Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The functional activity of cellular immunity was studied in 26 patients with opticochiasmatic arachnoiditis as a model of autoimmune involvement of the brain after administration of common anesthetics of different pharmacological groups. Injection of ketamine as the induction and basic component of general combined anesthesia leads to reduction of neurosensitization induced by the pathologic process; it is paralleled by the optimal activation of the suppressor component of lymphocytes and a reduction of sensitization to brain antigen. In contrast to ketamine, barbiturates augment neurosensitization and lead to depression of the lymphocyte activity, this confirming the anti-immunopathological effect of barbituric acid derivatives. Ketamine is advisable for patients with various immunopathological states.
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PMID:[The characteristics of the functional activity of cellular immunity factors in relation to the use of general anesthetics from different pharmacological groups in operations for optic nerve neurolysis]. 896 14

We report the effect of a single daily dose of ketamine in a 54 year old woman with fibromyalgia and severe post-traumatic neuropathic pain. A number of different approaches for pain relief had been tried with little effect. An intramuscular test dose of 0.4 mg/kg ketamine combined with 0.05 mg/kg midazolam lead to analgesia which lasted for almost two days. Long-term analgesia was also obtained by 250 mg/kg ketamine hydrochloride taken orally in the form of capsules every night at bedtime. The patient has now used this dose for nine months. Ketamine is an NMDA receptor antagonist. A single sub-anaesthetic dose of ketamine causes a long-term depression of pain intensity in some, but not in all, patients suffering chronic pain. This effect is distinctly different from the short-lasting (10-30 min) analgesic effect in cases of acute nociceptive pain. The long-term depression of the intensity of chronic pain states may be due to a reversal of NMDA receptor-dependent long-term potentiation of synapses in central pain pathways. By giving ketamine as a single dose at night the mental side-effects are reduced or avoided.
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PMID:[Analgesic effect of ketamine in a patient with neuropathic pain]. 899 75

Opiates remain the most common form of analgesic therapy in the burn patient today. Because of increased opiate requirements, optimal relief of burn pain continues to be a problem for these patients. The purpose of this article is to summarize those alternative pain control methods that appear in the literature. For instance, in minor burns acetominophen continues to be a useful first line analgesic. Non-steroidal anti-inflammatory drugs (NSAID) and benzodiazepine are generally combined with opiates while entonox seems to be used commonly in the adolescent patients to relieve procedural pain. Antidepressants appear to enhance opiate-induced analgesia while anticonvulsants are useful in the treatment of sympathetically maintained pain following burns. Ketamine has been extensively used during burn dressing changes but its psychological side-effects have limited its use. Clonidine, however, has shown promise in reducing pain without causing pruritus or respiratory depression. Other forms such as transcutaneous electrical nerve stimulation (TENS), psychological techniques, topical and systemic local anaesthetics are also useful adjuncts.
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PMID:Adjunctive methods of pain control in burns. 942 10

Effects of ketamine on the sodium (INa) and L-type calcium currents (ICa) were examined by using whole-cell patch clamp techniques in guinea pig single ventricular myocytes. The mode of action of ketamine was compared with those of quinidine, a sodium channel blocker, and verapamil, a calcium channel blocker. Ketamine (30-300 microM) inhibited both INa and ICa in a concentration-dependent manner. Quinidine (30 microM) and verapamil (0.1 microM) produced use-dependent depression of INa and ICa, respectively. The amplitude of INa elicited by the first depolarizing pulse after a long quiescent period was slightly decreased by quinidine. During a train of depolarizing pulse the current amplitude decreased gradually, and reached a steady state level in the quinidine-treated cell (use-dependent block, UDB). Verapamil produced a similar mode of inhibition of ICa, i.e., UDB. In contrast, ketamine produced significant decrease in INa and ICa elicited by the first depolarizing pulses and the decreases of both currents were not augmented during a train of depolarizing pulses. From these results, it can be concluded that ketamine produces tonic block of the cardiac sodium and calcium channels and the mode of inhibition is clearly different from UDB by quinidine and verapamil.
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PMID:Tonic block of the sodium and calcium currents by ketamine in isolated guinea pig ventricular myocytes. 959 21

Sixteen colts were premedicated with acepromazine and anaesthesia was induced with detomidine and ketamine. Ponies were randomly allocated to receive halothane (HAL) or infusion of detomidine, ketamine and guaiphenesin (DKG) to maintain anaesthesia. Heart and respiratory rate, ECG, mean arterial blood pressure (MABP), cardiac index (CI), blood gases and plasma cortisol, ketamine and guaiphenesin were measured. Surgical castration took place between 45 and 75 min and anaesthesia lasted 90 min. MABP with DKG was significantly higher than with HAL, and, with HAL, MABP increased from pre-surgery (64 +/- 6 mmHg) to mid-surgery (80 +/- 5 mmHg) but did not change with DKG. At 30 min, CI was similar in both groups (57 +/- 7 ml/kg bwt/min); it decreased during surgery with HAL and remained low, but it increased slightly with DKG, and was higher than with HAL at 60 and 90 min. Plasma cortisol decreased in both groups until 40 min then increased with HAL only during surgery. Ketamine concentration reached a plateau (1.3-1.8 microg/ml) between 20 and 90 min and guaiphenesin concentration between 60 and 90 min (99-101 microg/ml). Recovery was generally smooth in both groups. This study demonstrated that during HAL the increase in blood pressure associated with surgical stimulus is accompanied by decreased CI; this did not occur during DKG which is likely to lead to better tissue perfusion than HAL. The adrenocortical activity seen during HAL was absent during DKG which may result from pituitary depression, analgesic effects of total intravenous anaesthesia (TIVA) or better perfusion.
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PMID:Cardiovascular effects of surgical castration during anaesthesia maintained with halothane or infusion of detomidine, ketamine and guaifenesin in ponies. 970 13

This study evaluated if adding low-dose ketamine to fentanyl could offer a haemodynamically stable drug combination with little respiratory side-effects. Eight healthy, consenting male volunteers received in a random, cross-over and double-blind fashion both fentanyl 2 micrograms.kg-1 + ketamine 0.25 mg.kg-1 and fentanyl 2 micrograms.kg-1 + placebo. The fentanyl and placebo reduced minute ventilation, alveolar ventilation and oxygen consumption (p < 0.05), with little effect on haemodynamics. After fentanyl and ketamine, the decrease in minute ventilation and alveolar ventilation was attenuated compared to the placebo-containing combination (p < 0.05), but with a simultaneous increase in oxygen consumption (p < 0.05) and stimulation of haemodynamics (p < 0.05). Both treatments decreased oxygen saturation and arterial oxygen pressure similarly. Ketamine thus attenuated the fentanyl-induced reduction in ventilation without preventing the decrease in blood oxygenation. In conclusion, combining low-dose ketamine to fentanyl offers no benefits in terms of preventing respiratory depression.
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PMID:The effect of low-dose ketamine on fentanyl-induced respiratory depression. 989 40

We examined the role of N-methyl-D-aspartate (NMDA) receptors in chronic (pathological) pain in humans by using the NMDA receptor antagonist ketamine as a probe. Thirty patients with neuropathic pain in the trigeminal area were given an i.m. injection of ketamine 0.4 mg/kg combined with midazolam 0.05 mg/kg. Pethidine 1.0 mg/kg served as a control. Three different response patterns were observed. Ketamine caused a long-term (6-24 h) analgesic effect partly dissociated from the mental side effects in 8 of the 26 patients who completed the study; these patients also had a slight analgesic effect of pethidine. In nine patients, ketamine caused a short-lasting (<2 h) analgesic effect closely associated with the mental side effects, whereas pethidine caused little or no analgesia. The remaining nine patients did not experience any reduction of pain after either drug in spite of characteristic side effects. One week after the i.m. challenge the patients received either 4.0 mg/kg ketamine hydrochloride or placebo capsules to be taken orally as a nightly dose for three consecutive nights. Five of the eight patients who had a long-term analgesic effect of the i.m. challenge reported decreased pain on days after ketamine. None of the others reported an analgesic effect. The phenomenon of long-term depression of pain in a subgroup of patients was thus confirmed when ketamine was given p.o. These findings indicate that NMDA receptors are involved in the perception and maintenance of pathological pain in some patients. In others, pain appears to be mediated by NMDA receptor-independent mechanisms. We suggest that NMDA receptor-independent transmission in central pain pathways may contribute to the reduced efficiency of analgesic drugs often seen in chronic pain states.
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PMID:Prolonged analgesic effect of ketamine, an N-methyl-D-aspartate receptor inhibitor, in patients with chronic pain. 1021 88

The effect of the AMPA antagonist NBQX (10 microM), NMDA antagonist ketamine (100 microM) and 5-HT1A agonist 8-OH-DPAT (1, 10 and 100 microM) on the properties of a KCl-induced spreading depression (SD) was studied in parietal cortical slices of adult rats. Whereas NBQX did not significantly affect the SD, ketamine significantly (p < 0.01) reduced the amplitude of the first SD peak (12.8 +/- 4.6 mV) and blocked the second SD peak when compared with the controls (19.8 +/- 5.2 mV and 25 +/- 5 mV, respectively). Ketamine also decreased the SD duration at half maximal amplitude from 34.9 +/- 12.4 s to 22.2 +/- 12 s (p < 0.05). 8-OH-DPAT attenuated the duration of the SD from 42 +/- 15.6 s to 21.2 +/- 10.6 s (p < 0.05, 100 microM). These data indicate that not only NMDA receptor blockade, but also activation of the 5-HT1A receptor attenuates the SD and may be beneficial in the reduction of ischemic injury following focal cerebral ischemia.
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PMID:Effects of ionotropic glutamate receptor blockade and 5-HT1A receptor activation on spreading depression in rat neocortical slices. 1057 86

Migraine aura is probably caused by cortical-spreading depression. No treatment for acute and severe migraine aura has been described previously. The effect of ketamine (25 mg intranasally) was studied in 11 patients with severe, disabling auras resulting from familial hemiplegic migraine. In five patients ketamine reproducibly reduced the severity and duration of the neurologic deficits, whereas in the remaining six patients no beneficial effect was seen. Ketamine offers, for the first time, a possible treatment option for severe and prolonged aura.
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PMID:Aura in some patients with familial hemiplegic migraine can be stopped by intranasal ketamine. 1089 26

In this study, anesthesia levels obtained with tiletamine-zolazepam (TZ) and ketamine-midazolam (KM) with or without xylazine (X) were compared in rabbits. Reflexes (corneal, palpebral and withdrawal), blood parameters (PaO2, PaCO2, pH and ions HCO3-), cardiovascular function (heart rate and mean arterial blood pressure) and body temperature were evaluated before and after the injections of the anesthetic combination in the same rabbits (n = 10). With KM and TZ, no suppression of reflexes occurred. The body temperature and pH decreased and HCO3- increased similarly to KMX et TZX. Some physiological and blood parameters were less (PAM, PaCO2) and not (PaO2) affected comparatively to KMX et TZX. These protocols were of short duration of action and did not offer any anesthesia or analgesia. Therefore, their utilization should be restricted to short procedures where no painful manipulations are performed. Ketamine-midazolam-xylazine and tiletamine-zolazepam-xylazine on the other hand are indicated for interventions that require anesthesia. With these combinations, all reflexes were absent for 30-45 and 60-90 min following injections of KMX et TZX, respectively. However, these combinations induce cardiac depression, as well as a decrease of all measured blood parameters and body temperature and a reduction of PaO2. Supplementation with oxygen is recommended with the introduction of xylazine in the protocol.
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PMID:[Anesthesia of the New Zealand rabbit using the the combination of tiletamine-zolazepam and ketamine-midazolam with or without xylazine]. 1142 77


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