Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027497 (nausea)
 23,468 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of physostigmine on the respiratory depression induced by morphine was studied in human subjects who received morphine as part of their preanesthetic medication. After pretreatment with droperidol (2.5-5 mg, iv) to prevent nausea, the change in minute ventilation was measured in 16 patients in response to increasing concentrations of inspired CO2 (CO2-response curve) by the rebreathing method. This was repeated 30 min after morphine (0.166 mg/kg, iv) in nine subjects and in seven controls who did not receive morphine and again 5-10 min after physostigmine (13-33 micrograms/kg, iv) in all subjects. All subjects were given N-butylhyoscine hydrobromide (5 mg, iv) to antagonize any peripheral cholinergic effects of physostigmine. Morphine decreased the mean slope of the CO2-response curve from 1.78 +/- 0.18 to 1.12 +/- 0.14 1 X min-1 X mmHg-1 (P less than 0.01) and increased the alveolar PCO2 for a fixed minute ventilation (position of curve) from 45.0 +/- 1.3 to 51.9 +/- 1.5 mmHg (P less than 0.001). Physostigmine restored the mean slope after morphine to control value, i.e., 1.79 +/- 0.231 X min-1 X mmHg-1, and position to 46.2 +/- 1.2 mmHg (P less than 0.001). Physostigmine did not increase the slope or alter the position of the CO2-response curves of subjects given droperidol alone. The authors conclude that physostigmine can reverse the respiratory depressant effect of morphine and restore the sensitivity of the respiratory center of CO2, presumably by raising acetylcholine levels in the brain after these have been reduced by morphine.
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PMID:Physostigmine antagonizes morphine-induced respiratory depression in human subjects. 640 65

The effects of epinephrine 1/200,000 as an adjuvant to epidural morphine were investigated in three healthy male volunteers, during 26-h observation sessions. Peak blood concentrations of morphine were 44 +/- 12.9 ng/ml after plain morphine and 13.7 +/- 6.7 ng/ml after epinephrine-morphine. Cutaneous hypalgesia was more intense, faster in onset, and longer in duration after epinephrine-morphine than after plain morphine, and analgesia to ice-water immersion of extremities lasted longer. Adverse side effects of pruritus, nausea, vomiting, and difficulty of micturition were also more intense after epinephrine-morphine, and respiratory sensitivity to CO2 was depressed more severely between 6 and 16 h. The results indicated that epinephrine 1/200,000 reduces vascular absorption of epidural morphine and intensifies all the manifestations of cord and brainstem uptake.
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PMID:Influence of epinephrine as an adjuvant to epidural morphine. 682 60

Despite standardization, marked interindividual variation in the severity of the disulfiram-alcohol reaction (DAR) has been observed. We studied the DAR in 51 consecutive alcoholics with (n = 16) and without (n = 35) significant alcoholic liver disease. Clinical signs of the DAR were much weaker in the patients with compared with those patients without liver disease. Because acetaldehyde is thought to be the main cause of the DAR, we studied ethanol and acetaldehyde kinetics in 13 patients (6 females, 7 males) with alcoholic liver disease (documented by biopsy, clinical and/or radiological findings, and by quantitative liver function) [galactose elimination capacity (GEC) 4.2 +/- SD 1.0 mg/min/kg; aminopyrine breath test (ABT) 0.14 +/- 0.10% dose x kg/mmol CO2] and 13 age- and sex-matched controls (alcoholics without significant liver disease, GEC 7.1 +/- 0.7; ABT 0.81 +/- 0.35). Clinical signs of acetaldehyde toxicity during the DAR (flush, nausea, tachycardia, and blood pressure drop) were absent in alcoholic liver disease, but clearly evident in controls. Blood ethanol kinetics were similar in both groups, Cmax and area under the concentration-time curve (AUC) being 6.27 +/- 1.82 and 368.9 +/- 72.9 mmol x min/liter in alcoholic liver disease, and 6.62 +/- 1.71 and 377.6 +/- 124.5 in controls, respectively. In contrast, there was a strong (p < 0.001) difference in Cmax and AUC of acetaldehyde, respective values being 33.46 +/- 21.52 and 1463.8 +/- 762.5 mumol x min/liter in alcoholic liver disease, and 110.87 +/- 56.00 and 4162.0 +/- 2424.6 in controls.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Divergence of ethanol and acetaldehyde kinetics and of the disulfiram-alcohol reaction between subjects with and without alcoholic liver disease. 762 69

Sevoflurane, a new volatile anesthetic agent, is of great potential interest in pediatric anesthesia. Its use for ENT surgery in children was compared with halothane in this study. Altogether 40 children participated in the investigation. In 18 (median age 4.2 years), halothane was used. The remainder (median age 4.0 years) were anesthetized with sevoflurane. After rectal premedication with midazolam and atropine, anesthesia was induced by mask (the agent in O2/N2O, 40/60) using a Mapleson D system. The trachea was intubated without the use of muscle relaxants and the children were then allowed to breathe spontaneously at fresh gas flows set high enough to avoid rebreathing. Hemoglobine oxygen saturation (SpO2), inspired and expired gas concentrations, respiratory rate (RR), heart rate (HR), ECG and blood pressure were followed. Equianesthetic concentrations of the agents were used and induction characteristics were comparable between the two agents. RR and end-tidal CO2 tensions were similar in the two groups. HR and systolic blood pressures were, however, higher with sevoflurane. Cardiac arrhythmias were seen more frequently with halothane (61%) than with sevoflurane (5%). During emergence, postoperative nausea/vomiting was more frequent after halothane anesthesia. Initially, postoperative excitement occurred more often after sevoflurane, when paracetamol was given during anesthesia, which was reduced (P < 0.01) when paracetamol was given at the time for premedication. It is concluded that sevoflurane is an excellent induction agent, and maintains heart rate and systolic blood pressure better than when halothane is used. The incidence of cardiac arrhythmia is lower with sevoflurane than with halothane.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sevoflurane for ENT-surgery in children. A comparison with halothane. 767 95

Acute altitude illnesses include acute mountain sickness (AMS), a benign condition involving headache, nausea, vomiting, irritability, insomnia, dizziness, lethargy, and peripheral edema, and potentially lethal high-altitude cerebral edema and pulmonary edema (HAPE). Recent evidence is summarized that AMS is related to cerebral edema secondary at least in part to hypoxic cerebral vasodilation and elevated cerebral capillary hydrostatic pressure. This results in reduced brain compliance with compression of intracranial structures in the absence of altered global brain metabolism. It is postulated that these primary intracranial events elevate peripheral sympathetic activity that acts neurogenically in the lung possibly in concert with pulmonary capillary stress failure to cause HAPE and in the kidney to promote salt and water retention. The adrenergic responses are likely modulated by striking increases of aldosterone, vasopressin and atrial natriuretic peptide. The effects of exercise on altitude-induced illness and various therapeutic regimens (acetazolamide, CO2 breathing, dexamethasone, and alpha adrenergic inhibitors) are discussed in light of this hypothesis.
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PMID:A neurogenic basis for acute altitude illness. 816 37

In this prospective, double-blind, randomized study of women undergoing elective cesarean birth, the hypothesis that epidural butorphanol in various doses could effectively reduce or eliminate the side effects caused by epidural morphine was tested. Patients were randomly assigned to one of four groups. All received a standard epidural anesthetic and 20 min after delivery each received 3 mg epidural morphine with either 1 mg butorphanol (Group A), 2 mg butorphanol (Group B), 3 mg butorphanol (Group C), or 3 mL normal saline (Group D). Patient evaluations were made preoperatively and 2, 8, and 24 h after delivery. These consisted of visual analog scores for pain, satisfaction, nausea, itch, and somnolence. At each evaluation, a CO2 challenge test, using portable equipment, was performed. Data from 71 patients were analyzed and all four groups were comparable in terms of age, height, weight, level of sensory block, and volume of local anesthetic used. There were no significant differences among groups in terms of pain, satisfaction, nausea, or pruritus. Groups A, B, and C had significantly higher somnolence scores at 8 h compared to Group D (P < 0.001). There were no significant differences among groups in CO2 challenge test data at any point during the study, but overall a reduced sensitivity to CO2 after opioid administration was observed across all groups. There were no clinically significant incidents of respiratory depression. Epidural butorphanol, in doses of 1-3 mg, failed to reduce the side effects from 3 mg epidural morphine given after cesarean birth. Patients who received epidural butorphanol reported significantly higher levels of somnolence.
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PMID:Epidural butorphanol does not reduce side effects from epidural morphine after cesarean birth. 748 37

Respiratory parameters, ventilatory response to carbon dioxide and quality of anaesthesia were studied in patients undergoing upper limb surgery under axillary blockade. Thirteen patients were randomly assigned to two groups, group A (n = 6), who were given 35 ml of 1.5% lidocaine with 1 in 200,000 of adrenaline, and group B (n = 7), who received 1 microgram.kg-1 of fentanyl with the same dose of lidocaine. Quality of the sympathetic, sensory and motor blocks were tested at 15 min (T1) and 45 min (T2) after the injection (T0). The other parameters measured at these three times, both with the patient in a half-sitting position breathing room air, and after a rebreathing test with CO2 through Read's circuit, were respiratory rate (FR), tidal volume (VT), minute ventilation (VE), and PetCO2. Fentanyl provided a better sensory and motor blockade at T1, without any difference in sympathetic blockade. The quality of the blocks was similar in both groups at T2. There were no significant differences in the respiratory parameters between the two groups. Moreover, there was no untoward effect due to fentanyl (nausea, pruritus). It is concluded that 1 microgram.kg-1 fentanyl added to a local anaesthetic solution may be useful, at least during the first hour of an axillary block, without any respiratory side-effects.
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PMID:[Respiratory response to carbon dioxide after brachial plexus block with fentanyl and lidocaine]. 833 61

A closed gas pressure pistol was used in 50 patient CO2 angiography as a supplementary method to conventional injection with liquid contrast medium. These were diagnostic pelvis-leg angiographies (n = 36), therapeutic angiographies (n = 8), haemodialysis fistulas (n = 3), suspected stenosis of a renal transplant artery (n = 1) and suspected renal artery stenosis (n = 1). 246 renal angiography series were performed with CO2. Dosages varied in accordance with the imaged vascular area between 10 ccm;(shunt imaging) and up to 100 cm3 (pelvis-leg angiography), at pressures between 400 mbar in case of haemodialysis fistulas up to 2000 mbar in the pelvis-leg area. Short-term feeling of fullness and even nausea were accompanying symptoms in 4 patients. The image quality was slightly inferior to that of conventional contrast medium images due to an elevated signal-to-noise ratio. Injector-monitored CO2 angiographies enabled imaging of the distal aorta or of peripheral vascular sections, imaging of the upper extremity and presentation of kidney transplants in patients with a relative or absolute contraindication to iodised contrast media.
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PMID:[Carbon dioxide as an alternative contrast medium in peripheral angiography]. 863 9

Intravenous opioids cause analgesia and increase release of ACh in spinal cord dorsal horn in animals, and these effects are enhanced by intrathecal neostigmine injection. The purpose of the current study was to test whether intrathecal neostigmine enhanced analgesia and increased cerebrospinal fluid concentrations of ACh over those induced by i.v. alfentanil in volunteers, and also to test whether neostigmine enhanced alfentanil-induced side effects. After human studies committee approval, 40 healthy volunteers received an intrathecal injection of saline or neostigmine (50, 100 or 200 microg) followed in 60 min by a computer-controlled, stepped i.v. infusion of alfentanil to escalating targeted plasma concentrations. Pain report to hand and foot immersion in ice water, sedation, nausea, weakness, vital signs, end-tidal CO2 and oxyhemoglobin saturation were measured 60 min after spinal injection and at the end of each 20-min alfentanil infusion. Cerebrospinal fluid was sampled once after drug administration. Intrathecal neostigmine alone caused analgesia in the foot but not in the hand, and was accompanied by leg weakness, whereas IV alfentanil alone caused equivalent analgesia in both the hand and the foot and was accompanied by nausea, sedation, increased end-tidal CO2 and decreased oxyhemoglobin saturation. Neostigmine enhanced analgesia but not respiratory effects induced by i.v. alfentanil; it also enhanced nausea and sedation. Intravenous alfentanil increased cerebrospinal fluid ACh concentration, and neostigmine enhanced this change. These data in humans are consistent with a spinal cholinergic mechanism of i.v. opioid analgesia. Because neostigmine enhances both analgesia and side effects induced by i.v. alfentanil, the clinical utility of their use in combination will depend on the relative strength of these interactions.
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PMID:Enhancement of analgesia from systemic opioid in humans by spinal cholinesterase inhibition. 922 43

After laparoscopic cholecystectomy, CO2 remains within the peritoneal cavity, commonly causing pain. This prospective randomized study was performed to determine the efficacy of intraperitoneal normal saline and bupivacaine infusion on postoperative pain after laparoscopic cholecystectomy. Three hundred patients were randomly assigned to one of six groups of 50 patients each. Group A patients served as controls. In group B patients, normal saline was infused under the right hemidiaphragm and suctioned after the pneumoperitoneum was deflated. After suction, a subhepatic closed drain was left for 24 h. In group C patients, bupivacaine 1.5 mg/kg in solution 2.5 mg/ml, minus 15 ml of this solution, which was infiltrated in the trocar wounds, was infused under the right hemidiaphragm at the end of the cholecystectomy. In group D patients, bupivacaine was given as in group C, but a subhepatic drain was left for 24 h. In group E patients, normal saline was used as in group B plus bupivacaine as in group C. Group F patients were treated as in group E, but a subhepatic drain was left for 24 h. In all groups, 15 ml of a 2.5 mg/ml bupivacaine solution was infiltrated in the trocar wounds. Postoperatively, analgesic medication usage, nausea, vomiting, and pain scores were recorded at 2, 6, 12, 24, 36, 48, and 72 h. Postoperative pain was reduced significantly in the patients of the treatment groups vs. the controls. Between treatment groups, patients in groups B, E, and F had the best results, while those in groups C and D had significantly greater pain than those in groups B, E, and F. It is concluded that postoperative pain after laparoscopic cholecystectomy can be significantly reduced by intraperitoneal normal saline infusion subdiaphragmatically and after its postdeflation suction, bupivacaine infusion in the same area, or without bupivacaine in case a subhepatic drainage has been needed.
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PMID:Intraperitoneal normal saline and bupivacaine infusion for reduction of postoperative pain after laparoscopic cholecystectomy. 986 6


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