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Query: UMLS:C0278134 (anesthesia)
 110,339 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Naloxone, when administered for the purpose in reversing opiate-induced respiratory depression after morphine- or fentanyl-anesthesia may precipitate an increase in sympathetic tone with subsequent cardiovascular reactions. In order to investigate which variable of the cardiovascular system is affected most and to compare whether the effects after fentanyl anesthesia (0.05 mg/kg) differ markedly from those after sole equianesthetic meperidine-anesthesia (20 mg/kg), naloxone (5 microgram/kg) was given shortly (15 min.) after opiate injection. In the fentanyl group (n = 7) compared to the anesthetic level the antagonist induces an increase in heart-rate by 100%, in LV dP/dt max (inotropic state of the myocardium) by 90%, in mean peripheral blood pressure (afterload of the heart by 80%, in myocardial oxygen consumption by 50% and in left ventricular pressure by 42%. After 32 minutes all variables had returned to anesthesia values. In the meperidine-group (n = 7) naloxone induced an increase in heart-rate by 13%, in LV dP/dt max by 75%, in mean peripheral blood pressure by 65%, in myocardial oxygen consumption by 25% and in left ventricular pressure by 78%. After 25 minutes all increased variables had returned to prenaloxone values. The study indicates that the more potent the opiate agonist, the more naloxone is liable to induce a hyperexcitatory state of the cardiovascular system. This excitatory state is also reflected in an elevated myocardial oxygen consumption. Therefore caution is advised in administering naloxone to patients after sole opiate-anesthesia, who have an impaired myocardial oxygen supply. (Acta anaesth. belg., 1982, 33, 89-97).
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PMID:Naloxone induces excitation of the cardiovascular system and a rise in myocardial oxygen consumption in fentanyl and meperidine-anesthetized dogs. 712 22

The recovery of patients following neurolept or fentanyl/nitrous oxide anesthesia is extremely variable due to variations in drug dosage, biotransformation and excretion idiosyncracies among individuals. The respiratory depressant effects of fentanyl or fentanyl/droperidol can far outlast the analgesic duration and can recur after having dissipated. The level of consciousness and the quality of breathing can be misleading indicators of complete recovery from neurolept anesthesia. Respiratory rate has been observed to return to control levels when simultaneous response to CO2 rebreathing was reduced and resting PeCO2 was increased. Naloxone can be used in dosages which will help ensure adequate ventilation without attenuating postoperative analgesia.
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PMID:Biphasic respiratory depression from neurolept anesthesia. 718 Mar 69

1. An investigation was carried out to determine the effect of intracerebroventricular (I.C.V.) micro-injections of morphine on vasopressin (AVP) release in the urethane-anaesthetized rat. 2. Plasma AVP levels at different time intervals, following I.C.V. injection of 10-150 microgram morphine, were measured by radioimmunoassay. The effect of I.C.V. micro-injections of morphine on urine outflow was also studied in a group of water-loaded rats. 3. The vasopressin response to I.C.V. micro-injections of morphine was both dose- and time-dependent. High dose of 50 and 150 microgram morphine produced short latency stimulation of AVP release, followed by a fall. The low dose of 10 microgram morphine produced only a long latency inhibition. The most consistent response of I.C.V. injection of morphine was an inhibition of release. 4. Both stimulatory and inhibitory effects of morphine on vasopressin release were naloxone reversible and stereospecific. 5. I.C.V. micro-injections of morphine produced a dose-dependent rise in mean arterial blood pressure of short latency. Naloxone (0.5 mg/kg) completely abolished the rise seen with 10 microgram morphine and diminished the rise with 50 microgram. 6. Doses of 10 and 50 microgram morphine injected I.C.V. produced an immediate antidiuresis in water-loaded rats under urethane anaesthesia. 7. The vasopressin response to I.C.V. micro-injections of morphine is independent of the effects on the cardiovascular system and may involve different opiate receptor populations. The results also suggest the possibility that opiate receptors with different affinities for morphine may be responsible for the stimulatory and inhibitory effects of morphine on vasopressin release.
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PMID:The effect of intracerebroventricular injections of morphine on vasopressin release in the rat. 726 75

Many ophthalmic procedures are performed in elderly patients who have serious concurrent disease. Local anesthesia with sedation can be a safe, advantageous method of management. Uneventful ophthalmic surgery under local anesthesia depends on proper patient selection, preparation, and perioperative management. Patients should understand the procedures and be cooperative. Preparation includes a through medical evaluation. Medical problems must be stable and appropriately managed. The goal of premedication is to have a calm, cooperative patient. Narcotic and an antiemetic sedative such as either promethazine, hydroxyzine, or droperidol should be given according to age and weight. A benzodiazepine may be added for amnesia and anxiolytic effect. Naloxone or physostigmine are available to specificity reverse the effects of narcotics or benzodiazepines, respectively. Awareness of the toxicity and limitations of local anesthetics is important for their safe use.
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PMID:Local anesthesia for ophthalmic surgery: patient preparation and management. 728 26

The clinical impressions of enhanced arousal from halothane anesthesia and improvement of postanesthesia recovery scores after doxapram, physostigmine, or naloxone have not been verified in laboratory studies based on the effect of these drugs on MAC. With induction of anesthesia, a shift in the amplitude of the EEG from low to high occurs at anesthetic concentrations well below MAC and appears to coincide with the loss of consciousness. The authors examined the effect of arousal agents on the end-tidal halothane concentration required to produce this shifting EEG. In 24 unmedicated dogs, the end-tidal halothane concentration was elevated to 20 per cent above the shift point concentration (from 0.61 +/- 0.03 to 0.73 +/- 0.03 per cent) and maintained at this level for 30 min. Doxapram, 1 mg/kg, iv, and physostigmine, 0.03 mg/kg, iv, converted the EEG from a high amplitude to a low amplitude tracing in 22 +/- 3 s in eight of eight, and 225 +/- 37 s in seven of eight dogs, respectively. The end-tidal halothane concentration required to restore the shifting EEG was elevated above control for 50 +/- 7 min and 109 +/- 7 min, respectively. Naloxone, 0.06 mg/kg, iv, produced an awake EEG in two of eight dogs in 233 +/- 18 s which persisted for 22 +/- 4 min, and a transiently shifting EEG in three of eight dogs between 200 and 240 s. Naloxone 0.006, mg/kv, iv, produced an awake EEG in 80 +/- 8 s in four of four dogs who had previously received doxapram 3 h earlier. In this model doxapram and physostigmine paralleled the clinically observed onset and duration of arousal. The inconstant arousal from halothane anesthesia induced by naloxone was interpreted in terms of an opiate receptor independent action.
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PMID:Electroencephalographic evidence of arousal in dogs from halothane after doxapram, physostigmine, or naloxone. 729 74

Sixteen patients were studied to determine if naloxone could be shown to affect general anaesthesia with halothane and oxygen or nitrous oxide and oxygen with halothane. Changes in blood pressure, pulse rate, electroencephalogram and evidence of physical response were observed. The end-tidal halothane and carbon dioxide were controlled. The temperature and blood gases were held constant, as was the degree of neuromuscular blockade. Naloxone 1.2 mg was administered during general anaesthesia with either halothane in oxygen or halothane with nitrous oxide to 16 patients who were premedicated without a narcotic. No significant responses were recorded.
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PMID:The absence of antagonism by naloxone during halothane/nitrous oxide anaesthesia in man. 735 88

Both early post-ischaemic blood-brain barrier disruption and enhanced brain endogenous opioid system activity have been implicated in the pathogeneses of ischaemic neuronal damage; however, their roles in neonatal asphyxia have not been evaluated. Under alpha-Chloralose anaesthesia, 17 newborn lambs were asphyxiated until their mean arterial pressures were < or = 25 mmHg. They were then immediately resuscitated, and assigned to two groups. Group I, but not group II lambs received IV bolus of 10 mg kg-1 Naloxone within 5 min of resuscitation. The infusion was continued at the same dose hourly until sacrificed 24 h post-asphyxia. Arterial pH/gases, intracranial/arterial pressures, and rectal temperature were monitored. Neurological examinations were performed on both groups prior to sacrifice, and the blood-brain barrier integrity was assessed by Evans blue. Despite aggressive resuscitation, 5 lambs died during asphyxia, but 12 survived and were assigned according to the protocol. There were no significant group differences in the magnitude of asphyxia, arterial and intracranial pressures. However, blood-brain barrier disruption was observed in 5 out of 6 untreated, and in only 1 of the 6 lambs treated with Naloxone (p < 0.05). Severe neurological abnormalities were observed in 75% of lambs with disrupted, but in none of the animals with intact blood-brain barrier (p < 0.05). Our study suggests that post-asphyxia blood-brain barrier disruption is causally related to poor neurological outcome, and that Naloxone prevents both the disruption, and the neurological dysfunction among those survivors with intact blood-brain barrier.
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PMID:The effects of naloxone on the post-asphyxic cerebral pathophysiology of newborn lambs. 787 Feb 75

General anesthetics render a person unconscious and may produce respiratory paralysis at therapeutic doses. No pharmacological agent is available to restore respiration and the mechanism/s of anesthesia or apnea is not clearly understood. In this report, we present evidence to show that naloxone reversed respiratory failure induced by thiopental, ketamine, halothane but not that induced by phenobarbital. Furthermore, 25 mg/kg, i.v. thiopental, 140 mg/kg, i.v. ketamine, and 3% halothane produced anesthesia without significantly altering respiratory rate, increased GABA and decreased glutamate (except ketamine and phenobarbital) levels in rat brain stem and cortex, but not in caudate and cerebellum. Aspartate, glycine and alanine levels were not affected in four brain regions studied. Pretreatment with TSC for 30 minutes did not change GABA or glutamate contents, but abolished the anesthetic as well as the respiratory depressant actions of the anesthetics. Increasing the doses of anesthetics produced respiratory failure with further rise in GABA and fall in glutamate in brain stem and cortex. Naloxone reversed respiratory paralysis and restored GABA close to control values in rat brain stem and cortex with no changes in caudate or cerebellum. Data presented here suggest that GABA may be necessary to produce loss of consciousness and naloxone reverses anesthetic induced respiratory failure.
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PMID:Evidence for involvement of amino acid neurotransmitters in anesthesia and naloxone induced reversal of respiratory paralysis. 791 Dec 21

Intrathecal meperidine administration can provide surgical anaesthesia and postoperative analgesia for about two to six hours. We have observed two cases of respiratory depression associated with meperidine spinal anaesthesia. An 81-yr-old woman received 50 mg intrathecal meperidine for inguinal hernia repair. Supplemental oxygen was administered at 3 L.min-1 by nasal prongs. About 40 min later, the patient's oxygen saturation decreased from 97% to 87% and she was asked to take big breaths. She responded immediately and oxygen saturation returned to 97%. Two more similar episodes followed in the next five minutes. Naloxone 0.1 mg iv was administered and the oxygen saturation remained at 96-97% until completion of surgery about 15 min later. She had an uneventful recovery. A 24-yr-old healthy woman presented for tubal ligation eight hours after vaginal delivery of an infant. The surgical procedure was performed under spinal anaesthesia produced by 50 mg meperidine. During surgery, midazolam 2 mg iv was given for anxiolysis. About five minutes after admission to the postanaesthesia care unit, the patient's respiratory rate decreased to ten breaths per minute and oxygen saturation decreased to 89%. Supplemental oxygen at 3 L.min-1 was administered by nasal prongs. The patient was encouraged to take big breaths and the arterial oxygen saturation rapidly increased to 98-99%. Forty minutes later, nasal oxygen was discontinued. The patient maintained her oxygen saturation while breathing room air. She was then discharged to the ward and had an uneventful recovery course. We recommend that a patient's respiratory variables and oxygenation be closely monitored for at least one hour after intrathecal meperidine administration.
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PMID:Respiratory depression associated with meperidine spinal anaesthesia. 792 21

This report is of two adult patients who were scheduled for excision of carotid body tumours. One of the patients had bilateral tumours, while the second had a unilateral tumour. In the first, anaesthesia was maintained by nitrous oxide:oxygen and halothane 1-2%. Postoperatively, the intramuscular injection of meperidine 75 mg resulted in apnoea, cyanosis, and loss of consciousness. In the second, anaesthesia was maintained by nitrous oxide:oxygen, supplemented by fentanyl 2 micrograms.kg-1 and incremental doses of vecuronium. Following complete reversal of neuromuscular block, the patient became wide awake but spontaneous breathing was resumed at a rate of only two to three breaths per minute, and the oxygen saturation as monitored by pulse oximetry decreased to 50%. Naloxone 0.4 mg iv increased the respiratory rate to 14 per minute and the oxygen saturation to 98%. The report suggests that surgical excision of carotid body tumours, whether unilateral or bilateral, can be followed by severe postoperative respiratory depression. The complication may be attributed to opioid administration in the absence of peripheral chemoreceptor drive.
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PMID:Postoperative respiratory depression following excision of carotid body tumours. 800 36


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