Hypertonic saline-dextran suppresses burn-related cytokine secretion by cardiomyocytes

2001 ◽  
Vol 280 (4) ◽  
pp. H1591-H1601 ◽  
Author(s):  
Jureta W. Horton ◽  
David L. Maass ◽  
Jean White ◽  
Billy Sanders
Keyword(s):  
Hypertonic Saline ◽  
Burn Injury ◽  
Contractile Function ◽  
Total Body Surface Area ◽  
Isotonic Saline ◽  
Cytokine Secretion ◽  
Cardiac Contraction ◽  
Burn Trauma ◽  
Lps Challenge ◽  
Tnf Α

Whereas hypertonic saline-dextran (HSD, 7.5% NaCl in 6% D70) improves cardiac contractile function after burn trauma, the mechanisms of HSD-related cardioprotection remain unclear. We recently showed that cardiomyocytes secrete tumor necrosis factor-α (TNF-α), a response that was enhanced by burn trauma. This study addressed the question: does HSD modulate cardiac contraction/relaxation by altering cardiomyocyte TNF-α secretion? Wistar-Furth rats (325 g) were given a burn injury over 40% of the total body surface area and were then randomized to receive a bolus of either isotonic saline or HSD (4 ml/kg, n = 14 rats/group). Sham burn rats were given either isotonic saline or HSD ( n = 14 rats/group) to provide appropriate controls for the two burn groups. Hearts were isolated 24 h postburn for either Langendorff perfusion ( n = 8 hearts/group) or to prepare cardiomyocytes ( n = 6 hearts/group). Myocytes were stimulated with lipopolysaccharide (LPS) (0, 10, 25, or 50 μg for 18 h) to measure cytokine secretion. Burn trauma increased myocyte TNF-α and interleukin-1β and -6 secretion, exacerbated cytokine response to LPS stimulus, and impaired cardiac contraction. HSD treatment of burns decreased cardiomyocyte cytokine secretion, decreased responsiveness to LPS challenge with regard to cytokine secretion, and improved ventricular function. These data suggest that HSD mediates cardioprotection after burn trauma, in part, by downregulating cardiomyocyte secretion of inflammatory cytokines.

scholarly journals Hypertonic saline dextran after burn injury decreases inflammatory cytokine responses to subsequent pneumonia-related sepsis

2006 ◽  
Vol 290 (4) ◽  
pp. H1642-H1650 ◽  
Author(s):  
Jureta W. Horton ◽  
David L. Maass ◽  
D. Jean White
Keyword(s):  
Hypertonic Saline ◽  
Burn Injury ◽  
Inflammatory Responses ◽  
Contractile Function ◽  
Total Body Surface Area ◽  
Isotonic Saline ◽  
Ringer Solution ◽  
Myocardial Inflammation ◽  
Adult Rats ◽  
Tnf Α

The present study examined the hypothesis that hypertonic saline dextran (HSD), given after an initial insult, attenuates exaggerated inflammation that occurs with a second insult. Adult rats ( n = 15 per group) were divided into groups 1 (sham burn), 2 [40% total body surface area burn + 4 ml/kg isotonic saline (IS) + 4 ml·kg−1·% burn−1 lactated Ringer solution (LR)], and 3 (burn + 4 ml/kg HSD + LR), all studied 24 h after burns. Groups 4 (sham burn), 5 (burn + IS + LR), and 6 (burns + HSD + LR) received intratracheal (IT) vehicle 7 days after burns; groups 7 (burn + IS + LR) and 8 (burn + HSD + LR) received IT Streptococcus pneumoniae (4 × 106 colony-forming units) 7 days after burn. Groups 4–8 were studied 8 days after burn and 24 h after IT septic challenge. When compared with sham burn, contractile defects occurred 24 h after burn in IS-treated but not HSD-treated burns. Cardiac inflammatory responses (pg/ml TNF-α) were evident with IS (170 ± 10) but not HSD (45 ± 5) treatment vs. sham treatment (80 ± 15). Pneumonia-related sepsis 8 days after IS-treated burns ( group 7) exacerbated TNF-α responses/contractile dysfunction vs. IS-treated burns in the absence of sepsis ( P < 0.05). Sepsis that occurred after HSD-treated burns ( group 8) had less myocyte TNF-α secretion/better contractile function than IS-treated burns given septic challenge ( group 7, P < 0.05). We conclude that an initial burn injury exacerbates myocardial inflammation/dysfunction occurring with a second insult; giving HSD after the initial insult attenuates myocardial inflammation/dysfunction associated with a second hit, suggesting that HSD reduces postinjury risk for infectious complications.

Changes in cardiac contractile function and myocardial [Ca2+]i after burn trauma: NMR study

2001 ◽  
Vol 280 (4) ◽  
pp. H1916-H1922 ◽  
Author(s):  
Zhao-Fan Xia ◽  
Piyu Zhao ◽  
Jureta W. Horton
Keyword(s):  
Nmr Spectroscopy ◽  
Diastolic Pressure ◽  
Contractile Function ◽  
Total Body Surface Area ◽  
Left Ventricular ◽  
Cardiac Contraction ◽  
Free Calcium ◽  
Bicarbonate Buffer ◽  
Burn Trauma ◽  
Nmr Study

Cutaneous burn trauma causes cardiac contraction and relaxation defects, but the mechanism is unclear. Previous studies suggest that burn-related changes in myocyte handling of calcium may play an important role in postburn cardiac dysfunction. With the use of a high dissociation constant ( K d) calcium indicator 1,2-bis(2-amino-5,6-difluorophenoxy)-ethane- N,N,N′, N′-tetraacetic acid (TF-BAPTA) and 19F NMR spectroscopy, this study examined the correlation between the changes in cytosolic free calcium concentration ([Ca2+]i) and cardiac function after burn trauma. Sprague-Dawley rats were given scald burn (over 40% of the total body surface area) or sham burn. Twenty-four hours later, the hearts were excised and perfused by the Langendorff method with a modified phosphate-free Krebs-Henseleit bicarbonate buffer. Left ventricular (LV) developed pressure (LVDP), calculated from peak systolic LV pressure and LV end-diastolic pressure, was assessed through a catheter attached to an intraventricular balloon. At the same time, 31P and 19F NMR spectroscopy was performed before and after TF-BAPTA loading. LVDP measured in hearts from burned rats was <40% than that measured in hearts from sham burn rats (65 ± 6 vs. 110 ± 12 mmHg, P < 0.01); [Ca2+]i was increased fourfold in hearts from the burned group compared with that measured in the sham burn group (0.807 ± 0.192 vs. 3.891 ± 0.929 μM). Loading TF-BAPTA in hearts transiently decreased LVDP by 15%. Phosphocreatine-to-Pi ratio decreased, but ATP and intracellular pH remained unchanged by either TF-BAPTA loading or burn trauma. In conclusion, burn trauma impaired cardiac contractility, and this functional defect was paralleled by a significant rise in [Ca2+]i in the heart.

Bactericidal/permeability increasing protein attenuates the myocardial inflammation/dysfunction that occurs with burn complicated by subsequent infection

2007 ◽  
Vol 103 (3) ◽  
pp. 948-958 ◽  
Author(s):  
Jureta W. Horton ◽  
David L. Maass ◽  
D. Jean White ◽  
Joseph P. Minei
Keyword(s):  
Contractile Function ◽  
Total Body Surface Area ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Cytokine Secretion ◽  
Myocardial Inflammation ◽  
Susceptibility To Infection ◽  
Tnf Α ◽  
Total Body ◽  
T Values

Intubation and mechanical ventilation after burn contribute to pneumonia-related infection. Although postburn presence or absence of endotoxin has been described, inactivation of Toll-like receptor 4 signaling has been shown to improve postburn organ function, suggesting that LPS participates in burn-related susceptibility to infection. We hypothesized that bactericidal/permeability-increasing protein (rBPI) given postburn would attenuate myocardial inflammation/dysfunction associated with postburn septic challenge given 7 days postburn. Rats were given burn over 40% total body surface area, lactated Ringer 4 ml·kg−1·% burn−1; burns received either vehicle or rBPI, 1 mg·kg−1·h−1for 48 h postburn. Postburn day 7, subgroups of burns and shams were given intratracheal Klebsiella pneumoniae, 4 × 106CFU to produce burn complicated by sepsis; additional sham and burn subgroups received intratracheal vehicle to produce sham sepsis. Vehicle-treated groups: 1) sham burn + sham sepsis 2) sham burn + sepsis, 3) burn + sham sepsis, 4) burn + sepsis. rBPI-treated groups: 5) sham burn + sham sepsis, 6) sham burn + sepsis, 7) burn + sham sepsis, 8) burn + sepsis. Cardiomyocyte cytokine secretion and myocardial function were studied 24 h after septic challenge, postburn day 8. Pneumonia-related infection 8 days after vehicle-treated burn produced myocyte cytokine secretion (pg/ml), indicated by increased myocyte TNF-α, 549 ± 46; IL-1β, 50 ± 8; IL-6, 286 ± 3 levels compared with levels in sham myocytes (TNF-α, 88 ± 11; IL-1β, 7 ± 1; IL-6, 74 ± 10; P < 0.05). Contractile dysfunction was evident from lower left ventricular pressure ±dP/d t values in this group compared with sham. rBPI attenuated myocyte cytokine responses to septic challenge and improved contractile function, suggesting that burn-related mobilization of microbial-like products contribute to postburn susceptibility to infection.

Role of cytosolic vs. mitochondrial Ca2+ accumulation in burn injury-related myocardial inflammation and function

2005 ◽  
Vol 288 (2) ◽  
pp. H744-H751 ◽  
Author(s):  
David L. Maass ◽  
Jean White ◽  
Billy Sanders ◽  
Jureta W. Horton
Keyword(s):  
Room Temperature ◽  
Burn Injury ◽  
Imaging System ◽  
Total Body Surface Area ◽  
Myocardial Inflammation ◽  
Adult Rats ◽  
Burn Trauma ◽  
Fura 2 ◽  
Tnf Α

This study was designed to examine the role of mitochondrial Ca2+ homeostasis in burn-related myocardial inflammation. We hypothesized that mitochondrial Ca2+ is a primary modulator of cardiomyocyte TNF-α, IL-1β, and IL-6 responses to injury and infection. Ventricular myocytes were prepared by Langendorff perfusion of hearts from adult rats subjected to sham burn or burn injury over 40% of total body surface area to produce enzymatic (collagenase) digestion. Isolated cardiomyocytes were suspended in MEM, cell number was determined, and aliquots of myocytes from each experimental group were loaded with fura 2-AM (2 μg/ml) for 1) 45 min at room temperature to measure total cellular Ca2+, 2) 45 min at 30°C followed by incubation at 37°C for 2 h to eliminate cytosolic fluorescence, and 3) 20 min at 37°C in MnCl2 (200 μM)-containing buffer to quench cytosolic fura 2-AM signal. In vitro studies included preparation of myocytes from control hearts and challenge of myocytes with LPS or burn serum (BS), which have been shown to increase cytosolic Ca2+. Additional aliquots of myocytes were challenged with LPS or BS with or without a selective inhibitor of mitochondrial Ca2+, ruthenium red (RR). All cells were examined on a stage-inverted microscope that was interfaced with the InCyt Im2 fluorescence imaging system. Heat treatment or MnCl2 challenge eliminated myocyte cytosolic fluorescence, whereas cells maintained at room temperature retained 95% of their initial fluorescence. Compared with Ca2+ levels measured in sham myocytes, burn trauma increased cytosolic Ca2+ from 90 ± 3 to 293 ± 6 nM ( P < 0.05) and mitochondrial Ca2+ from 24 ± 1 to 75 ± 2 nM ( P < 0.05). LPS (25 μg/5 × 104 cells) or BS (10% by volume) challenge for 18 h increased cardiomyocyte cytosolic and mitochondrial Ca2+ and promoted myocyte secretion of TNF-α, IL-1β, and IL-6. RR pretreatment decreased LPS- and BS-related rise in mitochondrial Ca2+ and cytokine secretion but had no effect on cytosolic Ca2+. BS challenge in perfused control hearts impaired myocardial contraction/relaxation, and RR pretreatment of hearts prevented BS-related myocardial contractile dysfunction. Our data suggest that a rise in mitochondrial Ca2+ is one modulator of myocardial inflammation and dysfunction in injury states such as sepsis and burn trauma.

Caspase inhibition reduces cardiac myocyte dyshomeostasis and improves cardiac contractile function after major burn injury

2007 ◽  
Vol 103 (1) ◽  
pp. 323-330 ◽  
Author(s):  
Deborah L. Carlson ◽  
David L. Maass ◽  
Jean White ◽  
Patricia Sikes ◽  
Jureta W. Horton
Keyword(s):  
Cardiac Myocyte ◽  
Burn Injury ◽  
Contractile Function ◽  
Total Body Surface Area ◽  
Cysteine Proteases ◽  
Sodium Concentration ◽  
Sprague Dawley ◽  
Cardiac Contractile Function ◽  
Caspase 1 ◽  
Major Burn

In the heart, thermal injury activates a group of intracellular cysteine proteases known as caspases, which have been suggested to contribute to myocyte inflammation and dyshomeostasis. In this study, Sprague-Dawley rats were given either a third-degree burn over 40% total body surface area plus conventional fluid resuscitation or sham burn injury. Experimental groups included 1) sham burn given vehicle, 400 μl DMSO; 2) sham burn given Q-VD-OPh (6 mg/kg), a highly specific and stable caspase inhibitor, 24 and 1 h prior to sham burn; 3) burn given vehicle, DMSO as above; 4) burn given Q-VD-OPh (6 mg/kg) 24 and 1 h prior to burn. Twenty-four hours postburn, hearts were harvested and studied with regard to myocardial intracellular sodium concentration, intracellular pH, ATP, and phosphocreatine (23Na/31P nuclear magnetic resonance); myocardial caspase-1, -3,and -8 expression; myocyte Na+ (fluorescent indicator, sodium-binding benzofurzan isophthalate); myocyte secretion of TNF-α, IL-1β, IL-6, and IL-10; and myocardial performance (Langendorff). Burn injury treated with vehicle alone produced increased myocardial expression of caspase-1, -3, and -8, myocyte Na+ loading, cytokine secretion, and myocardial contractile depression; cellular pH, ATP, and phosphocreatine were stable. Q-VD-OPh treatment in burned rats attenuated myocardial caspase expression, prevented burn-related myocardial Na+ loading, attenuated myocyte cytokine responses, and improved myocardial contraction and relaxation. The present data suggest that signaling through myocardial caspases plays a pivotal role in burn-related myocyte sodium dyshomeostasis and myocyte inflammation, perhaps contributing to burn-related contractile dysfunction.

Cardiac effects of burn injury complicated by aspiration pneumonia-induced sepsis

2003 ◽  
Vol 285 (1) ◽  
pp. H47-H58 ◽  
Author(s):  
Jean White ◽  
James Thomas ◽  
David L. Maass ◽  
Jureta W. Horton
Keyword(s):  
Burn Injury ◽  
Contractile Function ◽  
Total Body Surface Area ◽  
Multiple Organ ◽  
Male Rats ◽  
Intratracheal Administration ◽  
Degree Burn ◽  
The Subject ◽  
Total Body ◽  
Factor Α

Early fluid resuscitation, antimicrobials, early excision, and grafting have improved survival in the early postburn period; however, a significant incidence of pneumonia-related sepsis occurs after burn injury, often progressing to multiple organ failure. Recent studies have suggested that this initial injury (burn injury) primes the subject, producing an exaggerated response to a second insult, such as pneumonia-related sepsis. We developed an experimental animal model that included a third-degree burn over 40% of the total body surface area, followed by sepsis (intratracheal administration of Streptococcus pneumoniae, 4 × 106 colony-forming unit), which was produced either 48 or 72 h after burn injury in adult male rats. Hearts harvested after either burn alone, sepsis alone, or burn plus sepsis were used to assess either contractile function (Langendorff) or cardiomyocyte secretion of tumor necrosis factor-α, interleukin (IL)-1β, IL-6, and IL-10 (ELISA). Experimental groups included the following: 1) sham (sham burn and no sepsis); 2) burn injury alone studied either 24, 48, or 72 h postburn; 3) pneumonia-related sepsis in the absence of burn injury; and 4) pneumonia-induced sepsis studied either 48 or 72 h after an initial burn injury. Burn injury alone (24 h) or sepsis alone produced myocardial contractile defects and increases in pro- and anti-inflammatory cytokine secretion by cardiomyocytes. Sepsis that occurred 48 h postburn exacerbated the cardiac contractile defects seen with either burn alone or sepsis alone. Sepsis that occurred 72 h postburn produced contractile defects resembling those seen in either burn alone or sepsis alone. In conclusion, our data suggest that burn injury primes the subject such that a second insult early in the postburn period produces significantly greater cardiac abnormalities than those seen with either burn alone or sepsis alone.

Arginine in burn injury improves cardiac performance and prevents bacterial translocation

1998 ◽  
Vol 84 (2) ◽  
pp. 695-702 ◽  
Author(s):  
Jureta W. Horton ◽  
Jean White ◽  
David Maass ◽  
Billy Sanders
Keyword(s):  
Blood Pressure ◽  
Bacterial Translocation ◽  
Fluid Resuscitation ◽  
Burn Injury ◽  
Total Body Surface Area ◽  
Cardiac Performance ◽  
Pharmacological Intervention ◽  
Adult Rats ◽  
Burn Trauma ◽  
Cardiac Contractile

Horton, Jureta W., Jean White, David Maass, and Billy Sanders. Arginine in burn injury improves cardiac performance and prevents bacterial translocation. J. Appl. Physiol. 84(2): 695–702, 1998.—This study examined the effects of arginine supplement of fluid resuscitation from burn injury on cardiac contractile performance and bacterial translocation after a third-degree burn comprising 43% of the total body surface area in adult rats. Before burn injury, rats were instrumented to measure blood pressure; after burn (or sham injury), paired groups of sham-burned and burned rats were given vehicle (saline), l-arginine,d-arginine, or N-methyl-l-arginine (300 mg/kg in 0.3 ml of saline 30 min, 6 h, and 23 h postburn) plus fluid resuscitation; sham-burned rats received drug only. Twenty-four hours after burn trauma, hemodynamics were measured; the animals were then killed and randomly assigned to Langendorff heart studies or to studies examining translocation of gut bacteria. Burn rats treated with vehicle,d-arginine, or N-methyl-l-arginine had well-defined cardiocirculatory responses that included hypotension, tachycardia, respiratory compensation for metabolic acidosis, hypocalcemia, cardiac contractile depression, and significant bacterial translocation. Compared with values measured in vehicle-treated burn rats, l-arginine given after burn improved blood pressure, prevented tachycardia, reduced serum lactate levels, improved cardiac performance, and significantly reduced bacterial translocation, confirming thatl-arginine administration after burn injury provided significant cardiac and gastrointestinal protection. Circulating neutrophil counts fell after burn trauma and serum glucagon levels rose, but these changes were not altered by pharmacological intervention. Our finding of significantly higher coronary perfusate guanosine 3′,5′-cyclic monophosphate concentration inl-arginine-treated burn rats suggests that the beneficial effects ofl-arginine were mediated by nitric oxide production.

scholarly journals IκB overexpression in cardiomyocytes prevents NF-κB translocation and provides cardioprotection in trauma

2003 ◽  
Vol 284 (3) ◽  
pp. H804-H814 ◽  
Author(s):  
Deborah L. Carlson ◽  
D. Jean White ◽  
David L. Maass ◽  
Robin C. Nguyen ◽  
Brett Giroir ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Cardiac Tissue ◽  
Nuclear Translocation ◽  
Total Body Surface Area ◽  
Nuclear Factor Κb ◽  
Cardiac Performance ◽  
Wild Type ◽  
Burn Trauma ◽  
Tnf Α ◽  
Cardiac Contractile Dysfunction

This study examined the effects of either IκBα overexpression (transgenic mice) or N-acetyl-leucinyl-leucinyl-norleucinal (ALLN) administration (proteosome inhibitor in wild-type mice) on cardiomyocyte secretion of tumor necrosis factor-α (TNF-α) and on cardiac performance after burn trauma. Transgenic mice were divided into four experimental groups. IκBα overexpressing mice were given a third-degree scald burn over 40% of the total body surface area or wild-type littermates were given either a scald or sham burn to provide appropriate controls. Pharmacological studies included ALLN (20 mg/kg) administration in either burned wild-type mice or wild-type shams. Burn trauma in wild-type mice promoted nuclear factor-κB (NF-κB) nuclear translocation, cardiomyocyte secretion of TNF-α, and impaired cardiac performance. IκBα overexpression or ALLN treatment of burn trauma prevented NF-κB activation in cardiac tissue, prevented cardiomyocyte secretion of TNF-α, and ablated burn-mediated cardiac contractile dysfunction. These data suggest that NF-κB activation and inflammatory cytokine secretion play a significant role in postburn myocardial abnormalities.

scholarly journals Burn injury induces intestinal inflammatory response mediated by Th17 in burn-primed endotoxemic mice

2020 ◽  
Author(s):  
Kazuhiko Sekine ◽  
Takayuki Shibusawa ◽  
Seitaro Fujishima ◽  
Naoki Aikawa ◽  
Junichi Sasaki
Keyword(s):  
Lamina Propria ◽  
Mononuclear Cells ◽  
Burn Injury ◽  
Inflammatory Responses ◽  
Total Body Surface Area ◽  
Vital Role ◽  
Mice Model ◽  
Th17 Response ◽  
Lamina Propria Mononuclear Cells ◽  
Tnf Α

Objective: This study aimed to elucidate the mechanism underlying the susceptibility to infection-related acute lung injury by focusing on the role of gut mucosal T-helper (Th) 17 cells that preferentially produce IL-17 with probiotics in a burn-primed endotoxemic mice model. Methods: Mice were subjected to a 15% total body surface area third-degree burn. Survival from lethal lipopolysaccharide (LPS) administration (3 mg/kg) on 11th day post burn was assessed in mice fed by chow with or without 1.2% Lactobacillus powder after burn injury. Lamina propria mononuclear cells were enzymatically isolated from the ileum removed on 11th day post burn and incubated along with 1 μg/mL LPS or 10 μg/mL anti-CD3 antibody for 24 h; subsequently, the following seven cytokines were analyzed in the supernatant: IFN-γ, TNF-α, IL-2, IL-4, IL-6, IL-10, and IL-17. Results: Lactobacillus treatment post-burn injury markedly improved survival after lethal endotoxemia in burn-primed mice (64.3% vs. 21.4%, p = 0.03). The production of proinflammatory cytokines such as TNF-α, IL-6, and IL-17 by lamina propria mononuclear T-lymphocytes and macrophages including Th17 response was augmented by burn injury but decreased with Lactobacillus treatment after burn injury. Conclusions: Th17- and Th17-mediated inflammatory responses in the gut mucosa may play a vital role, which could be attenuated by Lactobacillus treatment, in survival of lethal endotoxemia in burn-primed mice.

scholarly journals Burn injury decreases myocardial Na-K-ATPase activity: role of PKC inhibition

2007 ◽  
Vol 293 (4) ◽  
pp. R1684-R1692 ◽  
Author(s):  
Jureta W. Horton ◽  
Jing Tan ◽  
D. Jean White ◽  
David L. Maass
Keyword(s):  
Atpase Activity ◽  
Time Course ◽  
Burn Injury ◽  
Contractile Function ◽  
Myocardial Dysfunction ◽  
Total Body Surface Area ◽  
Ringer Solution ◽  
Sodium Accumulation ◽  
Major Burn ◽  
Myocardial Contractile

Cardiomyocyte sodium accumulation after burn injury precedes the development of myocardial contractile dysfunction. The present study examined the effects of burn injury on Na-K-ATPase activity in adult rat hearts after major burn injury and explored the hypothesis that burn-related changes in myocardial Na-K-ATPase activity are PKC dependent. A third-degree burn injury (or sham burn) was given over 40% total body surface area, and rats received lactated Ringer solution (4 ml·kg−1·% burn−1). Subgroups of rats were killed 2, 4, or 24 h after burn ( n = 6 rats/time period), hearts were homogenized, and Na-K-ATPase activity was determined from ouabain-sensitive phosphate generation from ATP by cardiac sarcolemmal vesicles. Additional groups of rats were studied at several times after burn to determine the time course of myocyte sodium loading and the time course of myocardial dysfunction. Additional groups of sham burn-injured and burn-injured rats were given calphostin, an inhibitor of PKC, and Na-K-ATPase activity, cell Na+, and myocardial function were measured. Burn injury caused a progressive rise in cardiomyocyte Na+, and myocardial Na-K-ATPase activity progressively decreased after burn, while PKC activity progressively rose. Administration of calphostin to inhibit PKC activity prevented both the burn-related decrease in myocardial Na-K-ATPase and the rise in intracellular Na+ and improved postburn myocardial contractile performance. We conclude that burn-related inhibition of Na-K-ATPase likely contributes to the cardiomyocyte accumulation of intracellular Na+. Since intracellular Na+ is one determinant of electrical-mechanical recovery after insults such as burn injury, burn-related inhibition of Na-K-ATPase may be critical in postburn recovery of myocardial contractile function.

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