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1.
Hyperreflexia is a common feature of spinal cord injury (SCI), and changes in reflex excitability have been reported to be useful in assessing treatments in animal models of cord damage. However, spinal reflexes are known to be dependent on anesthetic level. As a preliminary to its use in SCI, the excitability of the Hoffman reflex (H reflex) has been assessed under several commonly used anesthetics. The H reflex was recorded in the distal foot muscles (dorsal interossei) of adult rats, while the lateral plantar nerve was stimulated. Five different anesthetics were used: ketamine, halothane, Nembutal, Etomidate, and Saffan. Recording and stimulating electrodes were inserted directly through the skin to minimize the surgical procedure for each experiment, allowing repeated recording to be made in the same animal on a weekly basis. Suppression of the H reflex was tested using twin-pulse stimulation. Halothane and ketamine produced suppression of the H response when interpulse intervals were shortened to less than 1 s. The H-reflex suppression profiles recorded under Etomidate, Saffan, and Nembutal anesthesia were less sensitive to the stimulation rate, with little reduction until intervals were 200 ms or less. The suppression profiles of halothane and ketamine resemble that seen in unanesthetized humans, whereas that under the other anesthetics tried here resembles that observed in spinal-cord-injured animals. The results suggest a preferential action of some anesthetics on descending pathways involved in reflex modulation and the importance of assessing reflex excitability under anesthetics such as ketamine or halothane.  相似文献   

2.
The role of the N-methyl-D-aspartate (NMDA) receptor-channel complex in ketamine-induced anesthesia was examined in mice. General anesthetic potencies were evaluated on a rating scale, which provided the data for anesthetic scores, loss of righting reflex, sleeping time and recovery time. All drugs were administered intraperitoneally. NMDA (60-300 mg/kg), an NMDA receptor agonist, dose-dependently antagonized the general anesthetic potencies of ketamine at a dose of 100 mg/kg which produced loss of righting reflex in more than 90% of the mice. On the other hand, a high dose of N-methyl-L-aspartate (400 mg/kg), a stereoisomer of NMDA, did not. A dose of 300 mg/kg of NMDA significantly shifted the dose-response curve of ketamine for loss of righting reflex to the right. A high dose of D-cycloserine (200 mg/kg), an agonist at the glycine site on the NMDA receptor complex, slightly but significantly shortened the sleeping time caused by ketamine (100 mg/kg). However, neither a critical subconvulsive dose of kainate (15 mg/kg), a kainate receptor agonist, nor a subconvulsive dose of quisqualate (120 mg/kg), an alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptor agonist, reversed general anesthesia induced by 100 mg/kg of ketamine.(ABSTRACT TRUNCATED AT 250 WORDS)  相似文献   

3.
The neurotransmitters and receptor types involved in the afferent arm of the human pupillary light reflex are unknown. We hypothesized that the pupillary light reflex is mediated in part by NMDA receptors and that it would be depressed by the NMDA antagonists, nitrous oxide and ketamine. To study this question, sixteen patients received general anesthesia with desflurane, fentanyl, and muscular relaxation with rocuronium. After a stable level of general anesthesia had been obtained and at least 1 h after the start of the surgical procedure, ketamine 1 mg/kg (N = 8) or saline (N = 8) was injected intravenously by random selection. Heart rate, pupil size, pupillary light reflex, BIS scores, and blood pressure were measured every 2 min before and for 30 min after drug administration. A similar study of sixteen patients was then conducted with either addition of 60% nitrous oxide or 60% nitrogen to the gas mixture. We observed that the pupillary light reflex was depressed by ketamine and nitrous oxide by approximately 50%. The BIS score, representing the processed electroencephalogram, was elevated by ketamine and unchanged with nitrous oxide. Heart rate, pupil size, and blood pressure were unchanged by the drugs when compared to the control groups. We conclude that the two NMDA antagonists ketamine and nitrous oxide depress the human pupillary light reflex during general anesthesia whereas other monitored parameters were either unchanged or paradoxically elevated by the drugs. These findings present evidence that glutamate NMDA receptor activation is involved in generating the human pupillary light reflex.  相似文献   

4.
Systemic toxic reactions to local anesthetics are brought about by absolute overdosage, and, most commonly, inadvertent intravascular injections. The anti-convulsant action of ketamine has been studied. However, the effect of ketamine on lidocaine-induced convulsions has not been reported. This study investigated the effect of ketamine on lidocaine-induced seizures in mice. Mice (32-41 g) were divided into 2 groups, 15 in each group, and were pretreated with intraperitoneal normal saline solution or intraperitenoeal (ip) ketamine before lidocaine. Group 1 (N = 15) received 75 mg kg ip lidocaine; Group 2 (N = 15) received 20 mg kg ketamin ip; 5 min later 75 mg kg lidokaine ip were applied. Clinical features, incidences, latencies, durations, and mortality rate of convulsions were recorded. After 75 mg kg lidocaine injection, ataxia, loss of righting reflex, and generalized tonic-clonic convulsions were seen within 2-5 min in Group 1. Generalized tonic-clonic convulsions were seen in 8 mice and deep sedation was seen in 7 mice in Group 2 (p < .05). Generalized status epilepticus occurred in one mouse in both groups. Three mice from Group l and one mouse from Group 2 died during convulsions. There were no differences between the two groups with regard to the onset and duration of seizures (p > .05). It was concluded that ketamine significantly prevented lidocaine-induced generalized tonic-clonic seizures; on the other hand, the lethality of lidocaine was least reduced by ketamine.  相似文献   

5.
The effects of systemically and intrathecally administered ketamine on spinal wind-up of normal and monoarthritic rats were studied by using C-fiber reflex responses evoked by repetitive (0.6 Hz) electric stimulation. Both systemic and intrathecal ketamine induced dose-dependent depression of wind-up activity in normal rats, as revealed by the dose-related inhibitory effects of the drug. At the same intraperitoneal doses, ketamine produced a greater inhibitory effect on wind-up activity of monoarthritic rats, compared to normal animals. The intrathecal administration of ketamine also produced wind-up inhibition, the efficacy being higher in the monoarthritic rats. Results indicate that ketamine depresses spinal wind-up, specially in rats submitted to chronic pain, probably due to its antagonistic properties on dorsal horn NMDA receptors, which play a crucial role in the maintenance of chronic pain.  相似文献   

6.
The postoperative sleep disturbance (POSD) is characterized by reduction of sleep after surgical operation. However, its mechanism is not well known. Therefore, we hypothesized that anesthetics could contribute to the POSD, and studied the effects of isoflurane and ketamine on sleep in rabbits. Rabbit sleep was measured for 21 h after isoflurane exposure or intravenous injection of ketamine. Non-rapid eye movement sleep (NREMS) was decreased after isoflurane anesthesia. In contrast, ketamine anesthesia significantly enhanced NREMS. Both anesthetics did not affect rapid eye movement sleep. These results suggest that isoflurane may contribute to the POSD, but ketamine may decrease the POSD.  相似文献   

7.
A study of spontaneous and reflexly evoked activity of laryngeal abductor (posterior cricoarytenoid) and adductor (thyroarytenoid and lateral cricoarytenoid) muscles was carried out in cats anesthetized with chloraloseurethane or made decerebrate and supplemented with ketamine HCl. The posterior cricoarytenoid muscle was active largely during inspiration but showed tonic activity throughout the respiratory cycle; the thyroarytenoid and lateral cricoarytenoid muscles were rhythmically active during expiration. Anesthetic amounts of pentobarbital abolished adductor rhythmicity and enhanced cyclic inspiratory activity of the abductor muscle. Hyperventilation increased the tonic adductor muscle activity while diminishing abductor muscle activity prior to resolution of apnea. Glossopharyngeal (epipharyngeal branch) and superior laryngeal nerve stimulation evoked chiefly excitatory effects on adductors and largely and attenuating effect on the abductor during inspiration. Stimulation of caudal intercostal nerves caused similar effects but to a lesser degree. Peripheral phrenic nerve stimulation during inspiration facilitated reflex abductor muscle activity whereas such stimulation during expiration facilitated reflex adductor muscle activity. The collective evidence further supports the conclusion that the larynx has a dual function: that of a respiratory organ (widening of the glottis during inspiration and its narrowing during expiration) and of a guardian of the lower respiratory tract from invading foreign matter (reflex sphincter action of contracting adductor muscles with relaxation of the abductor).  相似文献   

8.
A growing body of evidence has suggested that the dysfunction of glutamatergic systems plays a pivotal role in major depressive disorder (MDD). In clinical studies, an N-methyl-d-aspartate receptor antagonist, ketamine, was shown to exert both rapid and sustained antidepressant effects in patients with treatment-resistant MDD. The objective of the present study was to confirm the rapid onset of action of ketamine and to investigate the mechanisms underlying both the rapid and sustained antidepressant-like effects of ketamine in rodent models of depression. The intraperitoneal administration of ketamine (10 mg/kg) 30 min prior to testing significantly reduced the number of escape failures in the learned helplessness (LH) paradigm in rats in which currently prescribed antidepressants exerted an effect only after repeated administrations. Ketamine also significantly reduced the immobility time in the tail suspension test (TST), and this effect lasted for 72 h, indicating that ketamine may possess a sustained antidepressant-like effect. The rapid antidepressant-like effects of ketamine in both the LH paradigm and the TST were significantly blocked by subcutaneous treatment with 2,3-dihydroxy-6-nitro-7-sulfoamoylbenzo(f)quinoxaline (NBQX), an α-amino-3-hydroxy-5-methylisoxazole-4-propionate (AMPA) receptor antagonist. In addition, the sustained antidepressant-like effect of ketamine in the TST was partially abolished by treatment with NBQX. In conclusion, we confirmed the faster onset of the action of ketamine, compared with clinically prescribed antidepressants. Moreover, the present results suggested that direct AMPA receptor activation may play an important role in both the rapid and sustained antidepressant-like effects of ketamine in animal models of depression, although other mechanisms might be involved in the sustained action.  相似文献   

9.
Systemic toxic reactions to local anesthetics are brought about by absolute overdosage, and, most commonly, inadvertent intravascular injections. The anti-convulsant action of ketamine has been studied. However, the effect of ketamine on lidocaine-induced convulsions has not been reported. This study investigated the effect of ketamine on lidocaine-induced seizures in mice. Mice (32–41 g) were divided into 2 groups, 15 in each group, and were pretreated with intraperitoneal normal saline solution or intraperitenoeal (ip) ketamine before lidocaine. Group 1 (N = 15) received 75 mg kg ip lidocaine; Group 2 (N = 15) received 20 mg kg ketamin ip; 5 min later 75 mg kg lidokaine ip were applied. Clinical features, incidences, latencies, durations, and mortality rate of convulsions were recorded. After 75 mg kg lidocaine injection, ataxia, loss of righting reflex, and generalized tonic-clonic convulsions were seen within 2–5 min in Group 1. Generalized tonic-clonic convulsions were seen in 8 mice and deep sedation was seen in 7 mice in Group 2 (p < .05). Generalized status epilepticus occurred in one mouse in both groups. Three mice from Group l and one mouse from Group 2 died during convulsions. There were no differences between the two groups with regard to the onset and duration of seizures (p > .05). It was concluded that ketamine significantly prevented lidocaine-induced generalized tonic-clonic seizures; on the other hand, the lethality of lidocaine was least reduced by ketamine.  相似文献   

10.
Ketamine is a non-competitive antagonist to the phencyclidine site of N-methyl-d-aspartate (NMDA) receptor. Clinical findings point to a rapid onset of action for ketamine on the treatment of major depression. Considering that classic antidepressants may take long-lasting time to exhibit their main therapeutic effects, the present study aims to compare the behavioral effects and the BDNF hippocampus levels of acute administration of ketamine and imipramine in rats. To this aim, rats were acutely treated with ketamine (5, 10 and 15 mg/kg) and imipramine (10, 20 and 30 mg/kg) and animal behavioral was assessed in the forced swimming and open-field tests. Afterwards, BDNF protein hippocampal levels were assessed in imipramine- and ketamine-treated rats by ELISA-sandwich assay. We observed that ketamine at the doses of 10 and 15 mg/kg, and imipramine at 20 and 30 mg/kg reduced immobility time compared to saline group, without affecting locomotor activity. Interesting enough, acute administration of ketamine at the higher dose, but not imipramine, increased BDNF protein levels in the rat hippocampus. In conclusion, our findings suggest that the increase of hippocampal BDNF protein levels induced by ketamine might be necessary to produce a rapid onset of antidepressant action.  相似文献   

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