Cardiovascular dysfunction following burn injury: What we have learned from rat and mouse models

Ashley Guillory, Robert P. Clayton, David Herndon, Celeste Finnerty

Research output: Contribution to journalArticle

15 Citations (Scopus)

Abstract

Severe burn profoundly affects organs both proximal and distal to the actual burn site. Cardiovascular dysfunction is a well-documented phenomenon that increases morbidity and mortality following a massive thermal trauma. Beginning immediately post-burn, during the ebb phase, cardiac function is severely depressed. By 48 h post-injury, cardiac function rebounds and the post-burn myocardium becomes tachycardic and hyperinflammatory. While current clinical trials are investigating a variety of drugs targeted at reducing aspects of the post-burn hypermetabolic response such as heart rate and cardiac work, there is still a paucity of knowledge regarding the underlying mechanisms that induce cardiac dysfunction in the severely burned. There are many animal models of burn injury, from rodents, to sheep or swine, but the majority of burn related cardiovascular investigations have occurred in rat and mouse models. This literature review consolidates the data supporting the prevalent role that α-adrenergic receptors play in mediating post-burn cardiac dysfunction and the idea that pharmacological modulation of this receptor family is a viable therapeutic target for resolving burn-induced cardiac deficits.

Original languageEnglish (US)
Article number53
JournalInternational Journal of Molecular Sciences
Volume17
Issue number1
DOIs
StatePublished - Jan 2 2016

Fingerprint

Burns
rats
mice
Rats
adrenergics
sheep
myocardium
heart rate
rodents
animal models
swine
mortality
Wounds and Injuries
organs
Adrenergic Receptors
Animals
drugs
Modulation
modulation
Pharmaceutical Preparations

Keywords

  • Animal models
  • Burns
  • Cardiac dysfunction
  • Thermal injury

ASJC Scopus subject areas

  • Physical and Theoretical Chemistry
  • Organic Chemistry
  • Spectroscopy
  • Inorganic Chemistry
  • Catalysis
  • Molecular Biology
  • Computer Science Applications

Cite this

Cardiovascular dysfunction following burn injury : What we have learned from rat and mouse models. / Guillory, Ashley; Clayton, Robert P.; Herndon, David; Finnerty, Celeste.

In: International Journal of Molecular Sciences, Vol. 17, No. 1, 53, 02.01.2016.

Research output: Contribution to journalArticle

@article{f6f7e537b7ad4ad38e8c60c7f07ae06d,
title = "Cardiovascular dysfunction following burn injury: What we have learned from rat and mouse models",
abstract = "Severe burn profoundly affects organs both proximal and distal to the actual burn site. Cardiovascular dysfunction is a well-documented phenomenon that increases morbidity and mortality following a massive thermal trauma. Beginning immediately post-burn, during the ebb phase, cardiac function is severely depressed. By 48 h post-injury, cardiac function rebounds and the post-burn myocardium becomes tachycardic and hyperinflammatory. While current clinical trials are investigating a variety of drugs targeted at reducing aspects of the post-burn hypermetabolic response such as heart rate and cardiac work, there is still a paucity of knowledge regarding the underlying mechanisms that induce cardiac dysfunction in the severely burned. There are many animal models of burn injury, from rodents, to sheep or swine, but the majority of burn related cardiovascular investigations have occurred in rat and mouse models. This literature review consolidates the data supporting the prevalent role that α-adrenergic receptors play in mediating post-burn cardiac dysfunction and the idea that pharmacological modulation of this receptor family is a viable therapeutic target for resolving burn-induced cardiac deficits.",
keywords = "Animal models, Burns, Cardiac dysfunction, Thermal injury",
author = "Ashley Guillory and Clayton, {Robert P.} and David Herndon and Celeste Finnerty",
year = "2016",
month = "1",
day = "2",
doi = "10.3390/ijms17010053",
language = "English (US)",
volume = "17",
journal = "International Journal of Molecular Sciences",
issn = "1661-6596",
publisher = "Multidisciplinary Digital Publishing Institute (MDPI)",
number = "1",

}

TY - JOUR

T1 - Cardiovascular dysfunction following burn injury

T2 - What we have learned from rat and mouse models

AU - Guillory, Ashley

AU - Clayton, Robert P.

AU - Herndon, David

AU - Finnerty, Celeste

PY - 2016/1/2

Y1 - 2016/1/2

N2 - Severe burn profoundly affects organs both proximal and distal to the actual burn site. Cardiovascular dysfunction is a well-documented phenomenon that increases morbidity and mortality following a massive thermal trauma. Beginning immediately post-burn, during the ebb phase, cardiac function is severely depressed. By 48 h post-injury, cardiac function rebounds and the post-burn myocardium becomes tachycardic and hyperinflammatory. While current clinical trials are investigating a variety of drugs targeted at reducing aspects of the post-burn hypermetabolic response such as heart rate and cardiac work, there is still a paucity of knowledge regarding the underlying mechanisms that induce cardiac dysfunction in the severely burned. There are many animal models of burn injury, from rodents, to sheep or swine, but the majority of burn related cardiovascular investigations have occurred in rat and mouse models. This literature review consolidates the data supporting the prevalent role that α-adrenergic receptors play in mediating post-burn cardiac dysfunction and the idea that pharmacological modulation of this receptor family is a viable therapeutic target for resolving burn-induced cardiac deficits.

AB - Severe burn profoundly affects organs both proximal and distal to the actual burn site. Cardiovascular dysfunction is a well-documented phenomenon that increases morbidity and mortality following a massive thermal trauma. Beginning immediately post-burn, during the ebb phase, cardiac function is severely depressed. By 48 h post-injury, cardiac function rebounds and the post-burn myocardium becomes tachycardic and hyperinflammatory. While current clinical trials are investigating a variety of drugs targeted at reducing aspects of the post-burn hypermetabolic response such as heart rate and cardiac work, there is still a paucity of knowledge regarding the underlying mechanisms that induce cardiac dysfunction in the severely burned. There are many animal models of burn injury, from rodents, to sheep or swine, but the majority of burn related cardiovascular investigations have occurred in rat and mouse models. This literature review consolidates the data supporting the prevalent role that α-adrenergic receptors play in mediating post-burn cardiac dysfunction and the idea that pharmacological modulation of this receptor family is a viable therapeutic target for resolving burn-induced cardiac deficits.

KW - Animal models

KW - Burns

KW - Cardiac dysfunction

KW - Thermal injury

UR - http://www.scopus.com/inward/record.url?scp=84953258214&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84953258214&partnerID=8YFLogxK

U2 - 10.3390/ijms17010053

DO - 10.3390/ijms17010053

M3 - Article

C2 - 26729111

AN - SCOPUS:84953258214

VL - 17

JO - International Journal of Molecular Sciences

JF - International Journal of Molecular Sciences

SN - 1661-6596

IS - 1

M1 - 53

ER -