Wherefore ketamine?

Persson, Jan

doi:10.1097/aco.0b013e32833b49b3

Cited by 65 publications

(59 citation statements)

References 70 publications

(64 reference statements)

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“…Aside from its major action –antagonism of NMDA-glutamatergic receptor– ketamine may have an effect on other receptors: nicotinic acetylcholine, serotonin, dopamine, opioid, muscarinic acetylcholine, and weakly influencing the GABA A and glycine receptors [24]. However, most of these receptors have less affinity for ketamine than the NMDA receptors, and require a higher (10–20 fold) concentration of ketamine to obtain the same antagonist effect [25].…”

Section: Discussionmentioning

confidence: 99%

Ketamine Attenuates the ACTH Response to Hypoxia in Late-Gestation Ovine Fetus

Chang

Wood²

2015

Neonatology

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Background: Ketamine, a noncompetitive N-Methyl-D-aspartate (NMDA) receptor antagonist, is a commonly used dissociative anesthetic in neonatology. We have proposed that ketamine reduces fetal stress responsiveness to stimuli that involve reduced oxygen supply to the fetal brain. Previously, we have shown that ketamine inhibits plasma ACTH levels in late-gestation fetal sheep subjected to brachiocephalic artery occlusion (BCO), an ischemic hypoxia model that might activate some of the same direct and reflex responses as hypoxia. Objectives: We performed the current study to test the hypothesis that ketamine pretreatment will reduce fetal ACTH responses to hypoxic hypoxia (HH). Methods: Fetal sheep were chronically catheterized at least 5 days prior to study. Ketamine (3 mg/kg) was administered intravenously to the fetus 10 min prior to normoxia or a period of hypoxia induced by administration of nitrogen gas to the maternal trachea for 30 min. Results: Hypoxia significantly increased both fetal ACTH and cortisol levels in both the control and ketamine groups (p < 0.0005, interaction effect of time·stimulus in two-way ANOVA), and the ACTH response was blunted by ketamine (p < 0.005). Conclusions: Ketamine reduced fetal ACTH responses to HH, possibly due to antagonism of the NMDA receptors in the fetal brain. Interestingly, in contrast to the responses to BCO, ACTH responses to HH were only partially inhibited, suggesting that multiple neurotransmitter pathways mediate the ACTH response to HH.

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Section: Discussionmentioning

confidence: 99%

Ketamine Attenuates the ACTH Response to Hypoxia in Late-Gestation Ovine Fetus

Chang

Wood²

2015

Neonatology

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“…On the other hand, ketamine produces hallucinatory effects in human (Moore and Bostwick, 1999) and has thus become a popular recreational drug for abusers (Topp et al, 2004). Acute side effects of ketamine use include nausea, tachycardia, and respiratory depression, but the chronic toxicity of ketamine has yet to be investigated (Persson, 2010). Increasing ketamine abuse has triggered growing concern about its toxic effects in prolonged use.…”

Section: Introductionmentioning

confidence: 99%

Ketamine effects on the urogenital system—changes in the urinary bladder and sperm motility

Tan

Chan

Wai

et al. 2011

Microscopy Res & Technique

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Different doses of ketamine (10 mg/kg, 20 mg/kg, 30 mg/kg, 40 mg/kg, 50 mg/kg, and 60 mg/kg) were injected i.p. (I.P.), respectively, to male ICR mice to determine the optimal dosage for chronic administration. At and above 40 mg/kg I.P. injection, mice had almost no hindlimb movement during swimming test. Subsequently, 30 mg/kg was used as the dose for the study in the toxicity of long-term ketamine administration on urinary bladder and sperm motility. The treatment group were subdivided into two (n = 10 each group); one received daily ketamine treatment i.p. for 3 months and another group for 6 months. Corresponding number of mice in control groups (n = 5 each group) received saline injection instead of ketamine. Terminal dUTP nick and labeling (TUNEL) study and Sirius red staining were carried out on the sectioned slides of the urinary bladders to study the degree of apoptosis in both epithelium and muscular layers of the urinary bladder and the relative thickness of the muscular layers in this organ was also computed. Apoptosis in the bladder epithelium was observed initially in the 3-month ketamine treated mice and the number of apoptotic cells was significantly different (P < 0.05) between the 3-month and 6-month ketamine treated mice and the control. The relative thickness of muscular layers in the bladder wall also decreased significantly (P < 0.05) when the 6-month treated mice and the control were compared. Sirius red staining revealed increase of collagen in the urinary bladder of the treated mice, most evidently 6 months after ketamine treatment. In addition, the sperm motility was studied and there was a statistically significant difference between the control and ketamine treated groups in the percentages of sperms which were motile (P < 0.05). This suggested that the chronic administration of ketamine affected the genital system as well.

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“…channels [34], and dopamine receptors, as well as other cholinergic, purinergic and adenosine receptor systems [25,35]. The ability of ketamine to block conductance of specific ion channels may be the reason it has local anesthetic properties after topical administration [36].…”

Section: Ketamine's Mechanism Of Actionmentioning

confidence: 99%

The Use of Ketamine in Neuropathic Pain

O’Brien

Pangarkar

Prager

2014

Curr Phys Med Rehabil Rep

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Hyperactivity of N-methyl-D-aspartate (NMDA) receptors may be one of the factors in the genesis of neuropathic pain (NP). Ketamine is a dissociative anesthetic and analgesic that is the most potent NMDA receptor antagonist currently available for human use. There is a growing body of literature for three decades suggesting efficacy of subanaesthetic doses of ketamine in the treatment of NP, particularly the pain in complex regional pain syndromes. The primary limitations of ketamine use are secondary to psychotomimetic and, to a lesser extent, sympathetic activation. The purpose of this article is to review the history, pharmacology, pharmacodynamics, clinical benefits, and limitations of ketamine for treatment of NP. Methods of administration and management of adverse effects are highlighted based on the clinical experience of the authors.

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Wherefore ketamine?

Cited by 65 publications

References 70 publications

Ketamine Attenuates the ACTH Response to Hypoxia in Late-Gestation Ovine Fetus

Ketamine Attenuates the ACTH Response to Hypoxia in Late-Gestation Ovine Fetus

Ketamine effects on the urogenital system—changes in the urinary bladder and sperm motility

The Use of Ketamine in Neuropathic Pain

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