Decreased contractility and compliance of the left ventricle as complications of thermal trauma

Adams, H. R.; Baxter, Charles R.; Izenberg, Seth

doi:10.1016/0002-8703(84)90695-1

Cited by 99 publications

(44 citation statements)

References 25 publications

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“…Altered vascular tone, cardiac contractile depression, and impaired diastolic relaxation have been described after burn trauma in animal models and in humans [1][2][3][4]. Decreased cardiac output was initially attributed by numerous investigators to fluid shifts, hypovolemia, and a fall in cardiac preload; however, other investigators have attributed postburn cardiac dysfunction to myocardial depressant factors in the serum and lymph [5][6][7].…”

Section: Introductionmentioning

confidence: 99%

Calcium Antagonists Improve Cardiac Mechanical Performance after Thermal Trauma

Horton

White

Maass

et al. 1999

Journal of Surgical Research

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Section: Introductionmentioning

confidence: 99%

Calcium Antagonists Improve Cardiac Mechanical Performance after Thermal Trauma

Horton

White

Maass

et al. 1999

Journal of Surgical Research

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“…Compromised cardiac function results in organ hypoperfusion leading to impaired peripheral microcirculation, burn zone extension, and reduced resistance to bacterial infection at the wound site. Burnassociated cardiac dysfunction has been shown previously to occur independently of intravascular volume loss (1)(2)(3). Assuming that circulating "myocardial depressant factors" trigger burn-induced cardiac contractility deficits, numerous experimental studies have been done to identify a causative factor (4 -11), but a single agent responsible for burn-induced myocardial dysfunction has not been found.…”

mentioning

confidence: 99%

C5a-Blockade Improves Burn-Induced Cardiac Dysfunction

Hoesel

Niederbichler²,

Schaefer

et al. 2007

The Journal of Immunology

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We previously reported that generation of the anaphylatoxin C5a is linked to the development of cardiac dysfunction in sepsis due to C5a interaction with its receptor (C5aR) on cardiomyocytes. Burn injury involves inflammatory mechanisms that can lead to C5a generation as well. In this study, we investigated the effects of C5a blockade on burn-induced cardiac dysfunction. Using a standardized rat model of full thickness scald injury, left ventricular pressures were recorded in vivo followed by in vitro assessment of sarcomere contraction of single cardiomyocytes. Left ventricular pressures in vivo and cardiomyocyte sarcomere contractility in vitro were significantly reduced following burn injury. In the presence of anti-C5a Ab, these defects were greatly attenuated 1, 6, and 12 h after burn injury and completely abolished 24 h after burn. In vitro incubation of cardiomyocytes with bacterial LPS accentuated the impaired contractility, which was partially prevented in cardiomyocytes from burned rats that had received an anti-C5a Ab. Based on Western blot analyses, real-time PCR, and immunostaining of left ventricular heart tissue, there was a significant increase in cardiomyocyte expression of C5aR after burn injury. In conclusion, an in vivo blockade of C5a attenuates burn-induced cardiac dysfunction. Further deterioration of contractility due to the exposure of cardiomyocytes to LPS was partially prevented by C5a-blockade. These results suggest a linkage between C5a and burn-induced cardiac dysfunction and a possible contribution of LPS to these events.

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“…Myocardial cellular disruption and hemodynamic alterations, including decreased cardiac output, shock, and left ventricular (LV) failure have been documented in burned patients (36,44,50,63). Deficits in myocardial contraction and relaxation have also been described in rats, guinea pigs, rabbits, and sheep after major burn injury (1,6,21,22,24,26,27,35,64). The contractile deficits are transient, appearing 2 h and resolving by 72 h after the burn, and occur despite fluid resuscitation to maintain adequate preload (21).…”

mentioning

confidence: 99%