We have located links that may give you full text access.
Journal Article
Research Support, Non-U.S. Gov't
Ca2+ cytochemical changes of hepatotoxicity caused by halothane and sevoflurane in enzyme-induced hypoxic rats.
World Journal of Gastroenterology : WJG 2005 August 29
AIM: To investigate the relation between hepatotoxicity of halothane and sevoflurane and altered hepatic calcium homeostasis in enzyme-induced hypoxic rats.
METHODS: Forty-eight rats were pretreated with phenobarbital and randomly divided into six groups (eight in each group) and exposed to O(2)/ N(2)/1.2 MAC anesthetics for 1 h: normal control (NC), 21% O(2)/79% N(2); hypoxic control (HC), 14% O(2)/86%N(2); normal sevoflurane (NS), 21% O(2)/ N(2)/1.2MAC sevoflurane; hypoxic sevoflurane (HS), 14% O(2)/ N(2)/1.2MAC sevoflurane; normal halothane (NH)21%O(2)/79%N(2)/1.2MAC halothane; hypoxic halothane (HH), 14% O(2)/N(2)/1.2MAC halothane. Liver specimens and blood were taken 24 h after exposure to calcium and determined by EDX microanalysis.
RESULTS: The liver of all rats given halothane (14% O(2)) had extensive centrilobular necrosis and denaturation. Morphologic damage was accompanied with an increase in serum glutamic pyruvic transminase. In groups NH and HH, more calcium was precipitated in cytoplasm and mitochondria.
CONCLUSION: These results suggest that halothane increases cytosolic Ca(2+) concentration in hepatocytes. Elevation in Ca(2+) concentration is implicated in the mechanism of halothane-induced hepatotoxicity. sevoflurane is less effective in affecting hepatic calcium homeostasis than halothane.
METHODS: Forty-eight rats were pretreated with phenobarbital and randomly divided into six groups (eight in each group) and exposed to O(2)/ N(2)/1.2 MAC anesthetics for 1 h: normal control (NC), 21% O(2)/79% N(2); hypoxic control (HC), 14% O(2)/86%N(2); normal sevoflurane (NS), 21% O(2)/ N(2)/1.2MAC sevoflurane; hypoxic sevoflurane (HS), 14% O(2)/ N(2)/1.2MAC sevoflurane; normal halothane (NH)21%O(2)/79%N(2)/1.2MAC halothane; hypoxic halothane (HH), 14% O(2)/N(2)/1.2MAC halothane. Liver specimens and blood were taken 24 h after exposure to calcium and determined by EDX microanalysis.
RESULTS: The liver of all rats given halothane (14% O(2)) had extensive centrilobular necrosis and denaturation. Morphologic damage was accompanied with an increase in serum glutamic pyruvic transminase. In groups NH and HH, more calcium was precipitated in cytoplasm and mitochondria.
CONCLUSION: These results suggest that halothane increases cytosolic Ca(2+) concentration in hepatocytes. Elevation in Ca(2+) concentration is implicated in the mechanism of halothane-induced hepatotoxicity. sevoflurane is less effective in affecting hepatic calcium homeostasis than halothane.
Full text links
Related Resources
Trending Papers
Challenges in Septic Shock: From New Hemodynamics to Blood Purification Therapies.Journal of Personalized Medicine 2024 Februrary 4
Molecular Targets of Novel Therapeutics for Diabetic Kidney Disease: A New Era of Nephroprotection.International Journal of Molecular Sciences 2024 April 4
The 'Ten Commandments' for the 2023 European Society of Cardiology guidelines for the management of endocarditis.European Heart Journal 2024 April 18
A Guide to the Use of Vasopressors and Inotropes for Patients in Shock.Journal of Intensive Care Medicine 2024 April 14
Diagnosis and Management of Cardiac Sarcoidosis: A Scientific Statement From the American Heart Association.Circulation 2024 April 19
Essential thrombocythaemia: A contemporary approach with new drugs on the horizon.British Journal of Haematology 2024 April 9
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app
All material on this website is protected by copyright, Copyright © 1994-2024 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.
By using this service, you agree to our terms of use and privacy policy.
Your Privacy Choices
You can now claim free CME credits for this literature searchClaim now
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app