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)

Several cases of recurrent respiratory depression progressing to apnoea and unconsciousness after apparent recovery from sufentanil have been reported recently. Alfentanil has the shortest elimination half-time of the narcotics used in anaesthesia, suggesting that it should be the least likely to cause postoperative respiratory depression. A case of recurrent unconsciousness and respiratory arrest after apparent recovery from alfentanil-isoflurane-nitrous oxide anaesthesia is reported. A total dose of 137 micrograms.kg-1 alfentanil was given over a 3.25-hr period to a 45-year-old female undergoing partial gastrectomy. Naloxone, 0.16 mg IV, rapidly restored spontaneous ventilation and consciousness. This case demonstrates that apnoea and unconsciousness can also recur after apparent recovery from alfentanil. Recovery room personnel should be aware of this phenomenon. Earlier detection may permit treatment before apnoea occurs. Patients given narcotic-supplemented anaesthesia should be monitored by capnography and/or pulse oximetry in the early postoperative period.
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PMID:Apnoea and unconsciousness after apparent recovery from alfentanil-supplemented anaesthesia. 231 Nov 53

The effects of bovine beta-casomorphin(1-7) (Tyr-Pro-Phe-Pro-Gly-Pro-Ile) on neonatal sleep in rats were studied. The pups received intraperitoneal injections of beta-casomorphin(1-7) (1 mg, 5 mg, 10 mg, 50 mg, or 100 mg/kg) or a corresponding volume of sodium chloride. In any of the doses used, beta-casomorphin(1-7) had no effect on waking. Only 100 mg/kg caused significant changes in sleep: the percentage of quiet state of the total recording time (TRT) increased and the percentage of active sleep decreased. Beta-casomorphin(1-7) did not cause significant respiratory depression. Naloxone pretreatment (1 mg/kg IP) reversed the effects of beta-casomorphin(1-7) on sleep, a finding which suggests that opiate mu-receptors are involved in mediating the sleep effects of beta-casomorphin.
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PMID:Effect of beta-casomorphin on neonatal sleep in rats. 234 85

Clonidine is an antihypertensive agent with central and peripheral alpha-2 adrenergic effects. One of the postulated mechanisms of action is the release of endogenous opioids and/or the stimulation of opioid receptors in the central nervous system (CNS). Naloxone, a pure opioid antagonist, has demonstrated reversal effects from clonidine intoxication. During the past 10 y, 25 children with a mean age of 2 y were admitted for clonidine intoxication. Dosage varied widely, but as little as 0.1 mg caused significant signs and symptoms. The most common presenting findings were somnolence-lethargy (96%), miosis (56%), and respiratory depression (48%), a paradoxical hypertensive response (44%) was more common than expected. Supportive management was the mainstay of therapy. Ten patients received naloxone, 50% demonstrated clinical improvement in vital signs and CNS depression. There were no complications as a result of naloxone therapy. Children seem to be unusually sensitive to the depressant effects of clonidine. Naloxone may be an important adjunct to therapy. Expect clonidine intoxications to become more common as the market for antihypertensive drugs expands.
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PMID:Pediatric clonidine intoxications. 235 31

An epidural catheter was inserted at T9-L2 interspace and 10 micrograms.kg-1 fentanyl with (E+) or without (E-) epinephrine 1:100,000 was given for 82 elective abdominal surgeries. N2O 66%, enflurane and muscle relaxant were used as needed. The onset and the duration of the action were estimated to be approximately 15 minutes and 4 hours, respectively. Anesthesia was maintained with enflurane below 0.4% (0.22 +/- 0.09%) in 70 patients (85.4%). E+ group needed significantly lower concentration of enflurane than E- group. There was no severe hemodynamic change during the operation. Systolic pressure, diastolic pressure and heart rate during the operation were 115.2 +/- 16.0 mmHg, 69.4 +/- 10.8 mmHg and 74.2 +/- 11.4 min-1, respectively, each of which was about 18% less than the values on arrival in the operating room. Sixty-one patients (82.5%) woke rapidly. Almost all patients felt well and had no pain during the recovery period. Naloxone 0.05-4 mg was administered intravenously in 21 patients (31.7%) whose respiratory rate was below 10 min-1. The patients with shorter operation time (shorter than 2.5 hours) needed more naloxone. Troubles of respiratory depression did not occur in the recovery room and in the ward in both naloxone and non-naloxone groups. This anesthesia method which induces mild depression of blood pressure and heart rate may be indicated for patients with ischemic heart disease or with poor cardiac function, but has no advantages in patients with poor respiratory function who need early extubation after a short operation.
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PMID:[Epidural anesthesia with high dose fentanyl for abdominal surgery]. 238 47

During progressive acute cardiac tamponade (CT) in conscious dogs, cardiac output (CO) falls continuously while arterial blood pressure (BP) is well maintained until an abruptly terminal decline. This response is primarily dependent on alpha-adrenergic mechanisms. During hemorrhagic shock, the opioid receptor blocker naloxone increases CO and BP and improves survival perhaps by reversing an opioid-induced cardiovascular depression. We produced 10 episodes of decompensated CT (DCT; 30% decline in BP) by intrapericardial saline infusion (20 ml/min) in five euvolemic conscious dogs. CT resulted in a decrease in CO and BP from base line (3.79 +/- 0.37 l/min and 89.6 +/- 5.2 mmHg, means +/- SE) to DCT (1.35 +/- 0.15 l/min and 57.5 +/- 3.1 mmHg; P less than 0.05). Naloxone (3 mg/kg iv) given at the onset of DCT resulted in a prompt sustained return of BP to base-line levels (P less than 0.05) with no change in CO. Four more animals were studied before and during naloxone (3 mg/kg iv then 0.3 mg.kg-1.min-1 iv). DCT occurred at a higher intrapericardial pressure (20.1 vs. 18.3 mmHg; P less than 0.025) if CT were induced during naloxone treatment than in its absence. Thus naloxone during DCT promptly reversed hypotension with no change in CO and, if present during induction of CT, naloxone allowed slightly higher levels of intrapericardial pressure to be tolerated. Further studies are needed to determine whether naloxone produced these effects solely by its actions on opioid receptors. This study suggests that the interaction between opioid and adrenergic influences plays a role in causing hypotension during CT.
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PMID:Influence of naloxone on response to acute cardiac tamponade in conscious dogs. 238 24

The effect of intrathecal (IT) cholecystokinin (CCK), substance P (SP) and morphine (MO) on spinal cord excitability was studied in decerebrate, spinalized rats. CCK had a weaker facilitatory effect on the nociceptive flexion reflex than SP. The possible functional significance of the coexistence of CCK and SP in neurons projecting to the spinal cord was tested by coadministration of the two peptides. At the doses tested no synergistic interaction on the reflex was found with CCK and SP. IT MO caused a brief enhancement followed by a prolonged depression of the reflex. A high dose of CCK injected prior to MO increased the facilitatory effect and decreased the depressive effect of the opiate on the reflex. The effect of desulfated (D) CCK was similar to CCK but at a higher dose. Naloxone (NAL) had a similar effect as CCK when administered prior to MO. The MO-induced depression of the reflex was readily reversed by NAL, but not by CCK. The results indicate that CCK may prevent the inhibitory effect of MO on spinal cord excitability to nociceptive stimulation, but does not reverse it. CCK may alter the balance of excitation-inhibition between various types of dorsal horn interneurons that are involved in the transmission of nociceptive information.
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PMID:Intrathecal cholecystokinin interacts with morphine but not substance P in modulating the nociceptive flexion reflex in the rat. 243 47

Cardiovascular, pulmonary, and behavioral effects of multiple doses of oxymorphone in 10 nonanesthetized, spontaneously breathing, healthy dogs were studied. Oxymorphone (0.4 mg/kg of body weight) was administered IV, and at 20, 40, and 60 minutes after the first injection was given, 0.2 mg of oxymorphone/kg was administered. Cardiovascular and pulmonary variables were measured before (base line) and at 5, 15, 35, 55, 75, 100, 120, 150, 180, 210, 240, 270, and 300 minutes after the first oxymorphone injection. Degree of sedation and behavioral effects also were recorded. Naloxone (0.04 mg/kg, IV) was administered 4.5 hours after the 4th oxymorphone injection, and behavioral changes were recorded. Oxymorphone induced mild respiratory depression. After transient apnea developed, respiratory rate increased to a pant, tidal volume decreased, and minute ventilation increased, but these values were not significantly (P = 0.05) different from base line. The PaCO2, physiologic dead space, and base deficit increased; alveolar tidal volume decreased; and alveolar minute ventilation did not change. The PaO2 decreased, hemoglobin and arterial O2 content increased, and O2 transport did not change. Venous admixture transiently increased. Oxymorphone induced minimal cardiovascular depression. Mean arterial blood pressure, stroke volume, central venous pressure, pulmonary artery pressure, and pulmonary wedge pressure increased. Heart rate decreased, systemic vascular resistance transiently increased, and cardiac output transiently decreased. Because the dogs moved spontaneously, responded to sound with sudden, vigorous movements, and breathed with excessive effort, oxymorphone alone was considered inadequate as a general anesthetic.
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PMID:Oxymorphone: cardiovascular, pulmonary, and behavioral effects in dogs. 244 2

Oxymorphone was administered IV to dogs 4 times at 20-minute intervals (total dosage, 1 mg/kg of body weight, IV) on 2 separate occasions. Minute ventilation, mixed-expired carbon dioxide concentration, arterial and mixed-venous pH and blood gas tensions, arterial, central venous, pulmonary arterial, and pulmonary wedge pressures, and cardiac output were measured. Physiologic dead space, base deficit, oxygen transport, and vascular resistance were calculated before and at 5 minutes after the first dose of oxymorphone (0.4 mg/kg) and at 15 minutes after the first and the 3 subsequent doses of oxymorphone (0.2 mg/kg). During 1 of the 2 experiments in each dog, naloxone was administered 20 minutes after the last dose of oxymorphone; during the alternate experiment, naloxone was not administered. In 5 dogs, naloxone was administered IV in titrated dosages (0.005 mg/kg) at 1-minute intervals until the dogs were able to maintain sternal recumbency, and in the other 5 dogs, naloxone was administered IM as a single dose (0.04 mg/kg). Naloxone (0.01 mg/kg, IV or 0.04 mg/kg, IM) transiently reversed most of the effects of oxymorphone. Within 20 to 40 minutes after IV naloxone administration and within 40 to 70 minutes after IM naloxone administration, most variables returned to the approximate values measured before naloxone administration. The effects of oxymorphone outlasted the effects of naloxone; cardiovascular and pulmonary depression and sedation recurred in all dogs. Four hours and 20 minutes after the last dose of oxymorphone, alertness, responsiveness, and coordination improved in all dogs after IM administration of naloxone. Cardiac arrhythmia, hypertension, or excitement was not observed after naloxone administration.
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PMID:Naloxone reversal of oxymorphone effects in dogs. 248 83

Sixty-six patients undergoing total knee arthroplasty were offered epidural morphine as a method of postoperative analgesia. Of the 66 patients, 50 completed the minimum protocol of 3 days in a special epidural monitoring unit and were thus available for study. In this study group, 86% stated that they obtained 75-100% relief of pain with each epidural injection. Greater than 90% of the patients rated the overall experience with epidural analgesia as excellent or good. Ninety percent stated that they would choose epidural morphine analgesia again if given the choice. Nausea and vomiting were the most common adverse effects, occurring in 34%. One patient experienced respiratory depression, which was reversed with Narcan. The most frequent complaint related to the procedure itself was the use of an apnea monitor; 18% of the patients considered this monitoring device intolerable. The progress of total knee arthroplasties in the epidural unit was monitored by range of motion achieved. At 72 hours the average motion was 10 degrees-87 degrees and at the end of the hospital stay was 6 degrees-98 degrees. The total hospital bill for epidural morphine analgesic patients was $469 more than for a conventional arthroplasty patient, though the mean duration of hospital stay was 1.7 days less for the epidural morphine patients. Epidural morphine provided excellent but inconsistent postoperative pain relief. When relief was present, aggressive in-house rehabilitation could be instituted, and a shorter overall hospital stay was achieved when compared with conventional analgesia. Nonetheless, the related adverse effects and inconsistent pain relief on many patients may preclude the use of epidural morphine as a single postoperative analgesic agent.
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PMID:The use of epidural morphine in patients undergoing total knee arthroplasty. 250 54

We studied the effect of nalbuphine on the ventilatory and occlusion pressure responses to carbon dioxide rebreathing in six healthy male volunteers (mean age 25.5 yr) in a single-blind laboratory study. On four separate days volunteers were assigned randomly to receive either placebo (0.9% sodium chloride) or three i.v. doses of nalbuphine (15, 30 and 60 mg 70 kg-1), followed 90 min later by naloxone 0.4 mg 70 kg-1. Duplicate rebreathing tests were performed and the mean intercept at PE'CO2 7 kPa and the slopes of the linear relationship between inspiratory minute ventilation (Vl) or occlusion pressure (P0.1) with PE'CO2 were measured. Nalbuphine significantly decreased the mean intercept of the Vl (P less than 0.01) and P0.1 (P less than 0.05) responses, but caused no changes in the slopes. No significant difference between the doses was noted, suggesting that an Effect maximum (E'max) for respiratory depression was reached with a dose of approximately 15 mg 70 kg-1. Naloxone was less effective in antagonizing the depression in Vl at the higher dose of nalbuphine. Similar P0.1 values were associated with the same inspiratory flow rate (1 litre s-1) before and after drug treatment, suggesting that nalbuphine acts centrally to depress ventilation. Sedation increased significantly following each dose of nalbuphine (P less than 0.001). No demonstrable difference between the doses was shown, suggesting an Effect maximum (E'max) for sedation was reached at about 15 mg 70 kg-1. Administration of nalbuphine was associated with pain at the injection site, dizziness, dreaming, nausea and vomiting. Cardiovascular stability was maintained in all subjects.
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PMID:Effect of nalbuphine hydrochloride on the ventilatory and occlusion pressure responses to carbon dioxide in volunteers. 250 65


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