Calcium Antagonists Improve Cardiac Mechanical Performance after Thermal Trauma

Horton, Jureta W.; White, D. Jean; Maass, David L.; Sanders, Billy; Thompson, Marita; Giroir, Brett P.

doi:10.1006/jsre.1999.5726

Cited by 33 publications

(33 citation statements)

References 42 publications

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“…Similar findings were demonstrated in the heart (33,34). In burn-induced cardiocyte apoptosis, however, cardiocyte proliferation remained unchanged causing cardiac impairment and dysfunction (33,34).…”

Section: Hepatic Changes In Response To a Burn And The Hepatic Acute supporting

confidence: 75%

“…In the same study, the authors showed that small bowel epithelial cell proliferation was not increased, leading to a loss of mucosal cells and hence mucosal mass (31,32). Similar findings were demonstrated in the heart (33,34). In burn-induced cardiocyte apoptosis, however, cardiocyte proliferation remained unchanged causing cardiac impairment and dysfunction (33,34).…”

Section: Hepatic Changes In Response To a Burn And The Hepatic Acute mentioning

confidence: 71%

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The Hepatic Response to Thermal Injury: Is the Liver Important for Postburn Outcomes?

Jeschke

2009

Mol Med

142

102

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Thermal injury produces a profound hypermetabolic and hypercatabolic stress response characterized by increased endogenous glucose production via gluconeogenesis and glycogenolysis, lipolysis, and proteolysis. The liver is the central body organ involved in these metabolic responses. It is suggested that the liver, with its metabolic, inflammatory, immune, and acute phase functions, plays a pivotal role in patient survival and recovery by modulating multiple pathways following thermal injury. Studies have evaluated the role and function of the liver during the postburn response and showed that liver integrity and function are essential for survival, and that hepatic acute phase proteins are strong predictors for postburn survival. This review discusses these studies and delineates the pivotal role of the liver in patients following severe thermal injury.

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Section: Hepatic Changes In Response To a Burn And The Hepatic Acute supporting

confidence: 75%

Section: Hepatic Changes In Response To a Burn And The Hepatic Acute mentioning

confidence: 71%

The Hepatic Response to Thermal Injury: Is the Liver Important for Postburn Outcomes?

Jeschke

2009

Mol Med

142

102

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“…Similar findings were demonstrated in the heart (33,34). Burn-induced cardiocyte apoptosis; however, cardiocyte proliferation remained unchanged causing cardiac impairment and dysfunction (33,34). The mechanisms whereby a cutaneous burn induces programmed cell death in hepatocytes are not defined.…”

Section: Wwwintechopencommentioning

confidence: 64%

“…In the same study, the authors showed that small bowel epithelial cell proliferation was not increased, leading to a loss of mucosal cells and hence mucosal mass (31,32). Similar findings were demonstrated in the heart (33,34). Burn-induced cardiocyte apoptosis; however, cardiocyte proliferation remained unchanged causing cardiac impairment and dysfunction (33,34).…”

Section: Wwwintechopencommentioning

confidence: 73%

The Hepatic Acute Phase Response to Thermal Injury

Jeschke¹

2011

Acute Phase Proteins - Regulation and Functions of Acute Phase Proteins

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“…Ventricular myocytes isolated from hearts 24 h after burn injury showed an increase in both systolic and resting Ca 2ϩ concentrations (4,19,20,36). In addition, it has been reported that when animals were treated with inhibitors that regulate cellular Ca 2ϩ cycling, such as diltiazem, a Ca 2ϩ channel blocker; dantrolene, an inhibitor of the sarcoplasmic reticulum (SR) Ca 2ϩ efflux; or ruthenium red, an inhibitor of mitochondrial Ca 2ϩ accumulation, cardiac contractile performance was improved compared with untreated animals (17,20,36). However, the mediators or cellular mechanisms responsible for burn-induced contractile dysfunction are not well understood (16).…”

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confidence: 99%