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Titolo:
Development of an acute burn model in adult mice for studies of cardiac function and cardiomyocyte cellular function
Autore:
White, J; Maass, DL; Giroir, B; Horton, JW;
Indirizzi:
Univ Texas, SW Med Ctr, Dept Surg, Dallas, TX 75216 USA Univ Texas DallasTX USA 75216 W Med Ctr, Dept Surg, Dallas, TX 75216 USA
Titolo Testata:
SHOCK
fascicolo: 2, volume: 16, anno: 2001,
pagine: 122 - 129
SICI:
1073-2322(200108)16:2<122:DOAABM>2.0.ZU;2-2
Fonte:
ISI
Lingua:
ENG
Soggetto:
NECROSIS-FACTOR-ALPHA; GUINEA-PIGS; CONTRACTILE DYSFUNCTION; THERMAL-INJURY; LEFT-VENTRICLE; SEPTIC SHOCK; INTERLEUKIN-1-BETA; APOPTOSIS; ANTIBODY; TRAUMA;
Keywords:
Langendorff perfusion; cardiomyocyte isolation by collagenase digestion; cardiomyocyte secretion of TNF alpha; thermal trauma; Fura-2AM; myocyte [Ca (2+)](i);
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
38
Recensione:
Indirizzi per estratti:
Indirizzo: Horton, JW Univ Texas, SW Med Ctr, Dept Surg, 5323 Harry Hines Blvd, Dallas, TX 75216USA Univ Texas 5323 Harry Hines Blvd Dallas TX USA 75216 X 75216USA
Citazione:
J. White et al., "Development of an acute burn model in adult mice for studies of cardiac function and cardiomyocyte cellular function", SHOCK, 16(2), 2001, pp. 122-129

Abstract

The increasing availability of mice with gene supplementation (transgenic), site-specific inactivation mutations (gene "knock-outs"), or site-specific genetic modification mutations (gene "knock-ins") has spurred interest inthe development of murine trauma models. In this study, C57 BL/6 mice (28 g) were given a cutaneous burn over 40% total body surface area by applyingbrass probes (1 x 2 x 0.003 cm) heated to 100 degreesC in boiling water tothe animals side and back for 5 s. Shams received anesthesia alone and notburn. Mice were killed 24 h post-burn to determine presence of partial-thickness or full-thickness burn injury, cardiac contractile function (Langendorff perfusion, n = 7 or 8 mice/group) or to examine cardiac myocyte cytokine secretion in isolated cardiomyocytes (collagenase perfusion, n = 4 or 5 mice/group). All mice were killed 24 h post-burn for subsequent cardiac or cardiomyocyte studies. Our studies confirm that this murine model of burn trauma produced mixed partial- or full-thickness burn injury, whereas there was no necrosis or inflammation in sham burn mice. Baseline hematocrits were similar in all mice (44 +/- 1) but decreased after burn trauma (37 +/- 1), likely because of the volume of fluid resuscitation and hemodilution. Burn trauma impaired cardiac contraction and relaxation as indicated by the lower left ventricular pressure (LVP) measured in burn (56 4) compared to that measured in shams (84 +/- 1 mmHg, P < 0.001), a lower rate of LVP rise (+dP/dt max, 1393 +/- 10 vs. 2000 +/- 41 mmHg/s, P < 0.002), and reduced LVP fall (-dP/dt max, 1023 +/- 40 vs. 1550 +/- 50, P < 0.001). These differences occurred despite similar coronary perfusion pressures and heart rates in both sham and burn mice. Ventricular function curves were shifted downward in the burn mice in the direction of contractile failure; in addition, hearts from burn mice had reduced LVP and +/- dP/dt responses to increases in coronary flow rate, increases in perfusate Ca2+, and to isoproterenol challenge (P < 0.05). Burn trauma promoted cardiac myocyte secretion of tumor necrosis factor (TNF alpha) (175 +/- 6 pg/mL) compared to that measured in shams (72 +/- 9 pg/mL, P < 0.05); burn trauma also increased cardiac myocyte secretion of interleukin 10 (IL-1 beta) (sham: 2 +/- 0.5; burn: 22 +/- 1 pg/mL, P < 0.05) and IL-6 (sham: 70 +/- 6; burn: 148 +/- 16 pg/mL, P < 0.05). Anti-TNF alpha strategies prevented burn-mediated cardiac contractile deficits. Burn trauma altered Ca2+ homeostasis in murine cardlomyocytes (Fura-2 AM loading). [Ca (2+)](i) in myocytes from burns (185 +/- 4 nM) was higher than values measured in myocytes from shams (86 +/- nM, P < 0.05). These data confirm that the murine burn model provides a reasonable approach to study the molecular and cell biology of inflammation in organ dysfunction after burn trauma.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 01/12/20 alle ore 22:00:45