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 effects of +/- ketamine were tested on the excitability of frog sciatic nerves using a sucrose gap apparatus and skeletal muscle fibers using intracellular microelectrodes. When applied extracellularly by perfusion, ketamine depressed the action potential of sciatic nerves in a dose-dependent manner. This depression was partially antagonized by the simultaneous treatment with a small concentration of naloxone. However, when the ketamine was applied intracellularly by placing it in a compartment with a cut end of the nerve, only very small and inconsistent decreases were produced. Ketamine also blocked excitability in skeletal muscle by depressing the sodium conductance (gNa). This also could be partly antagonized by the addition of a small concentration of naloxone to the solution bathing the muscle. These results support previous findings by other workers that ketamine has a stereospecific opioid agonist effect in addition to its other actions.
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PMID:Opioid effects of racemic ketamine on the excitability of sciatic nerve and skeletal muscle fibers of the frog. 262 89

Ketamine (0.3 mg/kg) administered intravenously to 12 halothane anesthetized horses caused a significant respiratory depression during ten minutes when respiration was spontaneous. Significant hemodynamic effects were not observed except for cardiac index. Clinical application was also discussed.
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PMID:[Circulatory and respiratory effects of ketamine in horses anesthetized with halothane]. 296 32

The cardiopulmonary consequences of diazepam (0.5 mg/kg, IV) followed by ketamine (10 mg/kg, IV) were evaluated in 11 dogs. Diazepam did not exhibit a tranquilizing effect and was frequently associated with excessive excitement. It produced minimal cardiopulmonary effects, except for a significant increase in heart rate. Ketamine administration was associated with less cardiovascular stimulation when administered after diazepam than it did when administered alone; the respiratory depression was greater. Compared with ketamine alone, the diazepam-ketamine combination was associated with more vomition, less muscle hypertonus, less seizure activity, and less salivation.
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PMID:Cardiovascular changes in dogs given diazepam and diazepam-ketamine. 308 35

Six healthy, consenting volunteer males received ketamine iv in five logarithmically scaled doses totaling 3 mg/kg on three occasions each. The sessions differed only in the initial injection of an unknown drug: placebo, morphine sulfate 0.2 mg/kg, or morphine sulfate 0.4 mg/kg. Initial and terminal steady-state ventilatory responses to CO2 (VERCO2) and isohypercapnic ventilation (end-tidal CO2 49.8 +/- 2.4 mmHg) during drug administration assessed CO2-mediated ventilatory drive. Oxygen concentration of 40% ablated hypoxic drive contribution. Morphine caused a decrease of isohypercapnic ventilation (VE) of 8.2 +/- 1.2 l/min after 0.2 mg/kg. Doubling the dose to 0.4 mg/kg gave a further depression of 6.6 +/- 1.8 l/min. No subject lost consciouness after morphine. Over a dose range of 0.39 to 3.0 mg/kg ketamine caused log-linear dose-related depression of 1.6 +/- 0.3 l/min for each doubling of dose, although the first significant depression of 4.9 +/- 1.1 l/min did not occur until the third dose (1.1 mg/kg) in the absence of morphine. All subjects were unconscious after 1.8 mg/kg ketamine. Slopes of the VERCO2 did not differ from control, regardless of the pretreatment, placebo, or morphine in the two doses. Ketamine alone, 3.0 mg/kg, caused a displacement of VERCO2 of +2.0 +/- 1.2 mmHg in CO2, while combination of ketamine and morphine in either dose caused a +10 mmHg displacement of VERCO2. Thus, ketamine appears qualitatively similar but less potent than premedicant doses of morphine in depressing respiration despite near equipotency in producing loss of consciousness.
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PMID:Respiratory interactions of ketamine and morphine. 310 49

Ketamine was the normal anaesthetic drug for carrying out the baths of severely burnt patients. It was compared with propofol in a study of 50 patients (greater than 50 UBS) randomly assigned to two groups: 2.5 mg . kg-1 propofol and 2 mg . kg-1 ketamine. The speed of induction was the same for both groups, surgery beginning within the same time intervals. In the propofol group, however, apnoea was seen more often and lasted longer (p less than 0.05) than in the ketamine group. The times between repeat injections were short (about 5 min) and constant with propofol, whereas they were larger and irregular with ketamine; this was due to the shorter distribution half-life and lack of accumulation of propofol. During anaesthesia with propofol, haemodynamic parameters remained steady after an initial period of cardiovascular depression. Respiratory rate increased, because of the lack of analgesia. Recovery was very quick, complete and with no bothersome adverse effects in the propofol group. These hypercatabolic patients could therefore be fed early postoperatively; also, there was no deleterious psychological interference in these deeply disturbed patients.
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PMID:[Comparative trial of propofol and ketamine in anesthesia for the baths of severely burnt patients]. 330 50

Ketamine 4 micrograms/kg/minute produced pain relief similar to that from morphine 33 micrograms/minute in a double-blind study that compared analgesia from constant-rate intravenous infusions of the two drugs in 60 patients. The analgesic efficacy of the infusions, as assessed by pain scores and the requirement for supplementary self-administered morphine, was poor. Ventilatory depression, the most significant side effect, occurred only in patients who received morphine infusion. The low dose ketamine infusion did not provide clinically useful analgesia even though adequate plasma concentrations were achieved.
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PMID:Analgesia from morphine and ketamine. A comparison of infusions of morphine and ketamine for postoperative analgesia. 331 43

Ketamine (KET)-induced blockade of cortical spreading depression (CSD) was examined in rats (n = 51) anesthetized with pentobarbital (50 mg/kg). CSD was elicited by intracortical injection of 1 microliter of 0.15 mol/l potassium acetate 10-40 min after i.p. injection of 6-50 mg/kg KET. KET was almost ineffective at 6 mg/kg but prevented CSD propagation at 12 mg/kg and at higher dosages. The blockade was maximal 20 min after injection. Terminal anoxic depolarization elicited by N2 breathing developed in control rats after a latency which was not significantly different from that in rats pretreated with 50 and 100 mg/kg KET. The failure of CSD blocking dosages of KET to delay the onset of terminal anoxic depolarization indicates that excitotoxic amino acids play different roles in the mechanism of the anoxia-elicited and CSD-related autoregenerative ionic shifts.
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PMID:Systemic ketamine blocks cortical spreading depression but does not delay the onset of terminal anoxic depolarization in rats. 343 42

Ketamine and xylazine used in combination have been shown to be effective, easily administered, cost efficient agents for surgical anesthesia in the rabbit. The effect of xylazine on the central nervous system has been shown to be mediated through alpha-2 adrenergic receptors. Yohimbine, an alpha-2 adrenergic antagonist has been shown to reverse xylazine induced depression and partially antagonize ketamine in other species. We evaluated the antagonistic effect of yohimbine on ketamine/xylazine anesthesia in the rabbit. Six New Zealand White rabbits were anesthetized with intramuscular ketamine (50 mg/kg) and xylazine (10 mg/kg) to establish baseline parameters including respiratory rate, heart rate, and palpebral, pedal and postural reflex activity. Fourteen days later each rabbit was subjected to the same anesthetic regimen followed 30 minutes later by the intravenous administration of yohimbine (0.2 mg/kg). The duration of anesthesia estimated by the time elapsed between the loss and return of the palpebral reflex was reduced in the yohimbine treated trial (means = 29.7 +/- 1.9 minutes) compared to the control trial (means = 67.0 +/- 13.5 minutes). The palpebral reflex returned within 5 minutes following yohimbine treatment. Our results indicated that yohimbine is an effective antagonist of ketamine/xylazine anesthesia in the rabbit. Yohimbine decreases anesthetic duration after intravenous administration and also may aid in the control of undesirable anesthetic effects and overdosage.
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PMID:Reversal of ketamine/xylazine anesthesia in the rabbit with yohimbine. 366 1

Thirty-four patients of ASA physical status I or II scheduled for gall bladder surgery were studied in a comparative prospective trial to evaluate the efficacy of epidural and intramuscular ketamine for postoperative pain relief. They were divided randomly into three groups. Group I (11 patients) received 30 mg intramuscular ketamine. Group II (10 patients) and Group III (13 patients) received 10 and 30 mg ketamine in 10 ml saline respectively, through epidural catheters. Pain was evaluated every two hours for the first 24 hours post-operatively by using a linear analogue pain scale from 0-10. Ketamine was given on the patient's request and whenever the pain score exceeded three. Ketamine produced analgesia in all patients studied. The reduction of pain score after two and four hours in Group I and III was significant when compared to Group II. Seven patients (54 per cent) in Group III did not require further analgesia after the initial injection. However, following 10 mg epidural ketamine or 30 mg IM ketamine, post-operative pain was more frequent. Four patients who received epidural ketamine complained of transient burning pain in the back during injection. No patient developed respiratory depression, psychic disturbance, cardiovascular instability, bladder dysfunction or neurologic deficit. It is concluded that 30 mg epidural ketamine is a safe and effective method for postoperative analgesia.
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PMID:Epidural ketamine for postoperative analgesia. 394 42

Avoidance of ketamine has been recommended in children with pulmonary hypertension or with limited right ventricular reserve, despite absence of data about the effects of ketamine on pulmonary vascular resistance (PVR) in children. Ketamine has been associated with increased PVR in studies of adults; in these studies adults were spontaneously breathing through unprotected airways, despite ketamine's known effects of ventilatory depression and partial loss of airway. The authors measured pulmonary and systemic hemodynamic responses to ketamine during spontaneous ventilation in 14 intubated infants who were receiving minimal ventilatory support with an intermittent mandatory ventilation (IMV) of 4 at an FIO2 of 0.3-0.4. No significant changes were found in cardiac index (CI), pulmonary vascular resistance index (PVRI), or systemic vascular resistance index (SVRI) in a group of seven infants with normal PVRI or in another group of seven infants with preexisting increased PVRI. Results did not differ in infants receiving diazepam sedation. The authors conclude that ketamine has little effect on baseline hemodynamics in mildly sedated infants whose airway and ventilation are maintained; in particular, PVRI is little changed by ketamine administration in ventilated infants with either normal or increased baseline PVRI.
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PMID:Pulmonary and systemic hemodynamic responses to ketamine in infants with normal and elevated pulmonary vascular resistance. 397 14


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