Neuroprotective Effect of Low-dose Lidocaine in a Rat Model of Transient Focal Cerebral Ischemia

Lei, Baiping; Cottrell, James E.; Kass, Ira S.

doi:10.1097/00000542-200108000-00029

Cited by 78 publications

(49 citation statements)

References 29 publications

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“…The administration of progesterone before 2 hours of ischemia and after 48 hours of reperfusion was responsible for a smaller weight loss 24 . The administration of lidocaine before ischemia followed by 7 days of reperfusion caused a lower weight loss on treated animals than in controls 25 . The weight reduction observed in the present study may be attributed to the surgical procedure and to anesthesia.…”

Section: Discussionmentioning

confidence: 85%

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Evaluation of the neuroprotective effect of ketoprofen on rats submitted to permanent focal brain ischemia

Silva

Colli

Coimbra

et al. 2007

Arq. Neuro-Psiquiatr.

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-Objective: To study the neurobehavioral, biochemical and histopathological consequences of permanent focal brain ischemia, and the putative neuroprotective action of ketoprofen. Method: Onehundred-and-three Wistar rats divided into groups A and B were respectively submitted to 48 hours and 15 days of ischemia. Each group was divided into 4 subgroups: ischemic not treated, ischemic treated, sham not treated, and sham treated. Ischemic animals had the left middle cerebral artery coagulated. Ketoprofen was administered to treated subgroups 15 minutes before arterial coagulation (manipulation in the sham group). Results: Exploratory activity and defecation were reduced in all ischemic animals in the first postoperative days and constant histopathological changes were observed in each group. The total brain glutamate levels were higher in treated animals 48 hours after surgery. Conclusion: No clear parallelism among behavioral, biochemical and histopathological findings was observed. Ketoprofen demonstrated no neuroprotective effect on the behavioral or histopathological aspects of focal permanent brain ischemia.KEY WORDS: focal brain ischemia, rat, open field, glutamate, histopathology, neuroprotection, ketoprofen. Avaliação do efeito neuroprotetor do cetoprofeno em ratos submetidos à isquemia cerebral focal permanenteRESUMO -Objetivo: Estudar as conseqüências comportamentais, bioquímicas e histopatológicas da isquemia cerebral focal permanente e o possível efeito neuroprotetor do cetoprofeno. Método: Foram utilizados 103 ratos Wistar, divididos em grupos A e B, submetidos, respectivamente, a 48 horas e a 15 dias de isquemia. Cada grupo foi dividido em 4 subgrupos: isquêmico não tratado; isquêmico tratado; sham não tratado; sham tratado. Nos animais isquêmicos foi coagulada a artéria cerebral média esquerda. Os subgrupos tratados receberam cetoprofeno 15 minutos antes da oclusão ou manipulação arterial. Resultados: Os animais isquêmicos reduziram a atividade exploratória e as evacuações nos primeiros dias pós-operatórios e mostraram alterações histopatológicas constantes em cada grupo. As concentrações do glutamato total 48 horas após a cirurgia foram maiores nos animais tratados. Conclusão: Não houve um paralelismo entre os achados comportamentais, bioquímicos e histopatológicos. O cetoprofeno não apresentou efeito protetor contra isquemia cerebral focal permanente, nos aspectos comportamentais e histopatológicos.

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Section: Discussionmentioning

confidence: 85%

“…Variations in body weight have been used in recent studies as a parameter to evaluate transitory focal cerebral ischemia 24,25 . The administration of progesterone before 2 hours of ischemia and after 48 hours of reperfusion was responsible for a smaller weight loss 24 .…”

Section: Discussionmentioning

confidence: 99%

Evaluation of the neuroprotective effect of ketoprofen on rats submitted to permanent focal brain ischemia

Silva

Colli

Coimbra

et al. 2007

Arq. Neuro-Psiquiatr.

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“…As shown in Table 3, administration of lidocaine ameliorates the electrophysiological activities and reduces infarct volume during focal ischemia. Lei et al (2001) reported that continuous administration of lidocaine at a clinical dose reduced cerebral infarct size at 48 h and 7 days after MCA occlusion, improved neurologic outcome, and inhibited post-ischemic weight loss in rats. As shown in Table 4, administration of lidocaine has been reported to delay the onset of depolarization (Ayad et al, 1994;Liu et al, 1997;Raley-Susman et al, 2001;Seyfried et al, 2005), reduce the amplitude of negative DC deflection (Ayad et al, 1994;Raley-Susman et al, 2001), and facilitate the recovery of membrane potential from depolarization (Weber and Taylor, 1994;Niiyama et al, 2005).…”

Section: Discussionmentioning

confidence: 99%

“…In 2 randomized, double-blinded, prospective clinical studies, continuous administration of lidocaine significantly ameliorated postoperative cognitive dysfunction in patients undergoing cardiac surgery for left heart valve procedures (Mitchell et al, 1999) or coronary artery bypass surgery with cardiopulmonary bypass (Wang et al, 2002). In animal models of ischemia, administration of lidocaine has been shown to ameliorate cognitive dysfunction (Popp et al, 2011) and reduce infarct volume (Shokunbi et al, 1990;Lei et al, 2001Lei et al, , 2004. Sodium entry and loss of membrane potential comprise some of the first steps in the development of ischemic neuronal damage.…”

Section: Introductionmentioning

confidence: 99%

Effect of lidocaine on dynamic changes in cortical reduced nicotinamide adenine dinucleotide fluorescence during transient focal cerebral ischemia in rats

et al. 2013

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Rats were subjected to 90 min of focal ischemia by occluding the left middle cerebral and both common carotid arteries. The dynamic changes in formation of brain ischemic areas were analyzed by measuring the direct current (DC) potential and NADH fluorescence with ultraviolet irradiation. In the lidocaine group (n = 10), 30 min before ischemia, an intravenous bolus (1.5 mg/kg) of lidocaine was administered, followed by a continuous infusion (2 mg/kg/h) for 150 min. In the control group (n = 10), an equivalent amounts of saline was administered. Following the initiation of ischemia, an area of high-intensity NADH fluorescence rapidly developed in the middle cerebral artery territory in both groups and the DC potential in this area showed ischemic depolarization. An increase in NADH fluorescence closely correlated with the DC depolarization. The blood flow in the marginal zone of both groups showed a similar decrease. Five minutes after the onset of ischemia, the area of high-intensity NADH fluorescence was significantly smaller in the lidocaine group (67% of the control; P = 0.01). This was likely due to suppression of ischemic depolarization by blockage of voltage dependent sodium channels with lidocaine. Although lidocaine administration did not attenuate the number of peri-infarct depolarizations during the ischemia, the 4 high-intensity area and infarct volume were significantly smaller in the lidocaine group both at the end of ischemia (78% of the control; P = 0.046) and 24 h later (P = 0.02). A logistic regression analysis demonstrated a relationship between the duration of ischemic depolarization and histologic damage and revealed that lidocaine administration did not attenuate neuronal damage when the duration of depolarization was identical. These findings indicate that the mechanism by which lidocaine decreases infarct volume is primarily through a reduction of the brain area undergoing NADH fluorescence increases which closely correlates with depolarization.

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“…The local anesthetic lidocaine may provide some added benefit through its ability to block the Na + channel, reduce Na + K + transmembrane flux, and decrease basal energy expenditures. 15 Usually 1 to 2 mg/kg of lidocaine may be given as an intravenous bolus immediately prior to the ischemic event. Most effective neuroprotective techniques used today involve some combination of the above therapies associated with some level of hypothermia, which still seems to be the most effective for neural protection during periods of transient forebrain ischemia.…”

Section: Neurosurg Focus / Volume 12 / May 2002mentioning

confidence: 99%

Perioperative management of complex skull base surgery: the anesthesiologist's point of view

Jellish¹,

Murdoch²,

Jp³

2002

FOC

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The anesthetic management of complex skull base surgical procedures provides unique problems and concerns for the neuroanesthesiologist. Positioning to access the skull base could put the patient at risk for peripheral nerve injury and some of the positions may increase the risk for air emboli. In addition, tumor pathology and involvement with vital structures could increase the chances for substantive blood loss, destruction of associated nerves or vessels, and may require temporary occlusion of the carotid artery necessitating intraoperative neuroprotection. Neurophysiological monitors may also be used to safeguard nerve function and anesthetic techniques must be adjusted to accommodate their use. Finally, postoperative morbidity may be affected by surgical approach to the skull base and the anesthesiologist should be aware of which approach may produce a greater incidence of pain, nausea, and vomiting in the postoperative period. The authors discuss the anesthetic concerns and management for complex cranial base surgery. Different approaches will be discussed and comparisons of perioperative parameters between these approaches will be made with data provided by retrospective chart review of more than 600 skull base procedures performed at the authors' institution over the last 10 years. This information should help guide decision making concerning anesthetic management for these skull base procedures.

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Neuroprotective Effect of Low-dose Lidocaine in a Rat Model of Transient Focal Cerebral Ischemia

Abstract: The current study demonstrated that a clinical anriarrhythmic dose of lidocaine, when given before and during transient focal cerebral isehemia, significantly reduced infaret size, improved neurologic outcome, and inhibited postisehemic weight loss.

Cited by 78 publications

References 29 publications

Evaluation of the neuroprotective effect of ketoprofen on rats submitted to permanent focal brain ischemia

Evaluation of the neuroprotective effect of ketoprofen on rats submitted to permanent focal brain ischemia

Effect of lidocaine on dynamic changes in cortical reduced nicotinamide adenine dinucleotide fluorescence during transient focal cerebral ischemia in rats

Perioperative management of complex skull base surgery: the anesthesiologist's point of view

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