Transfusion Therapy

Miller, Ronald D.

doi:10.1016/b978-0-443-06959-8.00055-8

Cited by 101 publications

(173 citation statements)

References 117 publications

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“…Although optogenetics allows for precise temporal control of neuronal firing, it is likely that a large increase in extracellular DA is necessary to overcome the powerful hypnotic effects of general anesthesia, which takes several minutes to develop with optical stimulation. Accelerated time to emergence from an inhaled anesthetic has been reported for a number of pharmacological and circuit-level manipulations, but this end point is greatly affected by physiological variables such as minute ventilation and cardiac output (49). In contrast, this study was performed using CSSGA wherein the concentration of anesthetic in the brain is held constant, so changes in cardiopulmonary physiology cannot alter anesthetic depth (50).…”

Section: Discussionmentioning

confidence: 99%

Optogenetic activation of dopamine neurons in the ventral tegmental area induces reanimation from general anesthesia

Taylor

Dort

Kenny

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

219

179

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Dopamine (DA) promotes wakefulness, and DA transporter inhibitors such as dextroamphetamine and methylphenidate are effective for increasing arousal and inducing reanimation, or active emergence from general anesthesia. DA neurons in the ventral tegmental area (VTA) are involved in reward processing, motivation, emotion, reinforcement, and cognition, but their role in regulating wakefulness is less clear. The current study was performed to test the hypothesis that selective optogenetic activation of VTA DA neurons is sufficient to induce arousal from an unconscious, anesthetized state. Floxed-inverse (FLEX)-Channelrhodopsin2 (ChR2) expression was targeted to VTA DA neurons in DA transporter (DAT)-cre mice (ChR2+ group; n = 6). Optical VTA stimulation in ChR2+ mice during continuous, steady-state general anesthesia (CSSGA) with isoflurane produced behavioral and EEG evidence of arousal and restored the righting reflex in 6/6 mice. Pretreatment with the D1 receptor antagonist SCH-23390 before optical VTA stimulation inhibited the arousal responses and restoration of righting in 6/6 ChR2+ mice. In control DAT-cre mice, the VTA was targeted with a viral vector lacking the ChR2 gene (ChR2− group; n = 5). VTA optical stimulation in ChR2− mice did not restore righting or produce EEG changes during isoflurane CSSGA in 5/5 mice. These results provide compelling evidence that selective stimulation of VTA DA neurons is sufficient to induce the transition from an anesthetized, unconscious state to an awake state, suggesting critical involvement in behavioral arousal.anesthesia | ventral tegmental area | dopamine | optogenetics | arousal

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Section: Discussionmentioning

confidence: 99%

Optogenetic activation of dopamine neurons in the ventral tegmental area induces reanimation from general anesthesia

Taylor

Dort

Kenny

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

219

179

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“…While midazolam is thought to cause minimal hemodynamic effects, it does have the potential to cause loss of airway reflexes, respiratory depression, and even apnea [1]. If an effective, reliable and safe sedative could be used in general practice, this would benefit a wide range of patients, especially those who are frail, anxious, severely phobic or uncooperative.…”

Section: Introductionmentioning

confidence: 99%

Dexmedetomidine versus Midazolam in Procedural Sedation. A Systematic Review of Efficacy and Safety

et al. 2017

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ObjectivesTo systematically review the literature comparing the efficacy and safety of dexmedetomidine and midazolam when used for procedural sedation.Materials and MethodsWe searched MEDLINE, EMBASE and COCHRANE for clinical trials comparing dexmedetomidine and midazolam for procedural sedation up to June 20, 2016. Inclusion criteria: clinical trial, human subjects, adult subjects (≥18 years), article written in English, German, French or Dutch, use of study medication for conscious sedation and at least one group receiving dexmedetomidine and one group receiving midazolam. Exclusion criteria: patients in intensive care, pediatric subjects and per protocol use of additional sedative medication other than rescue medication. Outcome measures for efficacy comparison were patient and clinician satisfaction scores and pain scores; outcome measures for safety comparison were hypotension, hypoxia, and circulatory and respiratory complications.ResultsWe identified 89 papers, of which 12 satisfied the inclusion and exclusion criteria; 883 patients were included in these studies. Dexmedetomidine was associated with higher patient and operator satisfaction than midazolam. Patients receiving dexmedetomidine experienced less pain and had lower analgesic requirements. Respiratory and hemodynamic safety were similar.ConclusionsDexmedetomidine is a promising alternative to midazolam for use in procedural sedation. Dexmedetomidine provides more comfort during the procedure for the patient and clinician. If carefully titrated, the safety profiles are similar.

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“…For example, several clinically utilized volatile anesthetics (e.g., isoflurane, sevoflurane, and desflurane) have effects on systemic and pulmonary BP, cardiac inotropy, heart rate, and airway smooth muscle tone. 17 Since the first successful administration of the general anesthesia with ethyl ether by Morton in 1846, 18 significant efforts have been made to develop stable and nonflammable anesthetics. The first nonflammable halogenated volatile anesthetic gas, methoxyflurane, was first synthesized in 1948 by a team of chemists involved in the Manhattan Project during World War II.…”

Section: Historical Volatile Anesthetics and Their Effect On Renal Fumentioning

confidence: 99%

Volatile Anesthetics and AKI

Fukazawa

Lee

2014

Journal of the American Society of Nephrology

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AKI is a major clinical problem with extremely high mortality and morbidity. Kidney hypoxia or ischemia-reperfusion injury inevitably occurs during surgery involving renal or aortic vascular occlusion and is one of the leading causes of perioperative AKI. Despite the growing incidence and tremendous clinical and financial burden of AKI, there is currently no effective therapy for this condition. The pathophysiology of AKI is orchestrated by renal tubular and endothelial cell necrosis and apoptosis, leukocyte infiltration, and the production and release of proinflammatory cytokines and reactive oxygen species. Effective management strategies require multimodal inhibition of these injury processes. Despite the past theoretical concerns about the nephrotoxic effects of several clinically utilized volatile anesthetics, recent studies suggest that modern halogenated volatile anesthetics induce potent anti-inflammatory, antinecrotic, and antiapoptotic effects that protect against ischemic AKI. Therefore, the renal protective properties of volatile anesthetics may provide clinically useful therapeutic intervention to treat and/or prevent perioperative AKI. In this review, we outline the history of volatile anesthetics and their effect on kidney function, briefly review the studies on volatile anesthetic-induced renal protection, and summarize the basic cellular mechanisms of volatile anesthetic-mediated protection against ischemic AKI.

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Transfusion Therapy

Cited by 101 publications

References 117 publications

Optogenetic activation of dopamine neurons in the ventral tegmental area induces reanimation from general anesthesia

Optogenetic activation of dopamine neurons in the ventral tegmental area induces reanimation from general anesthesia

Dexmedetomidine versus Midazolam in Procedural Sedation. A Systematic Review of Efficacy and Safety

Volatile Anesthetics and AKI

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