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

Five groups of 10 patients received thiamylal, enflurane, nitrous oxide-oxygen anesthesia for elective cholecystectomy. The common bile duct was intubated via the cystic duct with a 16-g plastic catheter, and the control intraductal pressure was measured. Patients then were given equi-analgesic doses of fentanyl, morphine, meperidine, butorphanol, or placebo intravenously, and the common bile duct pressure was recorded for 20 min. Fentanyl, morphine, and meperidine significantly increased pressure in the common duct (P less than 0.001). Butorphanol produced only insignificant changes. Naloxone given 20 min later significantly (P less than 0.001) decreased pressure in patients given fentanyl, morphine, and meperidine. Naloxone given without narcotics caused an increase in pressure that, although statistically significant (P less than 0.03), was clinically insignificant. In five additional patients anesthetized with thiamylal, nitrous oxide-oxygen and intermittent doses of fentanyl, common bile duct pressures were normal.
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PMID:Common bile duct pressure changes after fentanyl, morphine, meperidine, butorphanol, and naloxone. 670 71

The effect of a specific opioid antagonist, naloxone, was studied in two comparable groups of patients who received i.v. the dose of an anaesthetic agent required to produce loss of consciousness in 50% of subjects. The first group received naloxone 0.006 mg kg-1 5 min before induction of anaesthesia; the second group received a similar volume of saline solution. Thiopentone, Althesin, diazepam, ketamine and propanidid were studied. The differences in percentage of unconscious patients between the naloxone-treated group and the control group were statistically significant for diazepam, ketamine and propanidid. Naloxone did not modify the induction of anaesthesia with thiopentone or Althesin.
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PMID:Effect of naloxone on the loss of consciousness induced by i.v. anaesthetic agents in man. 671 51

Many vasoactive mediators have been implicated in causing or maintaining the hypotension of endotoxic shock. What has yet to be firmly established is the relative importance of each of these mediators in a given shock model. In a canine endotoxic shock model (LD100), we studied the effects of opiate and prostaglandin inhibition 60 min after endotoxin administration. After thiopental anesthesia, the animals were instrumented to measure various cardiovascular parameters. Endotoxic shock was induced by injecting E. coli endotoxin (0111:B4) (1 mg/kg i.v.). Drug intervention occurred 60 min after endotoxin administration. Naloxone (2 mg/kg i.v.) improved mean arterial pressure (MAP) transiently. A more significant increase of MAP (85% of preshock levels) was attained after ibuprofen (12.5 mg/kg i.v.) administration secondary to an increase in total peripheral resistance (TPR). All groups had 0% 24-hour survival. These data suggest that the endogenous opioids, presumably inhibited by naloxone, seem to contribute little to this lethal canine endotoxic shock model. By contrast, the prostanoids which are inhibited by ibuprofen appear to be more hemodynamically significant in this model.
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PMID:The effects of vasoactive mediator antagonists on endotoxic shock in dogs. I. 672 95

The effects of naloxone hydrochloride and morphine sulfate on the proestrous surge of PRL and gonadotropins (LH and FSH) were investigated in normal cycling Sprague-Dawley rats. Blood samples (0.45-0.50 ml) were withdrawn without anesthesia every 20 min from 1400-2000 h through an atrial cannula implanted the same morning. RIA revealed that a single iv injection of naloxone (0.2 mg/kg) at 1400 h completely suppressed the surge of PRL, and this was reversed by a concomitant injection of morphine (10 mg/kg). Morphine itself did not alter the peak of the PRL surge. Morphine suppressed only the early phase of the LH surge, and this was reversed by naloxone. Naloxone alone did not change the peak of the LH surge but maintained higher levels than controls during the declining phase. The FSH surge was not altered by either morphine or naloxone. These results suggest that endogenous opioid peptides may have a role in regulating the PRL and LH surges during proestrus in the rat.
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PMID:Effects of naloxone and morphine on the proestrous surge of prolactin and gonadotropins in the rat. 676 98

A 50-micrograms/kg dose of fentanyl, given intravenously in divided doses to dogs under enflurane-nitrous oxide anesthesia caused sharp decreases in heart rate (HR), arterial blood pressure (AP), left ventricular dP/dt, and plasma levels of catecholamines. Naloxone, 20 micrograms/kg given 65-70 min later, completely and rapidly reversed these changes. Because the cardiovascular effects of fentanyl and naloxone occurred in unparalyzed animals under surgical anesthesia without eliciting any motor responses, it seems unlikely that they can be ascribed to changes in awareness and surgical stimulation, especially pain. The brief duration of exposure to the narcotic makes it improbable that the naloxone response is due to acute dependence and precipitated withdrawal. Pretreatment with 20 micrograms/kg of atropine only attenuated the decrease in HR, indicating a minor role of vagal mechanisms under these conditions. Administration of 20 micrograms/kg of clonidine by slow infusion after fentanyl further reduced sympathetic activity and greatly attenuated the naloxone response. Injection of 5 mg/kg of tolazoline after administration of clonidine produced massive cardiovascular stimulation by antagonizing clonidine and unmasking the naloxone reversal of fentanyl. Thus, in fully anesthetized dogs, fentanyl decreased the level of cardiovascular function mainly by reducing sympathetic activity. This effect does not seem to be secondary to analgesia or other sensory depressant effects of the narcotic, but rather to an action on central opioid-sensitive mechanisms regulating cardiovascular function.
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PMID:Effects of fentanyl, naloxone, and clonidine on hemodynamics and plasma catecholamine levels in dogs. 682 30

The effects of naloxone (2 mg/kg body weight) on hemodynamics, oxygen transport, and some metabolic variables were studied in mongrel dogs under general anesthesia and controlled ventilation. All 19 dogs received Escherichia coli endotoxin (1.5 mg/kg) and subsequently were randomized into three groups. The first group (N = 7) served as a control group in which at 90 min after endotoxin (t 90), NaCl (0.65%, 4 ml/kg) was infused during 30 min. In the second group (N = 7) naloxone (2 mg/kg) dissolved in the same amount of fluid was administered at t 90 in 30 min. In the third group (N = 5) naloxone (2 mg/kg) was injected as a bolus in 5 ml NaCl (0.65%) at t 90, which was followed by NaCl (0.65%, 4 ml/kg) infused in 30 min. Differences in the three groups after intervention were tested statistically. After naloxone, blood pressure, cardiac output, and left ventricular stroke work increased significantly. Although oxygen availability increased, oxygen consumption and serum lactate did not change when compared with the control group. As to all other measured and calculated variables, no systematic differences were found in the three groups. In six dogs, plasma beta-endorphins were measured and were shown to rise substantially after induction of endotoxin shock. As to the hemodynamic changes, our observations confirm data from the literature. Naloxone apparently improves hemodynamics in endotoxin shock, but at least in this study fails to influence oxygen consumption and serum lactate levels.
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PMID:Effects of naloxone on hemodynamics, oxygen transport, and metabolic variables in canine endotoxin shock. 683 24

Three out of six patients who had received 1 mg of morphine and 0.22 ml plain bupivacaine 0.5%/segment as a subarachnoid spinal anaesthetic developed serious and delayed respiratory depression on several occasions. This was reversed by intravenous naloxone. It is postulated that the morphine had diffused to the level of the cisterna magnum and thence through brain tissue around the fourth ventricle. Naloxone did not reverse the analgesia.
Anaesthesia 1980 Nov
PMID:Respiratory depression after intrathecal narcotics. 689 89

A patient is reported in whom deep musculoskeletal pain apparently blocked transmission from nociceptive cutaneous fibers in an adjacent region. When the deep musculoskeletal pain was abolished with local anesthesia, the cutaneous hypalgesia disappeared. Naloxone did not influence the hypalgesia. Possible mechanisms are discussed.
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PMID:Inhibition of cutaneous nociception by deep musculoskeletal pain. A clinical observation. 698 49

The increase of plasma catecholamines that occurs during surgery can be reduced by administration of morphine. To test the hypothesis that morphine specifically blocks nociceptive stimulation during surgery, we compared the effects of morphine administration on the plasma catecholamine response to a laparotomy in pentobarbital-anesthetized dogs with the effect of morphine on the plasma catecholamine response to the neuroglucopenic agent, 2-deoxy-D-glucose (2DG, 300 mg/kg iv). In control dogs, plasma epinephrine (Epi) and plasma norepinephrine (NE) both increased progressively with time following a midline laparotomy (delta Epi by 50 min, +133 +/- 42 pg/ml, P less than 0.01 and delta NE by 50 min, +108 +/- 38 pg/ml, P less than 0.01, mean +/- SE, n = 12). 2-Deoxy-D-glucose produced a similar increase of both plasma NE and Epi. In dogs that received the anesthesia alone, plasma catecholamines did not increase from base line during the experiment. The analgesic morphine (15 mg iv), given 15 min after the completion of laparotomy, not only prevented the progressive rise of plasma catecholamines after laparotomy, but also caused a small but significant decline (P less than 0.05). Naloxone (0.4 mg iv) totally reversed the suppressive effects of morphine, restoring both catecholamines to the levels of their time-related control. In marked contrast, neither morphine nor naloxone affected the plasma NE and Epi increases following the administration of 2DG. These data suggest that morphine suppression of plasma catecholamines during surgery is not due to a generalized attenuation of sympathetic outflow, but rather to a specific interaction with an opiate receptor that either mediates analgesia or lies within the neural pathway stimulated by laparotomy but not by 2DG.
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PMID:Morphine suppresses plasma catecholamine responses to laparotomy but not to 2-deoxyglucose. 708 32

In pentobarbital-anaesthetized rats (60 mg/kg, i.p.) renal pelvis distension with a pressure of 80 cm H2O caused a decline in mean arterial blood pressure. This pressure response, which disappeared rapidly after cessation of the distension, was used to study the effects of analgesic drugs known to be effective in renal colic pain in man. Morphine (0.75 and 1 mg/kg, s.c.) and the decapeptide caerulein (1.6, 4 and 8 microgram/kg, s.c.) abolished the pressure response. The effects of the largest doses lasted for at least 30 min. Ineffective in this respect were (a) desulphated caerulein (40 microgram/kg, s.c.) and (b) additional doses of pentobarbital (20 and 40 mg/kg, s.c.). This shows (a) the importance of the sulphated tyrosine (known from previous studies on central effects) and (b) the missing influence of the depth of anaesthesia. Naloxone (0.5 mg/kg, s.c.) abolished the effect of morphine (1 mg/kg, s.c.) but failed to influence that of caerulein (8 microgram/kg, s.c.). Even a fourfold dose of naloxone (2 mg/kg, s.c.) did not weaken the effect of caerulein. Naloxone, per se, was ineffective. These results suggest different mechanisms of the present effects of morphine and caerulein. It appears that renal pelvis distension in the anaesthetized rat can serve as a model of renal colic.
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PMID:Caerulein and morphine in a model of visceral pain. Effects on the hypotensive response to renal pelvis distension in the rat. 711 Mar 76


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