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| 1 | Pyruvate-fortified resuscitation stabilizes cardiac electrical activity and energy metabolism during hypovolemia显示文摘AIM: To test the hypothesis that fluid resuscitation with Ringer's solution enriched with pyruvate(PR), a physiological antioxidant and energy substrate, affords protection of myocardial metabolism and electrophysiological performance superior to lactated Ringer's(LR) during hypovolemia and hindlimb ischemia-reperfusion.METHODS: Male domestic goats(25-30 kg) were exsanguinated to a mean arterial pressure of 48 ± 1 mm Hg. Right hindlimb ischemia was imposed for 90 min by applying a tourniquet and femoral crossclamp. LR or PR, infused iv, delivered 0.05 mmol/kg per minute L-lactate or pyruvate, respectively, from 30 min hindlimb ischemia until 30 min post-ischemia. Time controls(TC) underwent neither hemorrhage, hindlimb ischemia nor resuscitation. Goats were sacrificed and left ventricular myocardium biopsied at 90 min fluid resuscitation(n = 6 per group) or 3.5 h later(n = 9 LR, 10 PR, 8 TC).RESULTS: Myocardial 8-isoprostane content, phosphocreatine phosphorylation potential, creatine kinase activity, and heart rate-adjusted QT interval(QTc) vari- ability were evaluated at 90 min resuscitation and 3.5 h post-resuscitation. PR sharply lowered pro-arrhythmic QTc variability vs LR(P < 0.05); this effect persisted 3.5 h post-resuscitation. PR lowered myocardial 8-isoprostane content, a product of oxidative stress, by 39 and 37% during and 3.5 h after resuscitation, respectively, vs LR. Creatine kinase activity fell 42% post-LR vs TC(P < 0.05), but was stable post-PR(P < 0.02 vs post-LR). PR doubled phosphocreatine phosphorylation potential, a measure of ATP free energy state, vs TC and LR(P < 0.05); this energetic enhancement persisted 3.5 h post-resuscitation.CONCLUSION: By augmenting myocardial energy state and protecting creatine kinase activity, pyruvateenriched resuscitation stabilized cardiac electrical function during central hypovolemia and hindlimb ischemiareperfusion. | Hunaid A Gurji Daniel W White Besim Hoxha Jie Sun Albert H Olivencia-Yurvati Robert T Mallet | 2013 | World Journal of Critical Care Medicine2013，2，4： | 3 |
| 2 | Modeling cardiac arrest and resuscitation in the domestic pig显示文摘Cardiac arrest remains a leading cause of death and permanent disability worldwide. Although many victims are initially resuscitated, they often succumb to the extensive ischemia-reperfusion injury inflicted on the internal organs, especially the brain. Cardiac arrest initiates a complex cellular injury cascade encompassing reactive oxygen and nitrogen species, Ca2+ overload, ATP depletion, pro- and anti-apoptotic proteins, mitochondrial dysfunction, and neuronal glutamate excitotoxity, which injures and kills cells, compromises function of internal organs and ignites a destructive systemic inflammatory response. The sheer complexity and scope of this cascade challenges the development of experimental models of and effective treatments for cardiac arrest. Many experimental animal preparations have been developed to decipher the mechanisms of damage to vital internal organs following cardiac arrest and cardiopulmonary resuscitation(CPR), and to develop treatments to interrupt the lethal injury cascades. Porcine models of cardiac arrest and resuscitation offer several important advantages over other species, and outcomes in this large animal are readily translated to the clinical setting. This review summarizes porcine cardiac arrest-CPR models reported in the literature, describes clinically relevant phenomena observed during cardiac arrest and resuscitation in pigs, and discusses numerous methodological considerations in modeling cardiac arrest/CPR. Collectively, published reports show the domestic pig to be a suitable large animal model of cardiac arrest which is responsive to CPR, defibrillatory countershocks and medications, and yields extensive information to foster advances in clinical treatment of cardiac arrest. | Brandon H Cherry Anh Q Nguyen Roger A Hollrah Albert H Olivencia-Yurvati Robert T Mallet | 2015 | World Journal of Critical Care Medicine2015，4，1： | 2 |
| 3 | A putative mitochondrial mechanism for antioxidative cytoprotection by 17β-estradiol显示文摘 | Gottipati S Mallet T | 2004 | Exp Eye Res2004，78，5： | 1 |
| 4 | Recessively inherited L-Dopa-responsive dystonia caused by a point mutation(Q381K) in the tyrosine hydroxylase gene显示文摘 | Knappskog PM Flatmark T Mallet J | 1995 | Human Molecular Genetics1995，4，7： | 1 |
| 5 | A novel mechanism of antitumor response involving the expansion of CD3+/CD56+ large granular lymphocytes triggered by a tumor-expressed activating ligand 显示文摘 | Costello R T Sivori S Mallet F | 2002 | Leukemia2002，16，5： | 1 |
| 6 | Insu1in improves contracti1e function during moderate ischmia in canine left ventricle显示文摘 | TUNE J D MALLET R T DOWNEY H F | 1998 | Am J Physiol1998，274，： | 1 |
| 7 | Non metastatic advanced non small cell lung carcinoma:Systematic high dose brachy therapy following carative external radiotherapy显示文摘 | Nguyem T D picavet B Mallet F et at | 1999 | J Cancer-radother1999，3，6： | 1 |
| 8 | Current Zika virus epidemiology and recent epidemics显示文摘 | Ioos S Mallet HP Leparc Goffart I Gauthier V Cardoso T Herida M | 2014 | Med Mal Infect2014，44，7： | 1 |
| 9 | Pyruvate: metabolic protector o- cardiac per- formance 显示文摘 | MALLET R T | 2000 | Proceedings of the Society for Experimental Biolo- gyand Medicine2000，223，2： | 1 |
| 10 | Antioxidant properties of myocardial fuels显示文摘 | Mallet R T Sun J | 2003 | Mol Cell Biochem2003，253，12： | 1 |
| 11 | Hypoxia preconditioniong of ischemic canine myocardium显示文摘 | Mallet R T Lee S C | 1992 | Cardiovase Res1992，26，： | 1 |
| 12 | Rulation of CD80/B7-1 and CD86/BT-2 molecule expression in human primary acute myeloid leukemia and their role in allogenic immune recognition显示文摘 | Costello R T Mallet F Sainty D | 1998 | Eur J Immunol1998，28，： | 1 |
| 13 | Recessively inherited L-dopa-responsive dystonia caused by a point mutation (Q381K) in the tyrosine hydroxylase gene 显示文摘 | Knappskog PM Flatmark T Mallet J | 1995 | Hum Mol Gene1995，4，7： | 1 |
| 14 | Metabolic eardio protection by pyruvate: recent progress 显示文摘 | Mallet R T Sun J Knott E M | 2005 | Exp Biol Med (Mayweed)2005，23，7： | 1 |
| 15 | Disruption of a long distance regulatory region upstream of SOX9in isolated disorders of sex Development显示文摘 | BenkoS Gordon C T Mallet D | 2011 | J Med Genet2011，48，： | 1 |
| 16 | Enhanced fire escape training for mine workers using virtual reality simulation显示文摘 | Orr T J Mallet L G Margolis K A | 2009 | Mining Engineering2009，，11： | 1 |
| 17 | Antioxidant properties of myocardial fuels 显示文摘 | MALLET R T SUN J | 2003 | Mol Cell Biochem2003，253，2： | 1 |
| 18 | Regulation of CD80/B7-1 and CD86/B7-2 molecule expression in human primary acute myeloid leukemia and their role in allogenic immune recognition显示文摘 | Costello R T Mallet F Sainty D | 1998 | Eur J Immunol1998，28，： | 1 |
| 19 | LIGHT costimulates CD40 triggering and induces immunoglobulin secretion;a novel key partner in T cell-dependent B cell terminal differentiation 显示文摘 | Duhen T Pasero C Mallet F | 2004 | Eur J Immunol2004，34，12： | 1 |
| 20 | Human acute myeloid leukemia CD34 +/CD38 - progenitor ceils have decreased sensitivity to chemotherapy and Fas-induced apoptosis, reduced immunogenicity, and impaired dendritic cell transformation capacities显示文摘 | COSTELLO R T MALLET F GAUGLER B | 2000 | Cancer Res2000，60，： | 1 |
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