scholarly journals An evaluation of the protective effect of hyperbaric oxygenation on the central nervous system during circulatory arrest

1966 ◽  
Vol 52 (5) ◽  
pp. 618-628 ◽  
Author(s):  
Gordon F. Moor ◽  
Robert L. Fuson ◽  
George Margolis ◽  
Ivan W. Brown ◽  
Wirt W. Smith
1993 ◽  
Vol 3 (3) ◽  
pp. 308-316 ◽  
Author(s):  
Gil Wernovsky ◽  
Richard A. Jonas ◽  
Paul R. Hickey ◽  
Adré J. du Plessis ◽  
Jane W. Newburger

The dramatic reduction in surgical mortality associated with repair of congenital heart anomalies in recent decades has been accompanied by a growing recognition of adverse neurologic sequels in some of the survivors. Abnormalities of the central nervous system may be a function of coexisting cerebral abnormalities or acquired events unrelated to surgical management (such as paradoxical embolus, cerebral infection, or effects of chronic cyanosis), but insults to the central nervous system appear to occur most frequently during or immediately after surgery. In particular, techniques of support used during neonatal and infant cardiac surgery—cardiopulmonary bypass, profound hypothermia and circulatory arrest—have been implicated as important causes of cerebral injury. This paper will review the effects of bypass and deep hypothermic circulatory arrest on neurodevelopmental outcome.


1986 ◽  
Vol 41 (3) ◽  
pp. 255-259 ◽  
Author(s):  
James V. O'Connor ◽  
Todd Wilding ◽  
Peter Farmer ◽  
Joanna Sher ◽  
M. Arisan Ergin ◽  
...  

Resuscitation ◽  
2002 ◽  
Vol 52 (1) ◽  
pp. 109-115 ◽  
Author(s):  
Carla Bazzani ◽  
Chiara Mioni ◽  
Giuseppe Ferrazza ◽  
Maria Michela Cainazzo ◽  
Alfio Bertolini ◽  
...  

2010 ◽  
Vol 61 (1) ◽  
pp. 61-67
Author(s):  
Maja Petek ◽  
Ana Vrdoljak ◽  
Gordan Mršić

Qualitative GC-MS Assessment of TCP and Tamorf Elimination in RatsNerve agents are highly toxic organophosphorus (OP) compounds. They inhibit acetylcholinesterase (AChE), an enzyme that hydrolyses acetycholine (ACh) in the nervous system. Pathophysiological changes caused by OP poisonings are primarily the consequence of surplus ACh on cholinergic receptors and in the central nervous system. Standard treatment of OP poisoning includes combined administration of carbamates, atropine, oximes and anticonvulsants. In order to improve therapy, new compounds have been synthesised and tested. Tenocyclidine (TCP) and its adamantane derivative 1-[2-(2-thienyl)-2-adamantyl] morpholine (TAMORF) have shown interesting properties against soman poisoning. In this study, we developed a qualitative GC-MS method to measure elimination of TCP and TAMORF through rat urine in order to learn more about the mechanisms through which TCP protects an organism from OP poisoning and to determine the duration of this protective effect. GC-MS showed that six hours after treatment with TCP, rat urine contained only its metabolite 1-thienylcyclohexene, while urine of rats treated with TAMORF contained both TAMORF and its metabolites.


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