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)

Thirty elderly patients undergoing major hip surgery under spinal analgesia were randomly allocated in a double-blind manner into three groups. The aim was to evaluate the influence of intrathecal morphine and postoperative naloxone infusion on the regulation of ventilation. The Bupivacaine Group received spinal analgesia with 20 mg bupivacaine intrathecally. The Morphine Group received spinal analgesia with 20 mg bupivacaine + 0.3 mg morphine intrathecally. The Naloxone Group received spinal analgesia with 20 mg bupivacaine + 0.3 mg morphine intrathecally + postoperative naloxone infusion intravenously (1 microgram/kg/h over 12 h, 0.25 micrograms/kg/h over the next 12 h). Evaluation of resting ventilation and the ventilatory responses to hypercarbia and hypoxaemia was made on three occasions: before surgery, and 8, and 24 h after the intrathecal injection. Intrathecal morphine had no significant effect on ventilatory regulation in elderly patients undergoing major hip surgery performed under bupivacaine spinal analgesia. Postoperative administration of opioids or sedatives after intrathecal morphine as well as postoperative blood loss associated with a fall in blood pressure appeared to increase the risk of developing respiratory depression. Naloxone infusion seemed to reduce the risk of developing respiratory depression. Furthermore, one third of the elderly had a poor response to hypoxaemia before surgery.
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PMID:Influence of intrathecal morphine and naloxone intervention on postoperative ventilatory regulation in elderly patients. 163 66

A total of 88 somatosensory neurones were recorded from n. anterodorsalis, n. anteroventralis, n. lateralis dorsalis, n. lateralis posterior and n. centralis lateralis of rabbit thalamus. Among the 88 neurones, 50 were noxious-excited (convergent, n = 36; non-convergent with long latency responses, n = 14), 23 noxious-inhibited and 15 non-convergent neurones with short latency responses that were activated by innocuous stimuli only. Iontophoresis of etorphine predominantly depressed the late burst of the response to strong sural nerve stimulation in convergent neurones (25/26), the depression being readily blocked by iontophoresis of naloxone (16/16). After naloxone, the late burst was occasionally larger than that before etorphine. Etorphine depressed non-convergent neurones with long latency responses (13/13), but had no marked effects on non-convergent neurones with short latency responses. On the noxious-inhibited neurones, etorphine could enhance the inhibitory response when it was weak prior to drug administration (12/12). Contrary to etorphine, naloxone could block the inhibitory response when it was administered either iontophoretically (15/15) or intravenously (4/4). Naloxone could enhance the weak late burst of the evoked response in convergent neurones (2/2). Similarly to etorphine, electroacupuncture depressed noxious-excited neurones, convergent (18/18) and non-convergent neurones with long latency responses (6/6), the depression being blocked by naloxone (16/16). The results suggest that noxious inputs may activate the release of opioid peptides onto opiate receptors, the interaction of which mediates the modulation of thalamic nociceptive transmission.
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PMID:Effects of iontophoretic etorphine and naloxone, and electroacupuncture on nociceptive responses from thalamic neurones in rabbits. 164 66

In the present study, the effects of microiontophoretically applied U-50488 on the spontaneous discharge of respitation related units (RRUs) in nucleus ambiguus or rats were observed. Of 96 RRUs recorded, U-50488 produced depressant effect on 51 units, excitative effect on 11 units, excitation followed by depression on 6 units, depression followed by excitation on 3 units. The remaining 25 units were not influenced. Naloxone administered iontophoretically not only blocked U-50488-induced depression in 12 out of 16 units, but also blocked U-50488-induced excitation in 2 units. Duration of the depression produced by U-50488 was remarkably longer than that of excitation. The result suggested that kappa receptor might be involved in respiratory regulation and that the subtype of opiate receptors which mediates depression and excitation effect might not be the same.
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PMID:[Effects of microiontophoretically applied U-50488 on the spontaneous discharges, of respiration related units (RRUs) in the region of nucleus ambiguus or rat]. 164 94

Naloxone-depending potentiation of morphine antinociception by some non-opioidergic compounds between different classes of drugs was found in experiments on mice using nociceptive stimuli of different modality. This potentiation can or cannot be bound with elevation of sensitivity of opioid receptors, release of endogenous opioids or destruction of blood-brain barrier function mor morphine peripheral administration. This potentiation named as "release of functional reserve of opioid antinociceptive response" can or cannot be accompanied by an increase of breathing function depression. Taking into account the data of literature about the dissociation of analgetic positive-supporting morphine effects and also the capability of some compounds to lower the narcogenic opiates potential, the supposition about the real possibility of creating combined drugs is made.
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PMID:[Pharmacological regulation of opioidergic antinociceptive mechanisms]. 166 49

Self-aggression is a behavioural disorder in which an individual damages its own body parts by intense biting or scratching. Self aggression has been reported in human patients in Lesch-Nyhan syndrome and in cases of schizophrenia, depression, and congenital analgesia. In human patients as well as in experimental animals some kind of dysesthesia of the part of the body that is mutilated has been suggested. This study was conducted to find out the underlying pain mechanisms in self-aggressive behaviour arising out of stereotypy. The study was performed in 40 adult male rats. In all these animals, self-aggression was produced as part of amphetamine induced stereotyped behaviour. A predetermined scale was used for quantifying this behaviour. Reserpine and phenoxybenzamine pretreatment led to an increase in the incidence of self-aggression. Naloxone administration in reserpine pretreated animals led to a further significant increase in the incidence of self biting as compared to controls. From these studies it appears that self-aggressive behaviour may be associated with increased pain sensation.
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PMID:Role of opioid receptors in self-aggression in rats. 166 47

The cardiovascular and respiratory effects of dermorphin (D) have been evaluated in freely moving or anesthetized normotensive and spontaneously hypertensive male rats. Intravenously or intracerebroventricularly administration of D produced arterial hypotension with sinus bradycardia and respiratory depression. Naloxone antagonized the effects of D. Atrial natriuretic antipeptide IgG reduced the cardiovascular responses without any significant modification of respiratory response. ICI 174864, naloxonazine and binaltorphimine did not reduce the cardiovascular and respiratory effects. In hypertensive rats D produced more intense and longer cardiovascular effects than those seen in normotensive animals. D effects involve the activation of mu and k opioid receptors for cardiovascular responses and mu 2 opioid receptors for respiratory depression without any significant effect on delta receptors. The release of atrial natriuretic peptide also appears to be involved in the cardiovascular effects of D.
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PMID:Cardiovascular and respiratory effects of dermorphin in rats. 167 73

In anesthetized, artificially ventilated cats, pretreated with the muscarinic antagonist scopolamine, the effect of naloxone on the efficacy of nicotinic transmission in the superior cervical ganglion was used as a test of endogenous opioid release by the preganglionic axons. The cervical sympathetic trunk (CST) was split into two bundles. The compound action potential (CAP), evoked by supramaximal low-frequency stimulation (0.25 Hz) of one CST bundle, was recorded from a postganglionic nerve of the superior cervical ganglion. Partial block with hexamethonium was used to reduce the 'safety factor' of nicotinic transmission. A conditioning train (5 Hz, 40 s, supramaximal) to the other CST bundle (heterosynaptic conditioning) inhibited the CAP. At the peak of the inhibition the CAP was attenuated by 51 +/- 4%. Recovery was 90% complete in 201 +/- 28 s. The inhibition was antagonized in a dose-dependent manner by i.v. naloxone with an apparent IC50 of 60 +/- 12 micrograms/kg. The maximum effect obtained with naloxone was an 80% decrease in the magnitude of the inhibition. Magnitude and duration of the heterosynaptic inhibition were related to frequency, duration and intensity of the conditioning train. Naloxone-sensitive inhibition was observed with frequencies of the conditioning train as low as 0.5 Hz. A train (5 Hz, 40 s) to the postganglionic nerves produced a naloxone-insensitive depression of the orthodromic test CAP which was of smaller amplitude and duration than when the conditioning train was applied to the preganglionic axons.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Naloxone-sensitive inhibition of nicotinic transmission in the superior cervical ganglion of the cat. 167

The administration of narcotics in the subarachnoid or the epidural space is gaining acceptance for postoperative pain relief. However, the potential side effects of intrathecal and epidural use of opioids are the following: early and late respiratory depression, pruritus, nausea and vomiting, urinary retention. Early respiratory depression is low and may occur 6 or 12 hours after the epidural narcotics injection. Many factors contribute to the delayed phase of breathing disorders and a close respiratory monitoring is needed during at least 24 hours after epidural morphine injection. Naloxone can be used to reverse the depression. Pruritus can occur in 10 to 30% of patients receiving morphine; 10 to 30% nausea and vomiting, and urinary retention occurs in 20 to 50% of patients.
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PMID:[Secondary effects of opioids administered by the regional route]. 167 73

1. In decerebrated rabbits, repetitive stimulation of the high-threshold afferents of the left common peroneal (CP) nerve evokes prolonged depression of the sural-gastrocnemius medialis (GM) reflex recorded in the same limb. This inhibition is antagonized by co-administration of the opioid antagonist naloxone with the alpha 2-adrenoceptor antagonist idazoxan. The present study was designed to investigate whether such inhibition could be elicited from the contralateral hindlimb or the forelimbs. 2. The sural-GM reflex of decerebrated rabbits was depressed for more than 15 min after stimulation of either ipsilateral or contralateral common peroneal (CP) or median nerves with 500 pulses of 20 V, 1 ms given at 5 Hz. The order of efficacy for generating this inhibition was ipsilateral CP greater than contralateral CP greater than or equal to ipsilateral median = contralateral median. In three of thirty-nine rabbits, stimulation of the median nerves caused facilitation of the sural-GM reflex. 3. Idazoxan (1-2 mg/kg I.V.) did not significantly alter the depressant effect of ipsilateral CP stimulation but reduced that evoked by either median nerve and almost abolished the inhibition evoked from the contralateral CP nerve. 4. Naloxone (0.25 mg/kg I.V.) reduced the effects of ipsilateral CP stimulation, did not alter the inhibition evoked from contralateral CP, and had equivocal actions on the responses to median nerve stimulation. 5. When given together, the two antagonists almost abolished the effects of stimulating the median nerves and the contralateral CP nerve, and markedly reduced the inhibition evoked from the ipsilateral CP nerve. 6. These data show that prolonged inhibition of the sural-GM reflex can be evoked by stimulation of nerves in all four limbs and that in each case the inhibition can be blocked or reduced by co-administration of antagonists to opioid and alpha 2-adrenergic receptors. Such persistent inhibition of reflexes may serve to inhibit withdrawal reflexes in situations where interruptions to normal movement would be disadvantageous.
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PMID:Prolonged inhibition of a spinal reflex after intense stimulation of distant peripheral nerves in the decerebrated rabbit. 167 55

A case of respiratory depression which occurred following administration of epidural meperidine during Caesarean section is described. Epidural meperidine, 75 mg (10 mg.ml-1) was given after delivery of the infant to provide postoperative analgesia. Oxygen desaturation (SaO2 90%) and a decrease in respiratory rate (4.min-1) were noted 30 min after epidural meperidine was administered. Naloxone, 0.1 mg, was given iv which resulted in prompt improvement in both respiratory rate and oxygen saturation. Vascular absorption of meperidine from the epidural venous plexus is the most probable explanation for this case of early respiratory depression. We recommend a maximum bolus dose of 50 mg of epidural meperidine for pain management after Caesarean section. It is also important to monitor oxygen saturation continuously during the intraoperative period, and to monitor the patient closely in the recovery room for at least one hour for evidence of respiratory depression.
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PMID:Early respiratory depression during caesarean section following epidural meperidine. 173 38


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