Cardiovascular Dysfunction Following Burn Injury: What We Have Learned from Rat and Mouse Models

• Published in: International Journal of Molecular Sciences Vol. 17; no. 1; p. 53
• Main Authors: Guillory, Ashley N, Clayton, Robert P, Herndon, David N, Finnerty, Celeste C
• Format: Journal Article Book Review
• Language: English
• Published: Switzerland MDPI AG 02.01.2016; MDPI
• Subjects: animal models; Animals; Burns; Burns - complications; Burns - drug therapy; Burns - metabolism; Burns - physiopathology; cardiac dysfunction; Cardiovascular disease; Cardiovascular Diseases - drug therapy; Cardiovascular Diseases - etiology; Cardiovascular Diseases - metabolism; Cardiovascular Diseases - physiopathology; Cardiovascular System - drug effects; Cardiovascular System - metabolism; Cardiovascular System - physiopathology; Disease Models, Animal; Humans; Mice; Molecular Targeted Therapy; Rats; Receptors, Adrenergic, beta - metabolism; Review; Rodents; thermal injury; animal models; cardiac dysfunction; thermal injury; burns
• ISSN: 1422-0067; 1661-6596; 1422-0067
• DOI: 10.3390/ijms17010053

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 β-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.