no effects have been observed for the antiepileptic drugs carbamazepine and oxcarbazepine, consistent with their lack of efficacy on migraine. Some molecules of interest for migraine have been tested for their effect on CSD. Specifically, blocking CSD may play an enabling role for novel benzopyran derivative tonabersat in preventing migraine with aura. Additionally, calcitonin gene-related peptide (CGRP) antagonists have been recently reported to inhibit CSD, suggesting the contribution of CGRP receptor activation to the initiation and maintenance of CSD not only at the classic vascular sites, but also at a central neuronal level. Understanding what may be lying behind this contribution, would add further insights into the mechanisms of actions for “gepants”, which may be pivotal for the effectiveness of these drugs as anti-migraine agents.CSD models are useful tools for testing current and novel prophylactic drugs, providing knowledge on mechanisms of action relevant for migraine.

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Anesthetic effects on susceptibility to cortical spreading depression

Cited by 46 publications

References 16 publications

Spreading Depression, Spreading Depolarizations, and the Cerebral Vasculature

Spreading Depression, Spreading Depolarizations, and the Cerebral Vasculature

Anesthesia in Experimental Stroke Research

Cortical spreading depression as a target for anti-migraine agents

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