Neuroprotective Effects of Anesthetic Agents

Kawaguchi, Masahiko; Furuya, Hitoshi

doi:10.2199/jjsca.29.358

Cited by 38 publications

(47 citation statements)

References 24 publications

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“…De plus, les agents anesthésiques réduisent la génération d'espèces réactives de radicaux libres; ils augmentent la tolérance ischémique en effectuant un conditionnement antérieur et postérieur, et inhibent les voies apoptotiques. 4 Ainsi, les données probantes soutenant qu'il existe des voies multiples par lesquelles les agents anesthésiques ont le potentiel d'exercer des bienfaits cliniquement importants sont foison. Mais quelles sont les données probantes expérimentales pour la neuroprotection anesthésique (soutenue)?…”

Section: Resultsunclassified

“…Additionally, anesthetics reduce the generation of reactive free radical species; they increase ischemic tolerance by pre-and post-conditioning, and they also inhibit apoptotic pathways. 4 Thus, there is considerable evidence that multiple pathways exist by which anesthetic agents have the potential to exert clinically important benefits. But what is the experimental evidence for (sustained) anesthetic neuroprotection?…”

mentioning

confidence: 99%

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Anesthetic drugs and sustained neuroprotection in acute cerebral ischemia: can we alter clinical outcomes?

Werner

2009

Can J Anesth/J Can Anesth

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Section: Resultsunclassified

mentioning

confidence: 99%

Anesthetic drugs and sustained neuroprotection in acute cerebral ischemia: can we alter clinical outcomes?

Werner

2009

Can J Anesth/J Can Anesth

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“…Maintenance was with a mixture of O 2 , air, and desflurane. Although propofol (and etomidate and thiopentane) has potential neuroprotective effects, they are unproven, particularly in humans [30,31,43].…”

Section: Methodsmentioning

confidence: 99%

Cerebral Microembolization during Primary Total Hip Arthroplasty and Neuropsychologic Outcome: A Pilot Study

Patel

Stygall

Harrington

et al. 2010

Clinical Orthopaedics &Amp; Related Research

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BackgroundIntraoperative cerebral microembolization occurs in a substantial proportion of patients undergoing THA. Historically, postoperative cognitive dysfunction has been attributed to different factors, including anesthesia, but the influence of the surgery has not been thoroughly examined. Questions/purposes We conducted a prospective, controlled clinical trial to assess intraoperative cerebral microembolization during THA and neuropsychologic outcome. Methods The presence of a patent foramen ovale (PFO) also was investigated, using transcranial Doppler, to determine whether this affected cerebral microembolic incidence and load and whether microemboli occurred as a result of specific surgical activity. Forty-five patients were recruited who underwent THA and neuropsychologic assessment; a battery of tests was administered preoperatively and at 6 weeks and 6 months postoperatively. Results Overall, patients showed improvement in total neuropsychologic change scores at both postoperative intervals. The incidence of cerebral microembolization for THA was 23%. The prevalence of PFO was 37%. PFO did not appear to influence microemboli load or incidence. More microemboli were seen during femoral component insertion and impaction. Conclusions Intraoperative cerebral microembolization occurs in a substantial proportion of patients during THA recorded by transcranial Doppler. The microemboli load is low and is not influenced by the presence of PFO. Certain surgical activities seem responsible for greater cerebral microemboli generation. However, neuropsychologic outcome was not affected postoperatively by microemboli or other operative or patient variables.

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“…Some intravenous anesthetics have been implicated to have neuroprotective properties. The effects of barbiturates on neuroprotection were at first attributed to the reduction in the cerebral metabolism, but recent studies have shown that this does not appear to be the sole mechanism involved (73). Although barbiturates are well-known to have neuroprotective properties, a review done with randomized or quasi randomized trials by Cochrane from December 1996 to April 1999 showed no evidences that barbiturates in severe head injury could improve outcomes (74).…”

Section: Neurologic Protectionmentioning

confidence: 99%