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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A nationwide follow-up survey was undertaken to study the use of extradural and intrathecal opioids in the management of pain, to estimate the incidence of delayed ventilatory depression and to study post-injection surveillance routines. A questionnaire was sent to all 93 anaesthetic departments in Sweden; 96% responded. The major indication for using extradural opioids was the treatment of postoperative, traumatic and cancer pain. During 1984 over 14,000 patients received extradural, and over 1100 patients intrathecal, opioids. Morphine was the predominant opioid for extradural administration and was used in 96% of patients. Extradural opioid analgesia constitutes about 25% of all extradural blocks performed in Sweden. Pruritus and urinary retention were considered as minor problems; however, the risk was considerably higher after intrathecal morphine. The incidence of delayed ventilatory depression was about 1:1100 (0.09%) following extradural morphine and 1:275 (0.36%) following intrathecal morphine. Risk factors for delayed ventilatory depression are discussed. Administration of extradural morphine for postoperative pain relief in patients undergoing major surgery is considered a high benefit-low risk technique by most Swedish anaesthetists. The results of the present nationwide survey suggests that, following extradural morphine, surveillance of patients for more than 12 h appears unnecessary.
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PMID:Present state of extradural and intrathecal opioid analgesia in Sweden. A nationwide follow-up survey. 288 44

The high-affinity mu-1 opioid binding site has been implicated in some opioid responses (e.g., supraspinal analgesia) but not others (e.g., respiratory depression) by comparing the actions of naloxone, a short-acting, non-selective antagonist, and naloxonazine, an irreversible and selective mu-1 antagonist. The mu-1 site has been implicated in the opioid component modulating free feeding and deprivation-induced feeding, but not glucoprivic feeding. The present study compared naloxone and naloxonazine antagonism of hyperphagia induced by morphine, ethylketocyclazocine (EKC), dynorphin and d-ala2,d-leu5-enkephalin (DADL) in rats. Morphine produced a dose-dependent (0.01-5 mg/kg) hyperphagia in mildly food-deprived rats that was blocked by naloxone (0.01-10 mg/kg). Naloxonazine (10 mg/kg) shifted the morphine hyperphagia dose-response curve to the right. These effects could not be fully accounted for by the intrinsic hypophagic properties of these antagonists. EKC produced a dose-dependent (0.5-5 mg/kg) hyperphagia which was blocked by naloxone (10 mg/kg) only at low effective EKC doses. Naloxonazine (10 mg/kg) failed to affect EKC hyperphagia. Naloxone, but not naloxonazine also blocked dynorphin and DADL hyperphagia. These results indicate that feeding induced by opiate and opioid agonists are differentially mediated by the mu-1 and other opioid binding sites; these data contrast with the modulation by the mu-1 site of the supraspinal analgesia induced by each of these agonists.
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PMID:Differential sensitivity of opioid-induced feeding to naloxone and naloxonazine. 289 39

Pain is a complex somato-psychic experience, and all pains do not respond equally to opioid analgesics. Muscle and deafferentation pains are best eased by alternative treatments. Bone pain responds best to the combined use of morphine and an NSAID. Nerve compression often necessitates the concurrent use of a corticosteroid. Few patients need neurolytic or neuro-ablative procedures. Opioid use is governed by three key principles: "By the mouth," "by the clock," and "by the ladder." Morphine remains the strong opioid of choice for most patients. Respiratory depression is not a problem, nor is tolerance. Addiction (psychological dependence) does not occur in patients with opioid responsive pains.
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PMID:The management of pain in cancer: a guide to drugs and dosages. 290 83

o-Iodosobenzoic acid (IBA), in a surfactant micellar medium, is a rapid and efficient catalyst for the hydrolysis of organophosphate (OP) esters. Since little is known about the toxicity of IBA, a primary screen of neurobehavioral toxicity was evaluated in male ICR mice. IBA was administered intraperitoneally in a pH 7.4 phosphate buffer solution containing 8% dimethylformamide. The predominant overt signs of toxicity included an immediate and transient writhing reflex and/or persistent spasmodic myotwitching of the abdomen, and conspicuous suppression of orienting/exploratory behavior and emotional defecation. The dose ranges for ED50 of writhing response, suppression of rearing and spontaneous motor activity overlapped at levels of about one-tenth the acute LD50, 742 (633-856) mumol/kg, being 94.9 (74.5-122.5), 69.8 (47.9-105.4) and 71.1 (49.9-101.3) mumol/kg, respectively; the dose ranges for ED50 of abdominal myotwitching and depression of emotional defecation in a novel environment also overlapped but at levels of about one-fifth the acute LD50, being 138.4 (115.3-167.2) and 146.2 (110.7-196.3) mumol/kg, respectively. Morphine (1.25-10 mg/kg s.c.) antagonized the IBA-induced writhing response and abdominal myotwitching in a dose-dependent manner, with a PD50 of 4.2 and 4.9 mg/kg, respectively. The present report demonstrates that acute intraperitoneal administration of IBA produces an intriguing, non-specific behavioral syndrome, probably resulting from nociceptive stimulation. This implies that IBA might be irritating to the skin and mucosa.
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PMID:Ortho-iodosobenzoic acid: its acute toxicity and neurobehavioral effects in mice. 291 7

Water-deprived rats were given a daily opportunity to take water or an ethanol solution. Prior to some opportunities to drink, some were injected with morphine (across procedures either 2.0, 7.5, or 20.0 mg/kg), diprenorphine (from 0.001 to 10.0 mg/kg), or a combination of diprenorphine and morphine. The small dose of morphine increased intake of alcoholic beverage and the large dose decreased intake, confirming previous observations. Diprenorphine, across a wide range of doses, increased intake of ethanol solution. Morphine and diprenorphine together produced more intake than either given alone. Diprenorphine reversed the depressing effects of large doses of morphine on intake of ethanol solution. Since diprenorphine is an antagonist with respect to opioid analgesia and behavioral depression and an agonist with respect to intake of alcoholic beverages, and since it potentiates the small dose morphine effect, it is concluded that only some effects of morphine are related to opioid-potentiation of intake of alcoholic beverages.
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PMID:Morphine and diprenorphine together potentiate intake of alcoholic beverages. 303 77

The literature regarding the intrathecal use of morphine, baclofen, and midazolam to treat spasticity is reviewed. Nine patients with significant spasticity due to different etiologies were treated. Morphine and midazolam decreased spasticity but did not change the patient's functional status. Baclofen improved patient status, but was associated with significant CNS depression in two cases.
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PMID:Intrathecal application of drugs for muscle hypertonia. 304 64

The usefulness of physostigmine in reversing post-narcotic depression after general anaesthesia is well proven; so is that of naloxone, a specific opioid analgetics antagonist, in reversing neuroleptic anaesthesia effects. Morphine-like analgetics are widely used as premedication agents, too; on the other hand, physostigmine reverses opioids as well as other psychotropic and narcotic agents. For that reason, positive post-narcotic physostigmine effects could be due to its anti-opioid potency as well. In a double-blind, randomised study, physostigmine and naloxone were evaluated using a clinically based vigilance protocol, and compared with saline solution. Naloxone did not have remarkable advantages as compared with placebo, while physostigmine led to a significantly higher level of vigilance; moreover, that level was reached sooner. The positive effects of physostigmine in restoring a sufficient level of vigilance after general anaesthesia are, in respect of our findings, unrelated to its antagonism to morphine-like analgetics.
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PMID:[Pharmacologic modification of vigilance in the postnarcotic phase-- naloxone or physostigmine?]. 305 53

The authors studied the respiratory and analgesic effects of nalbuphine (0.21 mg/kg, intravenous), naloxone (0.014 mg/kg, intravenous), and placebo (normal saline) when given after morphine (0.21 mg/kg, intravenous) in a double-blind, randomized fashion. Resting end-tidal CO2 (PETCO2), ventilatory and occlusion pressure responses to CO2 rebreathing, and pain threshold were measured in 12 healthy adult volunteers before, 5 min, and 30 min after morphine. Nalbuphine, naloxone, or saline were administered 55 min after morphine, and the above measurements were repeated 5 min later (60 min after morphine) as well as 90, 120, 180, and 240 min after morphine. Whereas naloxone reversed respiratory depression as measured by all three respiratory parameters, nalbuphine either further depressed (resting PETCO2) or did not affect (ventilatory and occlusion pressure responses to CO2 rebreathing) respiratory drive. Morphine produced a significant elevation of the pain threshold. Significant decreases in the pain threshold were seen only after naloxone. Saline and nalbuphine did not significantly alter the pain threshold. The data indicate that nalbuphine may not reliably antagonize moderate doses of morphine.
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PMID:Failure of nalbuphine to antagonize morphine: a double-blind comparison with naloxone. 308 51

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

In postoperative patients using patient-controlled analgesia (PCA) to administer i.v. doses of morphine sulfate, respiratory rates and subjective rankings of pain, sedation, and liking for the drug were correlated with plasma morphine concentrations. In 12 patients selected before surgery, the initial morphine sulfate dose of 0.6 mg/sq m was increased or decreased as needed. Every two hours, cumulative morphine sulfate dose, respiratory rate, and sedation were recorded by the nurse, along with the patient's evaluation of pain and liking for the drug. Plasma was collected in the morning and evening during PCA therapy for morphine analysis. Data were analyzed by analysis of covariance. Dosing rates and rankings of pain, sedation, and liking decreased as a function of time postoperatively, but respiratory rates did not. Sedation and respiratory rates were independent of morphine concentration. Liking of the drug increased directly with plasma morphine concentration but decreased with time. A high level of pain was directly related to morphine use. For all significant relationships, there was high interpatient variability, with the exception of changes in pain rankings induced by morphine. Patients defined a minimum effective plasma morphine concentration of 20-40 ng/mL. The maximum plasma morphine concentration achieved by self-administration was 82 ng/mL. These postoperative patients used patient-controlled analgesia to deliver morphine sulfate i.v. for pain relief, not for euphoria, and did not exhibit sedation or respiratory depression. Morphine was consistently effective at plasma concentrations of 40 ng/mL or greater.
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PMID:Relationship between plasma morphine concentrations and pharmacologic effects in postoperative patients using patient-controlled analgesia. 315 20


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