Pituitary Adrenal Response to Ketamine and the Inhibition of the Response by Catecholaminergic Blockade

Fahringer, E.E.; Foley, E.L.; Redgate, E. S.

doi:10.1159/000122255

Cited by 16 publications

(5 citation statements)

References 10 publications

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“…(Lister et al 1976;Cooper et al 1980). Others have shown that the drug was effective in reducing stress-induced biochemical and hormonal in man (Tsuji et al 1980) and rat (Fahringer et al 1974) Administration of propranolol (0.05 mg . kg -1 ) to goats subjected to the stress of transportation failed to inhibit the cortical and glucose stress responses (Sanhouri et al 1991b).…”

Section: Adrenergic Antagonists 121 Propranololmentioning

confidence: 99%

Evaluation of Drugs Used in the Control of Stressful Stimuli in Domestic Animals: a Review

Ali¹,

Al‐Qarawi²

2002

Acta Vet. Brno

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Section: Adrenergic Antagonists 121 Propranololmentioning

confidence: 99%

Evaluation of Drugs Used in the Control of Stressful Stimuli in Domestic Animals: a Review

Ali¹,

Al‐Qarawi²

2002

Acta Vet. Brno

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“…Polystyrene beads coated with a purified polyclonal goat antibody specific for ACTH [26][27][28][29][30][31][32][33][34][35][36][37][38][39] was incubated for 24 hours at room temperature with fetal plasma (200µL) and 125 I ACTH tracer (50µL) labeled monoclonal antibody specific for ACTH [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17] . The unbound radioactivity was then washed with a provided buffer and the bound radioactivity measured with a gamma counter.…”

Section: Hormone Assaysmentioning

confidence: 99%

Ketamine inhibits fetal ACTH responses to cerebral hypoperfusion

Powers

Wood²

2007

American Journal of Physiology-Regulatory, Integrative and Comp

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The present study tested the effect of ketamine on the fetal reflex responses of late-gestation sheep to brachiocephalic occlusion (BCO), a stimulus that mimics the reduction in cerebral blood flow that results from severe fetal hypotension. Ketamine, a dissociative anesthetic and known noncompetitive antagonist of N-methyl D-aspartate (NMDA) receptors, has previously been shown to impair chemoreceptor responsiveness. Studies from this laboratory suggest that fetal reflex ACTH responses to hypotension are largely mediated by chemoreceptors; therefore we hypothesized that ketamine would inhibit the reflex hormonal response to BCO. Chronically catheterized fetal sheep were subjected to acute cerebral hypoperfusion through occlusion of the brachiocephalic artery. Fetal blood pressure and heart rate were continuously recorded and fetal blood samples drawn during the experiment were analyzed with specific hormone assays. Our results demonstrate that ketamine attenuates hemodynamic responses to cerebral hypoperfusion and is a potent inhibitor of adrenocorticotropin (ACTH) and proopiomelanocortin (POMC) / pro-ACTH release. These data support the hypothesis that fetal reflex responses hypotension are chemoreceptor mediated. Given the potency with which ketamine inhibits ACTH response to fetal hypotension, we suggest that the use of ketamine, or other anesthetic or analgesic drugs that block or otherwise interact with the NMDA-glutamate pathways, in late pregnancy or in pre-term newborns be reconsidered.

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“…In addition, ketamine is known to produce increases in plasma cortisol (Krystal et al 1994;Fahringer et al 1974;Clarke et al 1974;Oyama et al 1970) and glucose (Kaniaris et al 1975;Clarke et al 1974), and this group has reported cognitive effects of glucose and insulin (Newcomer et al 1994a; Newcomer et al in press;Craft et al 1993;Craft et al 1996) and glucocorticoids (Newcomer et al 1994b) in humans, motivating the measurement of these variables to rule out confounds to the interpretation of cognitive effects. For similar reasons, plasma epinephrine and norepinephrine were measured with a single isotope derivative (radioenzymatic) method (Shah et al 1985).…”

Section: Plasma Assaysmentioning

confidence: 99%

Ketamine-Induced NMDA Receptor Hypofunction as a Model of Memory Impairment and Psychosis

Newcomer

Farber

Jevtović-Todorović

et al. 1999

Neuropsychopharmacology

546

350

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Considerable research interest has recently been focused on the role of glutamate and related neural circuitry in the neurobiology of schizophrenia. The results of these investigations have emphasized hypofunction of glutamatergic neurons and/or the N-methyl-D-aspartate (NMDA) glutamate receptor (Tsai et al. 1995;Kim et al. 1980aKim et al. , 1980bSherman et al. 1991;Deutsch et al. 1989;Javitt and Zukin 1991;Olney 1988a;Olney 1988b;Olney and Farber 1995). An important element of several of these theoretical positions is that NMDA receptor hypofunction (NRH) produced by any mechanism can be psychotogenic. This has renewed interest in the clinical effects of NMDA glutamate receptor antagonists.Ketamine and phencyclidine (PCP) are non-competitive NMDA glutamate receptor antagonists (Zukin and Zukin 1979;Vincent et al. 1979;Lodge and Anis 1982;Lodge et al. 1987) which can produce a transient state of NRH in the brain. Early investigators characterized a PCP-induced clinical syndrome of schizophrenia-like Received March 18, 1998; revised June 19, 1998; accepted June 29, 1998. N EUROPSYCHOPHARMACOLOGY 1999 -VOL . 20 , NO . 2 NMDA Receptor Hypofunction Induced Memory Decrease 107 symptoms, including hallucinations, delusions, idiosyncratic and illogical thinking, poverty of speech and thought, agitation, disturbances of emotion, affect, withdrawal, decreased motivation, and dissociation (Johnstone et al. 1959;Luby et al. 1959;Rosenbaum et al. 1959;Luby et al. 1962;Corssen and Domino 1966;Bakker and Amini 1961;Davies and Beech 1960;Domino and Luby 1981). This PCP-induced syndrome can be indistinguishable from acute presentations of schizophrenia (Yesavage and Freeman 1978;Erard et al. 1980). Ketamine, a PCP analog still used in human anesthesia, has been reported to cause reactions similar to but not as severe as those caused by PCP, including brief, reversible "positive" and "negative" schizophrenia-like symptoms (Krystal et al. 1994;Malhotra et al. 1996). Both PCP and ketamine can exacerbate psychosis in schizophrenia Luby et al. 1962;Lahti et al. 1995a;Lahti et al. 1995b;Malhotra et al. 1997).Declarative, explicit or secondary memory and learning deficits in patients with schizophrenia occur early in the course of the illness and are quantitatively large compared with deficits in other differentiated elements of cognitive performance, showing stability "on" versus "off" antipsychotic medication and over repeated testing (Gruzelier et al. 1988;Saykin et al. 1991Saykin et al. , 1994Cannon et al. 1994). Clinical and preclinical investigations suggest the hypothesis that changes in NMDA glutamate receptor activity in patients with schizophrenia may be causally related to memory impairments found in this disorder. Relevant to this hypothesis, the activation of post-synaptic NMDA receptors is important for the induction of the activity-dependent synaptic modification called long-term potentiation (LTP) (Bliss and Collingridge 1993;Collingridge and Bliss 1995), and hippocampal LTP has been postulated to underlie cert...

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Pituitary Adrenal Response to Ketamine and the Inhibition of the Response by Catecholaminergic Blockade

Cited by 16 publications

References 10 publications

Evaluation of Drugs Used in the Control of Stressful Stimuli in Domestic Animals: a Review

Evaluation of Drugs Used in the Control of Stressful Stimuli in Domestic Animals: a Review

Ketamine inhibits fetal ACTH responses to cerebral hypoperfusion

Ketamine-Induced NMDA Receptor Hypofunction as a Model of Memory Impairment and Psychosis

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