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.

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.

scholarly journals Pediatric burn resuscitation: past, present, and future

2017 ◽  
Vol 5 ◽  
Author(s):  
Kathleen S. Romanowski ◽  
Tina L. Palmieri
Keyword(s):  
Fluid Resuscitation ◽  
Burn Injury ◽  
Total Body Surface Area ◽  
Burn Shock ◽  
Basic Principles ◽  
Future Directions ◽  
Number Of Children ◽  
History Of ◽  
Adults And Children ◽  
Total Body

Abstract Burn injury is a leading cause of unintentional death and injury in children, with the majority being minor (less than 10%). However, a significant number of children sustain burns greater than 15% total body surface area (TBSA), leading to the initiation of the systemic inflammatory response syndrome. These patients require IV fluid resuscitation to prevent burn shock and death. Prompt resuscitation is critical in pediatric patients due to their small circulating blood volumes. Delays in resuscitation can result in increased complications and increased mortality. The basic principles of resuscitation are the same in adults and children, with several key differences. The unique physiologic needs of children must be adequately addressed during resuscitation to optimize outcomes. In this review, we will discuss the history of fluid resuscitation, current resuscitation practices, and future directions of resuscitation for the pediatric burn population.

Cellular basis for burn-mediated cardiac dysfunction in adult rabbits

1996 ◽  
Vol 271 (6) ◽  
pp. H2615-H2621 ◽  
Author(s):  
J. W. Horton
Keyword(s):  
Cardiac Myocyte ◽  
Burn Injury ◽  
Total Body Surface Area ◽  
Ringer Solution ◽  
Polymorphonuclear Neutrophils ◽  
Experimental Conditions ◽  
Cardiac Contractile ◽  
Fetal Bovine ◽  
Total Body ◽  
And Control

We have shown that cutaneous burn injury impairs cardiac contractile performance; however, the mechanisms remain unclear. In this study, New Zealand White rabbits were anesthetized with isoflurane, given a full-thickness scald burn over 30% of total body surface area, and resuscitated with lactated Ringer solution (4 ml.kg-1.%burn-1 for 24 h); rabbits handled in an identical fashion were given a sham burn. Serum obtained from burned and control (sham-burned) rabbits was aliquoted and frozen at -70 degrees C until assay. Polymorphonuclear neutrophils (PMN) were isolated 24 h postburn from both sham and burned rabbits to yield preparations with > 95% PMN with > 95% viability. Cardiac myocytes were isolated by retrograde perfusion of hearts with Ca(2+)-free collagenase-Tyrode buffer, suspended in Krebs-Henseleit buffer containing 10% fetal bovine serum and 1.8 mM Ca2+, and incubated (1 x 10(5) cells/well) in a CO2 incubator under several experimental conditions, including buffer alone, buffer plus 10% burn serum, buffer plus 10% sham serum, or buffer plus either burn or sham PMN (25 x 10(5) cells/well). Myocyte viability (%) and creatine kinase (CK; units.ml-1.10(5) cells-1) were unchanged after incubation with sham plasma or sham PMN. Incubation of sham myocytes with burn plasma caused viability to fall (from 79 +/- 3 to 54 +/- 4%, P < 0.002), whereas CK rose (from 1,639 +/- 115 to 2,803 +/- 132 units.ml-1.10(5) cells-1, P < 0.01). Similarly, incubation of sham myocytes with burn PMN reduced viability (from 83 +/- 2 to 50 +/- 3%, P < 0.01), whereas CK remained unchanged (1,880 +/- 168 units.ml-1.10(5) cells-1). Our data indicate that circulating myocardial depressant factors after burn injury contribute to cardiac myocyte injury.

Alcohol ingestion before burn injury decreases splanchnic blood flow and oxygen delivery

2005 ◽  
Vol 288 (2) ◽  
pp. H716-H721 ◽  
Author(s):  
Mashkoor A. Choudhry ◽  
Zheng F. Ba ◽  
Shadab N. Rana ◽  
Kirby I. Bland ◽  
Irshad H. Chaudry
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Oxygen Delivery ◽  
Burn Injury ◽  
Total Body Surface Area ◽  
Intestinal Barrier ◽  
Alcohol Ingestion ◽  
Splanchnic Blood Flow ◽  
Intestinal Barrier Function ◽  
Proinflammatory Mediators

Recent studies from our laboratory have shown that alcohol and burn injury impair intestinal barrier and immune functions. Although multiple factors can contribute to impaired intestinal barrier function, such an alteration could result from a decrease in intestinal blood flow (BF) and oxygen delivery (Do2). Therefore, in this study, we tested the hypothesis that alcohol ingestion before burn injury reduces splanchnic blood flow and oxygen delivery. Rats (250 g) were gavaged with alcohol to achieve a blood ethanol level in the range of 100 mg/dl before burn or sham injury (25% total body surface area). Day 1 after injury, animals were anesthetized with methoxyflurane. Blood pressure, cardiac output (CO), ±dP/d t, organ BF (in ml·min−1·100 g−1), and Do2 (in mg·ml−1·100 g−1) were determined. CO and organ BF were determined using a radioactive microsphere technique. Our results indicate that blood pressure, CO, and +dP/d t were decreased in rats receiving a combined insult of alcohol and burn injury compared with rats receiving either burn injury or alcohol alone. This is accompanied by a decrease in BF and Do2 to the liver and intestine. No significant change in BF to the coronary arteries (heart), brain, lung, skin, and muscles was observed after alcohol and burn injury. In conclusion, the results presented here suggest that alcohol ingestion before burn injury reduces splanchnic BF and Do2. Such decreases in BF and Do2 may cause hypoxic insult to the intestine and liver. Although a hypoxic insult to the liver would result in a release of proinflammatory mediators, a similar insult to the intestine will likely perturb both intestinal immune cell and barrier functions, as observed in our previous study.

scholarly journals An alteration of the gut-liver axis drives pulmonary inflammation after intoxication and burn injury in mice

2014 ◽  
Vol 307 (7) ◽  
pp. G711-G718 ◽  
Author(s):  
Michael M. Chen ◽  
Anita Zahs ◽  
Mary M. Brown ◽  
Luis Ramirez ◽  
Jerrold R. Turner ◽  
...  
Keyword(s):  
Bacterial Translocation ◽  
Burn Injury ◽  
Pulmonary Inflammation ◽  
Bacterial Load ◽  
Total Body Surface Area ◽  
Alcohol Exposure ◽  
Hepatic Damage ◽  
Wall Thickening ◽  
Alveolar Wall ◽  
Gut Barrier Function

Approximately half of all adult burn patients are intoxicated at the time of their injury and have worse clinical outcomes than those without prior alcohol exposure. This study tested the hypothesis that intoxication alters the gut-liver axis, leading to increased pulmonary inflammation mediated by burn-induced IL-6 in the liver. C57BL/6 mice were given 1.2 g/kg ethanol 30 min prior to a 15% total body surface area burn. To restore gut barrier function, the specific myosin light chain kinase inhibitor membrane-permeant inhibitor of kinase (PIK), which we have demonstrated to reduce bacterial translocation from the gut, was administered 30 min after injury. Limiting bacterial translocation with PIK attenuated hepatic damage as measured by a 47% reduction in serum alanine aminotransferase ( P < 0.05), as well as a 33% reduction in hepatic IL-6 mRNA expression ( P < 0.05), compared with intoxicated and burn-injured mice without PIK. This mitigation of hepatic damage was associated with a 49% decline in pulmonary neutrophil infiltration ( P < 0.05) and decreased alveolar wall thickening compared with matched controls. These results were reproduced by prophylactic reduction of the bacterial load in the intestines with oral antibiotics before intoxication and burn injury. Overall, these data suggest that the gut-liver axis is deranged when intoxication precedes burn injury and that limiting bacterial translocation in this setting attenuates hepatic damage and pulmonary inflammation.

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.

Molecular and pharmacological approaches to inhibiting nitric oxide after burn trauma

2003 ◽  
Vol 285 (4) ◽  
pp. H1616-H1625 ◽  
Author(s):  
Jean White ◽  
Deborah L. Carlson ◽  
Marita Thompson ◽  
David L. Maass ◽  
Billy Sanders ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cardiac Function ◽  
Total Body Surface Area ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Contractile Dysfunction ◽  
Wild Type ◽  
Burn Trauma ◽  
Cardiac Contractile ◽  
Cardiac Contractile Dysfunction

Whereas controversial, several studies have suggested that nitric oxide (NO) alters cardiac contractility via cGMP, peroxynitrite, or poly(ADP ribose) synthetase (PARS) activation. This study determined whether burn-related upregulation of myocardial inducible NO synthase (iNOS) and NO generation contributes to burn-mediated cardiac contractile dysfunction. Mice homozygous null for the iNOS gene (iNOS knockouts) were obtained from Jackson Laboratory. iNOS knockouts (KO) as well as wild-type mice were given a cutaneous burn over 40% of the total body surface area by the application of brass probes (1 × 2 × 0.3 cm) heated to 100°C to the animals' sides and back for 5 s (iNOS/KO burn and wild-type burn). Additional groups of iNOS KO and wild-type mice served as appropriate sham burn groups (iNOS/KO sham and wild-type sham). Cardiac function was assessed 24 h postburn by perfusing hearts ( n = 7–10 mice/group). Burn trauma in wild-type mice impaired cardiac function as indicated by the lower left ventricular pressure (LVP, 67 ± 2 mmHg) compared with that measured in wild-type shams (94 ± 2 mmHg, P < 0.001), a lower rate of LVP rise (+dP/d tmax, 1,620 ± 94 vs. 2,240 ± 58 mmHg/s, P < 0.001), and a lower rate of LVP fall (–dP/d tmax, 1,200 ± 84 vs. 1,800 ± 42 mmHg/s, P < 0.001). Ventricular function curves confirmed significant contractile dysfunction after burn trauma in wild-type mice. Burn trauma in iNOS KO mice produced fewer cardiac derangements compared with those observed in wild-type burns (LVP: 78 ± 5 mmHg; +dP/d t: 1,889 ± 160 mmHg/s; –dP/d t: 1,480 ± 154 mmHg/s). The use of a pharmacological approach to inhibit iNOS (aminoguanidine, given ip) in additional wild-type shams and burns confirmed the iNOS KO data. Whereas the absence of iNOS attenuated burn-mediated cardiac contractile dysfunction, these experiments did not determine the contribution of cardiac-derived NO versus NO generated by immune cells. However, our data indicate a role for NO in cardiac dysfunction after major trauma.

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.

scholarly journals Direct Peritoneal Resuscitation Improves Survival in a Murine Model of Combined Hemorrhage and Burn Injury

2020 ◽  
Vol 185 (9-10) ◽  
pp. e1528-e1535
Author(s):  
Andrew D Jung ◽  
Lou Ann Friend ◽  
Sabre Stevens-Topie ◽  
Rebecca Schuster ◽  
Alex B Lentsch ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Lung Injury ◽  
Hemorrhagic Shock ◽  
Survival Time ◽  
Median Survival ◽  
Normal Saline ◽  
Median Survival Time ◽  
Burn Injury ◽  
Total Body Surface Area ◽  
Fatty Acid Binding

ABSTRACT Introduction Combined burn injury and hemorrhagic shock are a common cause of injury in wounded warfighters. Current protocols for resuscitation for isolated burn injury and isolated hemorrhagic shock are well defined, but the optimal strategy for combined injury is not fully established. Direct peritoneal resuscitation (DPR) has been shown to improve survival in rats after hemorrhagic shock, but its role in a combined burn/hemorrhage injury is unknown. We hypothesized that DPR would improve survival in mice subjected to combined burn injury and hemorrhage. Materials and Methods Male C57/BL6J mice aged 8 weeks were subjected to a 7-second 30% total body surface area scald in a 90°C water bath. Following the scald, mice received DPR with 1.5 mL normal saline or 1.5 mL peritoneal dialysis solution (Delflex). Control mice received no peritoneal solution. Mice underwent a controlled hemorrhage shock via femoral artery cannulation to a systolic blood pressure of 25 mm Hg for 30 minutes. Mice were then resuscitated to a target blood pressure with either lactated Ringer’s (LR) or a 1:1 ratio of packed red blood cells (pRBCs) and fresh frozen plasma (FFP). Mice were observed for 24 hours following injury. Results Median survival time for mice with no DPR was 1.47 hours in combination with intravascular LR resuscitation and 2.08 hours with 1:1 pRBC:FFP. Median survival time significantly improved with the addition of intraperitoneal normal saline or Delflex. Mice that received DPR followed by 1:1 pRBC:FFP required less intravascular volume than mice that received DPR with LR, pRBC:FFP alone, and LR alone. Intraperitoneal Delflex was associated with higher levels of tumor necrosis factor alpha and macrophage inflammatory protein 1 alpha and lower levels of interleukin 10 and intestinal fatty acid binding protein. Intraperitoneal normal saline resulted in less lung injury 1 hour postresuscitation, but increased to similar severity of Delflex at 4 hours. Conclusions After a combined burn injury and hemorrhage, DPR leads to increased survival in mice. Survival was similar with the use of normal saline or Delflex. DPR with normal saline reduced the inflammatory response seen with Delflex and delayed the progression of acute lung injury. DPR may be a valuable strategy in the treatment of patients with combined burn injury and hemorrhage.

Sign in / Sign up

Export Citation Format

Share Document