Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

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

Contradictory results have been reported regarding the participation of bulbospinal inspiratory (BSI) neurons in vomiting contractions of the diaphragm in dogs and cats maintained at low and high end-tidal CO2 levels, respectively. To resolve this discrepancy, effects of CO2 levels on vomiting activities were observed in 159 BSI-neurons of paralyzed decerebrate dogs. About half of the BSI-neurons exhibited a vigorous burst with each fictive retch regardless of the CO2 level and 28 of 51 BSI-neurons produced a burst during the early phase of expulsion. These BSI-neurons were not concentrated in any particular area. While these results do not resolve the above contradiction, they do suggest that some BSI-neurons participate in the vomiting contraction of the diaphragm.
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PMID:Bulbospinal augmenting inspiratory neurons may participate in contractions of the diaphragm during vomiting in decerebrate dogs. 770 May 90

Postoperative intestinal atonia is a complication which is likely to occur in patients predisposed for constipation and in patients after intra-abdominal operations. The postoperative delay of bowel movement, however, is often also related to the type of anaesthesia being used. In order to evaluate the magnitude of an anaesthetic-induced postoperative delay of bowel movement, two types of intravenous-based anaesthesia using fentanyl/midazolam (1 mg/25 mg; dosage 0.1 ml/kg/h), and ketamine/midazolam (250 mg/25 mg; dosage 0.1 ml/kg/h) respectively were compared with a volatile anaesthetic technique (enflurane; mean concentration 1.5 vol%). METHODS. In three groups of patients (each n = 15) undergoing elective surgery of the lower extremities, induction of anaesthesia was accomplished with methohexital (1-1.5 mg/kg) to facilitate intubation. For the maintenance of muscle relaxation vecuronium bromide was used. All patients were given droperidol to prevent postoperative emesis, and they were artificially ventilated with N2O/O2 (60:40) to normal end-expiratory CO2 concentrations. No anticholinergic agents were used at the end of operation since they are known to interfere with bowel motility. In order to determine gastro-intestinal motility, the H2 exhalation test was used. For this purpose 40 g lactulose in 100 ml of water was given to all patients via a gastral tube shortly before extubation. Lactulose is broken down by bacteria once it enters the colon, and H2 is released, taken up by the vascular system and exhaled. Postoperatively, patients were asked to exhale into a 20-ml syringe every 10 min. The content was analysed for hydrogen (ppm), using an electrochemical sensor (GMI exhaled hydrogen monitor). From the time of lactulose instillation to a threefold increase in end-expiratory hydrogen concentration (compared to the preoperative value), gastro-coecal transit time was computed. RESULTS. All three groups of patients were comparable in age, height and body weight. Also, the duration of operation was comparable in all three groups. Mean gastro-coecal transit time was 204 (+/- 19.6, SD) min following enflurane, 302 (+/- 32.8 SD) min following fentanyl/-midazolam and 210 (+/- 28.8 SD) min following ketamine/midazolam anaesthesia. The gastro-intestinal inhibition after the opioid-based anaesthetic technique was significantly prolonged (p < 0.001, Kruskal-Wallis test). There was no significance between patients after ketamine-based anaesthesia and those who had the volatile anaesthetic. DISCUSSION AND CONCLUSION. When using intravenous anaesthesia with an opioid, gastro-intestinal inhibition, especially in patients prone to have constipation, is likely to develop postoperatively. In classical neuroleptanaesthesia and in analgosedation in the ICU, the simultaneous use of the butyrophenone droperidol seems to counteract the inhibition of opioid-related gastrointestinal motility. In cases of opioid-related gastrointestinal atonia a gastrokinetic compound may be necessary to overcome this effect on intestinal motility.
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PMID:[No inhibition of intestinal motility following ketamine-midazolam anesthesia. A comparison of anesthesia with enflurane and fentanyl/midazolam]. 814 42

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

The roles of arterial and central chemoreceptors in the transition from retching to expulsion during vomiting were studied. In spontaneously breathing decerebrate dogs, actual vomiting induced by activation of abdominal vagal afferents always consisted of retching and subsequent expulsion phases. Pulmonary ventilation almost stopped during the retching phase. Arterial blood CO2 tension gradually increased and reached a maximum near the time of the transition from the retching phase to the expulsion phase. Similarly, when end-tidal CO2 was maintained higher than 4.6 +/- 0.7% in paralyzed, artificially ventilated decerebrate dogs, stimulation of abdominal vagal afferents induced fictive retching and fictive expulsion, which were identified from the characteristic discharge patterns of the motor nerves to the costal and hiatal parts of the diaphragm, the abdominal muscles and the digastric muscle. However, only fictive retching occurred at an end-tidal CO2 of less than 3.7 +/- 0.7%. Although end-tidal CO2 was at a low level, fictive retching was followed by fictive expulsion when artificial ventilation was interrupted during the fictive retching phase and when sinus nerve afferents were stimulated. Even after sino-aortic denervation, fictive retching and subsequent fictive expulsion could be induced by stimulation of either vagal afferents or the solitary tract and nucleus, but the threshold level of end-tidal CO2 which enabled the induction of fictive expulsion increased after denervation. These results indicate that the activity of arterial and/or central chemoreceptor afferents must exceed some critical level to induce the transition from the retching phase to the expulsion phase.
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PMID:Hypercapnia and hypoxia which develop during retching participate in the transition from retching to expulsion in dogs. 823 24

In six mongrel dogs under thiopental anesthesia, piezoelectric transducers and bipolar electromyographic (EMG) wires were installed onto left costal, medial crural and lateral crural segments of the diaphragm. During CO2 rebreathing, shortening and EMG activity increased significantly in all three regions of the diaphragm compared to resting breathing. During emesis, (1) both shortening and EMG activity significantly increased compared to resting in costal segment; however, (2) lateral crural shortening was not increased in spite of significant increase in EMG activity; furthermore, (3) the medial crural segment lengthened without any increased EMG activity. These results demonstrate a differential recruitment of costal and crural diaphragm segments, and an additional differential activity within the crural segment between medial and lateral crural regions, during emesis. This activity of the canine diaphragm is consistent with a central influence of emesis upon individual regions of the diaphragm.
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PMID:Differential function of the costal and crural diaphragm during emesis in canines. 846 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

Ingestion of sodium hypochlorite bleach is usually benign, leading most poison centers to advocate conservative, home management. We report a rare, fatal case of household bleach ingestion. A 66-y-old female ingested an unknown quantity of regular CLOROX bleach (5.25% sodium hypochlorite, pH = 11.4). Upon discovery, she was vomiting spontaneously, and had slurred speech and oral mucosal discoloration. On hospital arrival the patient became unresponsive with shallow respirations. Laboratory studies revealed hypernatremia (169 mEq Na/L), hyperchloremia (143 mEq Cl/L), and metabolic acidosis (5 mmol total CO2/L). Radiographic evaluation showed bilateral pneumothoraces and pneumoperitoneum. The patient was intubated and ventilated, hypotension was treated with fluid resuscitation, and metabolic acidosis corrected with sodium bicarbonate. Naloxone and flumazenil were given without effect, and thoracostomy tubes were placed. Rapid deterioration of vital signs and mental status ensued, with cardiorespiratory arrest from which she was resuscitated. A second cardiac arrest resulted in death. Autopsy revealed esophageal and gastric mucosal erosions, perforation at the gastroesophageal junction, and extensive necrosis of adjacent soft tissue. Stomach contents contained sodium hypochlorite, and pleural and peritoneal fluid had the aroma of bleach. Postmortem vitreous humor Na was 187 mEq/L and Cl was 169 mEq/L. Toxicologic analysis revealed meprobamate metabolites in the urine, and lidocaine in the blood. The literature regarding fatal bleach ingestion is reviewed.
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PMID:Fatal ingestion of sodium hypochlorite bleach with associated hypernatremia and hyperchloremic metabolic acidosis. 1019 36

Bartter's syndrome is characterized by hypochloremia, hypokalemia, metabolic alkalosis associated with renal potassium leakage, and normal blood pressure despite increased plasma renin activity. Although association of empty sella with Gitelman syndrome has been reported, no association has been reported with Bartter's syndrome. Here we report a patient with Bartter's syndrome and empty sella. A 12 month-old male patient presented with a history of nausea, vomiting, abdominal distension, constipation, and edema in the lower extremities that had begun in the early postnatal period. The patient was born at 32 weeks gestation by operative delivery for polyhydramnios. Blood pressure was normal. Serum sodium, potassium, calcium, phosphate, chloride, albumin and alkaline phosphatase levels were 129 mEq/l, 2.5 mEq/l, 9 mg/dl, 3.8 mg/dl, 72 mg/dl, 4.2 g/dl and 1285 IU/l, respectively. Serum magnesium level was normal. Arterial blood gas levels revealed pH 7.55 (normal, 7.35-7.45), PCO2 33.6 mm/Hg (36-46), base excess +7.1 (+/- 2.3), and total CO2 33.6 mmol/l (23-27). Renin and aldosterone levels were elevated. Urine had pH 8.0 and specific gravity 1.010. Urinary calcium excretion was 22.8 kg/day (urine calcium/creatinine ratio 0.46). Urinary potassium and chloride levels were elevated. MRI of the brain was normal except for partially empty sella. We present the first pediatric patient with the association of Bartter's syndrome and empty sella.
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PMID:Association of Bartter's syndrome and empty sella. 1451 87


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