Dose-Dependent Influence of Sevoflurane Anesthesia on Neuronal Survival and Cognitive Outcome After Transient Forebrain Ischemia in Sprague-Dawley Rats

Lasarzik, Irina; Noppens, Rüdiger; Wolf, Thorsten; Bauer, Henrike; Luh, Clara; Werner, Christian; Engelhard, Kristin; Thal, Serge C.

doi:10.1007/s12028-011-9562-3

Cited by 9 publications

(10 citation statements)

References 41 publications

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“…The results of the current study are also different from those of the study by Lasarzik et al, 17 in which higher concentrations of sevoflurane were associated with a better histologic outcome as compared with lower concentrations. Their experimental protocol was different from ours in 2 main ways.…”

Section: Discussioncontrasting

confidence: 99%

Preischemic Administration of Sevoflurane Does not Exert Dose-dependent Effects on the Outcome of Severe Forebrain Ischemia in Rats

Miura

Kanazawa²,

Nasu³

2015

Journal of Neurosurgical Anesthesiology

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We previously showed that preischemic administration of high-dose isoflurane worsened the outcome from severe forebrain ischemia in rats. Conversely, high doses of sevoflurane have been reported to improve the outcome from forebrain ischemia when the insult is moderate. To clarify the dose-dependent effects of sevoflurane on severe forebrain ischemia, we performed an outcome study using an identical protocol to that in our previous study with isoflurane. Fasting male Sprague-Dawley rats underwent surgical preparation for forebrain ischemia under halothane anesthesia. Anesthesia was changed to fentanyl/nitrous oxide to eliminate the halothane, after which 30 minutes of 0.5, 1.0, 1.5, 2.0, or 2.5 minimum alveolar concentration sevoflurane was administered. Ten minutes of ischemia was induced by bilateral carotid occlusion plus systemic hypotension, in which cessation of electroencephalographic activity was confirmed. Sevoflurane was discontinued and anesthesia continued with fentanyl/nitrous oxide for an additional 100 minutes. Outcome evaluation at 5 days postischemia included seizure incidence, mortality rate, neuromotor score, and histologic injuries to the cerebral cortex and hippocampal CA1 and CA3. Different doses of sevoflurane did not statistically affect seizure incidence (10.0% to 18.2%), mortality rate (20.0% to 46.7%), cortical damage (mild to moderate degree), or hippocampal CA1 damage (93.7% to 96.7% neuronal necrosis) or CA3 damage (36.3% to 41.7%). Dose-dependent effects of sevoflurane were not observed for any of the outcome variables assessed in this rat model of severe forebrain ischemia.

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Section: Discussioncontrasting

confidence: 99%

Preischemic Administration of Sevoflurane Does not Exert Dose-dependent Effects on the Outcome of Severe Forebrain Ischemia in Rats

Miura

Kanazawa²,

Nasu³

2015

Journal of Neurosurgical Anesthesiology

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“…This implies that the low rates of cell death in our study probably would not be in correlation with cognitive impairment. Lasarzik et al (2011) showed that sevoflurane in high doses (4%), similar to ours, are more neuroprotective in regards of cell death than low dose (1%) in an ischemia model. The rats receiving 4% had a median of 3222 viable cells in the CA1 region, also similar to our young rats, and they did not show neurocognitive dysfunction using object recognition test.…”

Section: Discussionsupporting

confidence: 86%

Systemic physiology and neuroapoptotic profiles in young and adult rats exposed to surgery: A randomized controlled study comprising four different anaesthetic techniques

Ibrahim

Krammer

Hansen

et al. 2015

Intl J of Devlp Neuroscience

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Combination of anaesthesia and surgery induces significant perturbations of physiological parameters in both young and adult spontaneously breathing rats undergoing surgery. These observations further enlighten the need for detailed physiological monitoring under these experimental conditions. Although some statistically significant differences in activated caspase-3 profiles were detected between experimental groups, the overall extent of neuronal cell death remained very low under all conditions questioning, thereby, the physiological significance of apoptotic neurodegeneration in the context of anaesthesia and surgery.

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“…Most neurons will die as a consequence of secondary energy failure, which occurs 6 to 15 h after injury [4]. The magnitude of primary cell death is dependent on the severity and duration of ischaemia/hypoxia and could not be observed in the neocortex within the first 13 min [28]. In the present study, we found that an insignificant increase of s100ß could be observed after 90 min of reperfusion.…”

Section: Discussionmentioning

confidence: 46%

“…For example, the basal ganglia and the hippocampus are more susceptible to ischaemia [28]. The proposed protective effects of levosimendan might become visible after a longer observation period and may not be associated with reduced glutamate release [39].…”

Section: Discussionmentioning

confidence: 99%

The effects of levosimendan on brain metabolism during initial recovery from global transient ischaemia/hypoxia

et al. 2012

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BackroundNeuroprotective strategies after cardiopulmonary resuscitation are currently the focus of experimental and clinical research. Levosimendan has been proposed as a promising drug candidate because of its cardioprotective properties, improved haemodynamic effects in vivo and reduced traumatic brain injury in vitro. The effects of levosimendan on brain metabolism during and after ischaemia/hypoxia are unknown.MethodsTransient cerebral ischaemia/hypoxia was induced in 30 male Wistar rats by bilateral common carotid artery clamping for 15 min and concomitant ventilation with 6% O2 during general anaesthesia with urethane. After 10 min of global ischaemia/hypoxia, the rats were treated with an i.v. bolus of 24 μg kg-1 levosimendan followed by a continuous infusion of 0.2 μg kg-1 min-1. The changes in the energy-related metabolites lactate, the lactate/pyruvate ratio, glucose and glutamate were monitored by microdialysis. In addition, the effects on global haemodynamics, cerebral perfusion and autoregulation, oedema and expression of proinflammatory genes in the neocortex were assessed.ResultsLevosimendan reduced blood pressure during initial reperfusion (72 ± 14 vs. 109 ± 2 mmHg, p = 0.03) and delayed flow maximum by 5 minutes (p = 0.002). Whereas no effects on time course of lactate, glucose, pyruvate and glutamate concentrations in the dialysate could be observed, the lactate/pyruvate ratio during initial reperfusion (144 ± 31 vs. 77 ± 8, p = 0.017) and the glutamate release during 90 minutes of reperfusion (75 ± 19 vs. 24 ± 28 μmol·L-1) were higher in the levosimendan group. The increased expression of IL-6, IL-1ß TNFα and ICAM-1, extend of cerebral edema and cerebral autoregulation was not influenced by levosimendan.ConclusionAlthough levosimendan has neuroprotective actions in vitro and on the spinal cord in vivo and has been shown to cross the blood–brain barrier, the present results showed that levosimendan did not reduce the initial neuronal injury after transient ischaemia/hypoxia.

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Dose-Dependent Influence of Sevoflurane Anesthesia on Neuronal Survival and Cognitive Outcome After Transient Forebrain Ischemia in Sprague-Dawley Rats

Cited by 9 publications

References 41 publications

Preischemic Administration of Sevoflurane Does not Exert Dose-dependent Effects on the Outcome of Severe Forebrain Ischemia in Rats

Preischemic Administration of Sevoflurane Does not Exert Dose-dependent Effects on the Outcome of Severe Forebrain Ischemia in Rats

Systemic physiology and neuroapoptotic profiles in young and adult rats exposed to surgery: A randomized controlled study comprising four different anaesthetic techniques

The effects of levosimendan on brain metabolism during initial recovery from global transient ischaemia/hypoxia

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