Ketamine prevents ischemic neuronal injury

Marcoux, F; Goodrich, James E.; Dominick, Mark A.

doi:10.1016/0006-8993(88)90037-6

Cited by 95 publications

(37 citation statements)

References 48 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Most of the studies reporting protection by the NMDA antagonists, especially those in gerbils (Gill et al, 1987a;Boast et al, 1988;Marcoux et al, 1988;Rod and Auer, 1989), neither maintained nor monitored body temperature. In others where body temperature was monitored (Church et al, 1988;Sauer et al, 1988;Swan et al, 1988), it is unclear whether normothermia was maintained equally in the vehicle-versus the drug-treated groups throughout both the ischemic and recirculation periods.…”

Section: Discussionmentioning

confidence: 99%

“…In gerbils, remarkable degrees of protection against ischemic injury to hippocampal neurons have been reported for the competitive NMDA antagonists, cis-4-(phosphonomethyl)-2-piperidine-carboxylic acid (CGS) and 4-(3-phosphonopropyl)-2-piperazine-carboxylic acid (CPP; Boast et al, 1988) and for the noncompetitive antagonists, MK-801 (Gill et al, 1987a) and ketamine (Marcoux et al, 1988). MK-80 1 was found to be highly effective at preventing hippocampal cell loss at doses ranging from 0.1 mg/kg to 10 mg/kg, i.p., when given 1 hr prior to ischemia.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

The N-methyl-D-aspartate antagonist, MK-801, fails to protect against neuronal damage caused by transient, severe forebrain ischemia in adult rats

1991

View full text Add to dashboard Cite

The neuroprotective effects of dizocilipine maleate (MK-801), a noncompetitive antagonist of the N-methyl-D-aspartate (NMDA) receptor/channel, were tested in the 4-vessel occlusion rat model of forebrain ischemia. Adult Wistar rats, treated intraperitoneally with MK-801 or saline using several different treatment paradigms were subjected to 5 (n = 208) or 15 (n = 62) min of severe, transient forebrain ischemia. In saline-treated animals, 15 min of ischemia (n = 13) produced extensive and consistent loss of pyramidal neurons in the CA1 zone of hippocampus. The degree and distribution of cell loss were not reduced by single dose preischemic administration of MK-801 at 1 (n = 7), 2.5 (n = 4), or 5 mg/kg (n = 8). In other animals subjected to 15 min of forebrain ischemia, multiple doses of MK-801 (5, 2.5, and 2.5 mg/kg) given immediately and at approximately 8 and 20 hr after cerebral reperfusion (n = 5) did not alter CA1 injury compared to saline-treated controls (n = 5). Five minutes of forebrain ischemia in saline-treated animals, (n = 82) resulted in significantly fewer (p less than 0.001) dead CA1 pyramidal cells and a greater variance compared to animals subjected to 15 min of ischemia. Power analysis of the preliminary saline-treated animals subjected to 5 min of ischemia (n = 22) indicated that 60 animals per group were necessary to detect a 15% difference between MK-801 and vehicle-treated groups. Multidose treatment with MK-801 (1 mg/kg) given 1 hr prior to 5 min of ischemia (n = 60) and again at approximately 8 and 16 hr after recirculation failed to attenuate hippocampal injury.(ABSTRACT TRUNCATED AT 250 WORDS)

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

The N-methyl-D-aspartate antagonist, MK-801, fails to protect against neuronal damage caused by transient, severe forebrain ischemia in adult rats

1991

View full text Add to dashboard Cite

show abstract

“…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

View full text Add to dashboard Cite

show abstract

“…Ketamine, a PCP derivative, is an NMDAnoncompetitive antagonist and has been proved by extensive studies to be a neuropro-tective substance [23][24][25][26]. Ketamine is able to combine with the PCP site in the NMDA receptor complex, to interfere with the combination of EAAs with NMDA receptors and to block the opening of the iron channel, thus alleviating the Ca 2+ influx and neuronal damage induced.…”

Section: Discussionmentioning

confidence: 99%

Role of Excitatory Amino Acids in Hypoxic Preconditioning

Xie

Hou

1999

Neurosignals

View full text Add to dashboard Cite

We examined the effects of the extrinsic ionotropic NMDA receptor agonist (aspartate) and antagonist (ketamine) on the hypoxic preconditioning of mice and the concentration changes of intrinsic excitatory amino acids (EAAs), aspartate and glutamate, in the whole brain and different brain regions during preconditioning by an HPLC method. Our results showed that aspartate and ketamine significantly prolonged and shortened the standard tolerance time of mice during preconditioning and survival time in hypobaric chambers, respectively. After the 1st exposure, EAA concentrations in the whole brain and brain regions were increased. After run 4, they were decreased or maintained. It is suggested that the activation and suppression of ionotropic NMDA receptors is harmful and beneficial to hypoxic preconditioning, respectively. Degradation and/or inactivation of EAAs might be beneficial to the tolerance of mice to hypoxia.

show abstract

Ketamine prevents ischemic neuronal injury

Cited by 95 publications

References 48 publications

The N-methyl-D-aspartate antagonist, MK-801, fails to protect against neuronal damage caused by transient, severe forebrain ischemia in adult rats

The N-methyl-D-aspartate antagonist, MK-801, fails to protect against neuronal damage caused by transient, severe forebrain ischemia in adult rats

Ketamine concentrations during cardiopulmonary bypass

Role of Excitatory Amino Acids in Hypoxic Preconditioning

Contact Info

Product

Resources

About