Browsing by keyword "Nitrous Oxide"
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Diffusion of nitrous oxide into the pleural cavityWe postulated that nitrous oxide transfer into the pleural cavity can occur by diffusion from the alveoli, independent of vascular transport. Under general anaesthesia, six sheep were studied in two phases, a control and an experimental phase. The sheep were anaesthetized, intubated, and received positive pressure mechanical ventilation. A catheter was placed in the right pleural cavity and 150 ml air injected. The animals were ventilated with 100% oxygen. The inspired gas was changed to a mixture of 50% nitrous oxide and 50% oxygen, and the rate of increase of nitrous oxide concentration in the pleural space was measured. The animals were then ventilated with 100% oxygen and then killed by exsanguination while ventilation was continued. The inspired mixture was changed to 50% nitrous oxide and 50% oxygen and the rate of increase in nitrous oxide concentration was measured in the pleural space again. During venitilation with nitrous oxide in the living animals, the concentration of nitrous oxide in the pleural cavity increased rapidly and decreased to zero during ventilation with 100% oxygen. During ventilation without circulation, the rate of increase in the concentration of nitrous oxide in the pleural cavity was the same as in the control phase. This suggests that nitrous oxide enters the pleural space by diffusion, rather than by vascular delivery. This mechanism may explain the rapid increase in the volume of pneumothorax if nitrous oxide is given in the inspired gas.
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Nitrous oxide promotes hyperhomocysteinemia in levodopa treated ratsBACKGROUND: This study investigated whether brief exposure to nitrous oxide (N(2)O) exacerbates levodopa-induced hyperhomocysteinemia, and if co-treatment with folate or entacapone could reduce total plasma homocysteine (tHcy) levels. METHODS: Male Wistar rats (N=9 per group) were randomly treated with vehicle/N(2)O (GROUP 1), levodopa/nitrogen (group 2), levodopa/N(2)O (group 3), levodopa/N(2)O+folate (group 4), or levodopa/N(2)O+entacapone (group 5). tHcy was measured at 12 min, 4, 8, and 12 h after anesthesia. RESULTS AND CONCLUSION: The combination of N(2)O-exposure and levodopa treatment significantly increased tHcy in rats. This hyperhomocysteinemia could be prevented by entacapone but not folate co-administration.
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Sites and artifacts related to Horace Wells in Hartford, ConnecticutHorace Wells, a contender for recognition as the discoverer of anesthesia, is celebrated in the town where he conducted most of his work, Hartford, CT. His only descendant was his son, Charles Thomas Wells (1839-1909), an influential and successful business executive at Aetna Insurance Company. He was a man of considerable influence, and he worked tirelessly with city officials and the Connecticut Dental Association in celebrating the 50th anniversary of his father's contribution to medicine. This discovery is unique because events and individuals in 1 country, the United States, contributed entirely to the birth of a medical specialty. Sites in Jefferson, GA; Hartford, CT; and Boston, MA and their environs celebrate this most precious contribution to modern medicine, especially since the introduction of safe anesthesia permitted the development of surgical specialties and obstetrics. We trace the history and relationship between Horace Wells and several sites and artifacts in Hartford, CT. These sites span the most important, distinctive, and attractive parts of the city: Bushnell Park, Trinity College, Cedar Hill Cemetery, the Athenaeum, and the Connecticut Historical Society.