Consideration in Selecting an Inhaled Anesthetic Agent in Liver Disease

Author(s):  
Chandra Pandey ◽  
Soumya Nath ◽  
Mukesh Tripathi
2017 ◽  
Vol 32 (4) ◽  
pp. 667-675 ◽  
Author(s):  
Jennifer Herzog-Niescery ◽  
Hans-Martin Seipp ◽  
Thomas Peter Weber ◽  
Martin Bellgardt

2016 ◽  
Vol 125 (5) ◽  
pp. 850-860 ◽  
Author(s):  
Katie J. Roddy ◽  
Vicki Starnes ◽  
Sukumar P. Desai

Abstract Background Crawford Williamson Long (1815 to 1878) was the first to use ether as an inhaled anesthetic for surgical operations. By not publishing his discovery for 7 yr, his pioneering work was largely overshadowed by that of Horace Wells (1815 to 1848), Charles Thomas Jackson (1805 to 1880), and William Thomas Green Morton (1819 to 1868). As a result, sites commemorating Long’s discovery are not offered the same recognition as those affiliated with Wells or Morton. Methods We highlight sites in Athens, Danielsville, and Jefferson, Georgia, that honor the first man to regularly use ether as an anesthetic agent. Extensive site visits, examination of museum artifacts, and genealogical research were used to obtain information being presented. Results Historic Oconee Hill Cemetery in Athens is where Long and members of his family are buried. Established in 1856, it is closely linked to the history of Athens and the University of Georgia (Athens, Georgia). The main site we describe is the Crawford W. Long Museum, located in Jefferson, Georgia, which opened to the public in 1957. It has undergone extensive renovations and holds an expansive collection of Long’s family heirlooms and personal artifacts. In addition, it displays an impressive art collection, depicting Long, surgical procedures, members of Long’s family, and homes associated with him. Visitors to the museum may also enjoy a walking audio tour that highlights the life of Long and his contribution to medicine. Conclusions We provide information on sites and artifacts that honor Georgia’s most celebrated physician. Much of this has not been published before, and it is our hope that Crawford Williamson Long’s legacy receives the attention it richly deserves.


2011 ◽  
Vol 11 (1) ◽  
Author(s):  
Jan FA Hendrickx ◽  
Harry Lemmens ◽  
Sofie De Cooman ◽  
André AJ Van Zundert ◽  
René EJ Grouls ◽  
...  

2002 ◽  
Vol 282 (6) ◽  
pp. H2134-H2140 ◽  
Author(s):  
David M. Roth ◽  
James S. Swaney ◽  
Nancy D. Dalton ◽  
Elizabeth A. Gilpin ◽  
John Ross

Anesthetics provide sedation and immobility facilitating echocardiography in mice, but influence cardiac function. We studied the effects of intraperitoneal and inhaled anesthetic agents on echocardiographic measurements. Mice were anesthetized with intraperitoneal tribromoethanol (TBE), ketamine-midazolam (K/M), ketamine-xylazine (K/X), or inhaled isoflurane (Isf), and echocardiographic parameters were assessed at 5, 10, 15, and 20 min. In C57BL/6N mice, Isf produced high initial heart rates (HR) that decreased to levels comparable to TBE at 15–20 min (∼450 beats/min) and the most stable percent fractional shortening (%FS) and end-diastolic dimension (EDD). With TBE, %FS initially was low, but increased comparable to Isf (∼45%) at 15 min. K/M produced similar time trends but lower absolute values compared with TBE for all parameters. K/X produced cardiac depression evidenced by low HR and %FS, and increased EDD. Isf was the most reproducible in repeat studies at 12 days. In C57BL/6J compared with C57BL/6N mice, K/M produced higher HR, and %FS and TBE produced smaller EDD. In conclusion, anesthetic agent, timing of echocardiographic measurements, and genetic background are all critical variables during echocardiography in mice.


2020 ◽  
Vol 48 (1) ◽  
pp. 545-545
Author(s):  
Zaid Noori ◽  
Jordan Swisher ◽  
Shahid Fawad ◽  
Samer AlSamman

Author(s):  
Francesco Giunta ◽  
Claudio Di Salvo ◽  
Antonio Rubino ◽  
Elena Marini

2013 ◽  
Vol 116 (6) ◽  
pp. 1272-1275 ◽  
Author(s):  
Adam C. Adler ◽  
Neil Roy Connelly ◽  
Abistanand Ankam ◽  
Karthik Raghunathan

Author(s):  
Odell T. Minick ◽  
Hidejiro Yokoo

Mitochondrial alterations were studied in 25 liver biopsies from patients with alcoholic liver disease. Of special interest were the morphologic resemblance of certain fine structural variations in mitochondria and crystalloid inclusions. Four types of alterations within mitochondria were found that seemed to relate to cytoplasmic crystalloids.Type 1 alteration consisted of localized groups of cristae, usually oriented in the long direction of the organelle (Fig. 1A). In this plane they appeared serrated at the periphery with blind endings in the matrix. Other sections revealed a system of equally-spaced diagonal lines lengthwise in the mitochondrion with cristae protruding from both ends (Fig. 1B). Profiles of this inclusion were not unlike tangential cuts of a crystalloid structure frequently seen in enlarged mitochondria described below.


2020 ◽  
Vol 134 (16) ◽  
pp. 2189-2201
Author(s):  
Jessica P.E. Davis ◽  
Stephen H. Caldwell

Abstract Fibrosis results from a disordered wound healing response within the liver with activated hepatic stellate cells laying down dense, collagen-rich extracellular matrix that eventually restricts liver hepatic synthetic function and causes increased sinusoidal resistance. The end result of progressive fibrosis, cirrhosis, is associated with significant morbidity and mortality as well as tremendous economic burden. Fibrosis can be conceptualized as an aberrant wound healing response analogous to a chronic ankle sprain that is driven by chronic liver injury commonly over decades. Two unique aspects of hepatic fibrosis – the chronic nature of insult required and the liver’s unique ability to regenerate – give an opportunity for pharmacologic intervention to stop or slow the pace of fibrosis in patients early in the course of their liver disease. Two potential biologic mechanisms link together hemostasis and fibrosis: focal parenchymal extinction and direct stellate cell activation by thrombin and Factor Xa. Available translational research further supports the role of thrombosis in fibrosis. In this review, we will summarize what is known about the convergence of hemostatic changes and hepatic fibrosis in chronic liver disease and present current preclinical and clinical data exploring the relationship between the two. We will also present clinical trial data that underscores the potential use of anticoagulant therapy as an antifibrotic factor in liver disease.


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