Ketamine Decreases Plasma Catecholamines and Improves Outcome from Incomplete Cerebral Ischemia in Rats

Hoffman, William E.; Pelligrino, Dale A.; Werner, Christian; Kochs, Eberhard; Albrecht, Ronald F.; Esch, J. Schulte am

doi:10.1097/00000542-199205000-00014

Cited by 128 publications

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“…1 4 Despite reports of potentially harmful effects during bolus administrations of phencyclidine derivatives the role of ketamine in neurosurgical anesthesia needs to be reevaluated as several experiments indicate substantial neuronal protection with these compounds. [6][7][8][9] The present study demonstrates a dose-dependent improvement in neurological outcome, following incomplete cerebral ischemia, with S(+)-ketamine. These results are consistent with previous observations where neurological deficit and histopathological damage were reduced with racemic ketamine in this model and following models of experimental brain injury.…”

Section: Resultsmentioning

confidence: 78%

“…[3][4][5] Studies in laboratory animals have shown that racemic ketamine exhibits some neuroprotective potential when infused prior to incomplete cerebral ischemia or following traumatic brain injury. [6][7][8][9] For example, studies in this animal model of incomplete hemispheric ischemia have shown that neurological outcome was improved at three days from insult with racemic ketamine. 6 Similarly, studies in rats using a non-penetrating impact have shown that racemic ketamine improved neurological outcome and decreased the extension of the lesion even when given two hours post trauma.…”

Section: Laboratory Investigationsmentioning

confidence: 99%

“…[6][7][8][9] For example, studies in this animal model of incomplete hemispheric ischemia have shown that neurological outcome was improved at three days from insult with racemic ketamine. 6 Similarly, studies in rats using a non-penetrating impact have shown that racemic ketamine improved neurological outcome and decreased the extension of the lesion even when given two hours post trauma. 7,8 More recently, studies in rat hippocampal neuronal cultures have shown that racemic ketamine and S(+)-ketamine attenuated the injury after glutamate exposure or axonal transsection.…”

Section: Laboratory Investigationsmentioning

confidence: 99%

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High-dose S(+)- ketamine improves neurological outcome following incomplete cerebral ischemia in rats

Reeker

Werner

Möllenberg

et al. 2000

Can J Anesth/J Can Anesth

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572CAN J ANESTH 2000 / 47: 6 / pp [572][573][574][575][576][577][578] Purpose: To determine the effects of the non-competitive NMDA-receptor antagonist S(+)-ketamine on neurological outcome in a rat model of incomplete cerebral ischemia. Methods: Thirty rats were anesthetized, intubated and mechanically ventilated with isoflurane, O 2 30% and nitrous oxide 70%. Following surgery animals were randomly assigned to one of the following treatment groups: Rats in group 1 (n=10, control) received fentanyl (bolus: 10 µg·kg -1 iv; infusion 25 µg·kg -1 ·h -1 ) and N 2 O 70% / O 2 . Rats in group 2 (n=10) received O 2 30% in air and low-dose S(+)-ketamine (infusion: 0.25 mg·kg -1 ·min -1 ). Rats in group 3 (n=10) received O 2 30% in air and high-dose S(+)-ketamine (infusion: 1.0 mg·kg -1 ·min -1 ). Following 30 min equilibration period ischemia was induced by combined unilateral common carotid artery ligation and hemorrhagic hypotension to 35 mmHg for 30 min. Plasma catecholamines were assayed before and at the end of ischemia. Neurological deficit was evaluated for three postischemic days. Results: Neurological outcome was improved with high-dose S(+)-ketamine when compared to fentanyl / N 2 O -anesthetized controls (9 vs 1 stroke related deaths, P < 0.05). Increases in plasma catecholamine concentrations were higher in fentanyl / N 2 O -anesthetized (adrenaline baseline 105.5 ± 92.1 pg·ml -1 , during ischemia 948 ± 602.8 pg·ml -1 , P < 0.05; noradrenaline baseline 407± 120.2 pg·ml -1 , ischemia 1267 ± 422.2 pg·ml -1 , P < 0.05) than in high-dose S(+)-ketamine-treated animals (adrenaline baseline 71 ± 79.5 pg·ml -1 , ischemia 237 ± 131.9; noradrenaline baseline 317.9 ± 310.5 pg·ml -1 , ischemia 310.5 ± 85.7 pg·ml -1 ). Conclusion: Neurological outcome is improved following incomplete cerebral ischemia with S(+)-ketamine. Decreases in neuronal injury may be related to suppression of sympathetic discharge. Résultats : L'évolution neurologique a été meilleure avec de fortes doses de S(+)-kétamine qu'avec l'alfentanyl / N 2 O (9 vs 1 décès reliés à un accident ischémique cérébral, P < 0,05). L'augmentation des concentrations plasmatiques de catécholamines a été plus marquée avec l'alfentanyl / N 2 O (l'adrénaline de base à 105,5 ± 92,1 pg·ml -1 ; pendant l'ischémie, 948 ± 602,8 pg·ml -1 , P < 0,05; la noradrénaline de base à 407± 120,2 pg·ml -1 ; pendant l'ischémie, 1267 ± 422,2 pg·ml -1 , P < 0,05) qu'avec de fortes doses de S(+)-kétamine (l'adrénaline de base à 71 ± 79,5 pg·ml -1 ; pendant l'ischémie, 237 ± 131,9; la noradrénaline de base à 317,9 ± 310,5 pg·ml -1 ; pendant l'ischémie, 310,5 ± 85,7 pg·ml -1 ). Conclusion : L'utilisation de S(+)-kétamine permet une évolution neurologique supérieure après une ischémie cérébrale incomplète. Cette situation peut être reliée à la suppression de décharge sympathique.

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Section: Resultsmentioning

confidence: 78%

Section: Laboratory Investigationsmentioning

confidence: 99%

Section: Laboratory Investigationsmentioning

confidence: 99%

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High-dose S(+)- ketamine improves neurological outcome following incomplete cerebral ischemia in rats

Reeker

Werner

Möllenberg

et al. 2000

Can J Anesth/J Can Anesth

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“…5 In animal models of cerebral ischemia and traumatic head injury ketamine and its enantiomere S(+)-ketamine showed brain protective potential even when administered one hour after the insult. [6][7][8] Although cerebrovascular autoregulation in the rat was intact with S(+)-ketamine, it is unclear whether total iv anesthesia (TIVA) using S(+)-ketamine in combination with propofol affects cerebrovascular autoregulation in humans. Therefore the present study investigates the effects of S(+)-ketamine and propofol (a combination adequate to provide anesthesia during surgery) on the dynamic component of cerebrovascular autoregulation in comparison to sevoflurane anesthesia.…”

Section: Discussionmentioning

confidence: 99%

S(+)-ketamine/propofol maintain dynamic cerebrovascular autoregulation in humans

Engelhard

Werner

Möllenberg

et al. 2001

Can J Anesth/J Can Anesth

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“…Patients were premeditated with diazepam (0.1 mg. kg -~ po) or Iorazepam (0.03 mg.kg -t sl), and morphine sulfate (0.15 mg.g -~ ira) with perphenazine (0.05 mg-kg -t im). Anaesthesia was induced with fentanyl (10)(11)(12)(13)(14)(15) lag.kg-I), midazolam (0.05 mg.kg -I) pancuronium (0.15 mg-kg-I). After intubation and placement of a pulmonary artery catheter, heart rate (HR), mean arterial pressure (MAP), mean pulmonary artery pressure (PAP) and thermodilution cardiac outputs (CO) were recorded.…”

Section: Methodsmentioning

confidence: 99%

Ketamine concentrations during cardiopulmonary bypass

et al. 1996

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Ketamine Decreases Plasma Catecholamines and Improves Outcome from Incomplete Cerebral Ischemia in Rats

Cited by 128 publications

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High-dose S(+)- ketamine improves neurological outcome following incomplete cerebral ischemia in rats

High-dose S(+)- ketamine improves neurological outcome following incomplete cerebral ischemia in rats

S(+)-ketamine/propofol maintain dynamic cerebrovascular autoregulation in humans

Ketamine concentrations during cardiopulmonary bypass

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