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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty patients with cervical esophageal dysphagia were treated by cricopharyngeal myotomy. Of these 20 patients, ten had pharyngoesophageal diverticula, four had a hypertensive upper esophageal sphincter (UES), four had bulbar palsy, and two has miscellaneous forms of cricopharyngeal dysfunction. Preoperative esophageal manometric examination revealed mean UES pressures of 37.2 mmHg +/- 4.8 SEM in patients with diverticula-markedly lower (p = 0.01) than in normal patients (55.9 mmHg +/- 5.0 SEM). In patients with hypertensive UES the mean pressure was 166.2 mmHg +/- 13.4, significantly higher (p less than 0.001) than normal. Incoordination of the deglutitive response of the UES characterised by premature relaxation and contraction was present in all patients with diverticula and in one other patient. Another patient exhibited incomplete sphincteric relaxation (achalasia). A 4-5 cm myotomy of the cricopharyngeus muscle and adjacent esophageal muscle was performed in all patients. On the patients with diverticula two also had diverticulectomy. No patient with bulbar palsy was benefited. All other patients were relieved of dysphagia by the operation, with the exception of one patient with a diverticulum. A subsequent diverticulectomy was required in this patient. Postoperative manometric examination revealed an average decrease in UES pressure of 63% and an average decreased in length of the high pressure zone of 1.4 cm.
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PMID:Cervical esophageal dysphagia: indications for and results of cricopharyngeal myotomy. 679 98

Doxacurium was administered by titrated infusion to 14 pediatric patients for 4.7-12.3 days after laryngotracheal reconstruction to produce minimum spontaneous movement and less than five posttetanic movements of the first toe after stimulation of the posterior tibial nerve. Recovery was documented by stimulation of the ulnar nerve with 2 Hz for 2 s (train-of-four [TOF]) at intervals of 1 min and measurement of the ratio of the fourth to the first response (TOF ratio) at the adductor pollicis. During spontaneous recovery, the TOF ratio was between 0.4 and 0.7 for 0.6-3.3 h, mean (SEM) 2.2 (0.31) h. The TOF ratio equaled 1 between 4.7 and 23.0 h, mean (SEM) 11.0 (2.1) h after termination of doxacurium infusion. In six of the patients, weakness and decreased coordination were noted for a few days to weeks postoperatively. There were no complications related to impairment of upper airway function or ventilation in those patients who had recovery of neuromuscular transmission to the extent of TOF ratio equal to 1 prior to extubation or in those patients in whom weakness or lack of coordination was noted after tracheal extubation.
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PMID:Recovery from doxacurium infusion administered to produce immobility for more than four days in pediatric patients in the intensive care unit. 902 19

The epidemiological association between black cherry trees and mare reproductive loss syndrome has focused attention on cyanide and environmental cyanogens. This article describes the toxicokinetics of cyanide in horses and the relationships between blood cyanide concentrations and potentially adverse responses to cyanide. To identify safe and humane blood concentration limits for cyanide experiments, mares were infused with increasing doses (1-12 mg/min) of sodium cyanide for 1 h. Infusion at 12 mg/min produced clinical signs of cyanide toxicity at 38 min; these signs included increased heart rate, weakness, lack of coordination, loss of muscle tone, and respiratory and behavioral distress. Peak blood cyanide concentrations were about 2500 ng/mL; the clinical and biochemical signs of distress reversed when infusion stopped. Four horses were infused with 1 mg/min of sodium cyanide for 1 h to evaluate the distribution and elimination kinetics of cyanide. Blood cyanide concentrations peaked at 1160 ng/mL and then declined rapidly, suggesting a two-compartment, open model. The distribution (alpha) phase half-life was 0.74 h, the terminal (beta phase) half-life was 16.16 h. The mean residence time was 12.4 h, the steady-state volume of distribution was 2.21 L/kg, and the mean systemic clearance was 0.182 L/h/kg. Partitioning studies showed that blood cyanide was about 98.5% associated with the red cell fraction. No clinical signs of cyanide intoxication or distress were observed during these infusion experiments. Mandelonitrile was next administered orally at 3 mg/kg to four horses. Cyanide was rapidly available from the orally administered mandelonitrile and the C max blood concentration of 1857 ng/mL was observed at 3 min after dosing; thereafter, blood cyanide again declined rapidly, reaching 100 ng/mL by 4 h postadministration. The mean oral bioavailability of cyanide from mandelonitrile was 57% +/- 6.5 (SEM), and its apparent terminal half-life was 13 h +/- 3 (SEM). No clinical signs of cyanide intoxication or distress were observed during these experiments. These data show that during acute exposure to higher doses of cyanide (~600 mg/horse; 2500 ng/mL of cyanide in blood), redistribution of cyanide rapidly terminated the acute toxic responses. Similarly, mandelonitrile rapidly delivered its cyanide content, and acute cyanide intoxications following mandelonitrile administration can also be terminated by redistribution. Rapid termination of cyanide intoxication by redistribution is consistent with and explains many of the clinical and biochemical characteristics of acute, high-dose cyanide toxicity. On the other hand, at lower concentrations (<100 ng/mL in blood), metabolic transformation of cyanide is likely the dominant mechanism of termination of action. This process is slow, with terminal half-lives ranging from 12-16 hours. The large volume of distribution and the long terminal-phase-elimination half-life of cyanide suggest different mechanisms for toxicities and termination of toxicities associated with low-level exposure to cyanide. If environmental exposure to cyanide is a factor in the cause of MRLS, then it is likely in the more subtle effects of low concentrations of cyanide on specific metabolic processes that the associations will be found.
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PMID:The toxicokinetics of cyanide and mandelonitrile in the horse and their relevance to the mare reproductive loss syndrome. 2002 Nov 60