Publications (28)119.76 Total impact
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Article: [Cost awareness at emergencies: Multicentric survey among prescribers.]
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ABSTRACT: AIM: Regular increasing of health-care expense brought about the development of medical implication in prescription control and the will to give more responsibility to prescribers. Emergency departments account for a large part of hospital expenses. This study was carried out to evaluate cost awareness among French emergency physicians. METHODS: A questionnaire was sent to 160 physicians (junior and senior grade) working at the emergency department of 12 hospitals in the Lyon region (France). Every participant had to estimate the true hospital costs of a selection of drugs, blood products, laboratory tests and imaging modalities. RESULTS: One hundred and seven questionnaires (68%) were returned and analysed: 48 filled in by juniors (45%), 59 by seniors (55%). Only 26 physicians accurately estimated costs within 50% of the true cost. Response errors were underestimations averaging 4695±226euros, i.e. -59±3% of the total sum (7899euros). Drug prescriptions were significantly (P<0.001) the most underestimated (-74±3%), when compared to both imaging modalities (-23±5%) or blood products prescriptions (-37±6%). High-cost drugs (>1000euros) were the most overestimated pharmaceuticals (-82±2%). Laboratory tests were rather overestimated (+12±8%). Junior grade physicians underestimated more costs than senior physicians (P=0.04). DISCUSSION: Physicians had a poor understanding of prescription costs at the emergencies, especially regarding high-cost drugs. Much progress is required to integrate the cost-containment problem in daily prescriptions at the emergency department.La Presse Médicale 02/2013; · 0.67 Impact Factor -
Article: [Necrotising community-acquired pneumonia due to Panton-Valentine leukocidin-secreting Staphylococcus aureus: a rare diagnosis to be evoked].
La Presse Médicale 07/2011; 40(10):966-70. · 0.67 Impact Factor -
Article: Noninvasive positive ventilation in the treatment of sleep-related breathing disorders.
Handbook of Clinical Neurology 01/2011; 98:459-69. -
Article: Inhibition of mitochondrial permeability transition to prevent the post-cardiac arrest syndrome: a pre-clinical study.
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ABSTRACT: Resuscitated cardiac arrest (CA), leading to harmful cardiovascular dysfunction and multiple organ failure, includes a whole-body hypoxia-reoxygenation phenomenon. Opening of the mitochondrial permeability transition pore (mPTP) appears to be a pivotal event in ischaemia-reperfusion injury. We hypothesized that pharmacological inhibition of mPTP opening may prevent the post-CA syndrome. Anaesthetized New Zealand White rabbits underwent a 15 min primary asphyxial CA and 120 min of reperfusion following resuscitation. At reflow, animals received an intravenous bolus of either cyclosporine A (CsA, 5 mg/kg) or NIM 811 (2.5 mg/kg), two potent inhibitors of mPTP opening, or the CsA vehicle (control). Short-term survival, haemodynamics, regional (sonomicrometry), and global cardiac function (dP/dt and aortic flow) were assessed. We measured markers of cellular injuries and/or organ failure, including troponin Ic release, lacticodehydrogenase, lactate, creatinine, and alanine aminotransferase. Cyclosporine A and NIM 811 significantly improved short-term survival, post-resuscitation cardiac function, as well as liver and kidney failure (P < 0.05). CsA and NIM 811 both attenuated in vitro mPTP opening (calcium retention capacity by spectrofluorimetry) and restored oxidative phosphorylation when compared with controls (P < 0.05). These data suggest that pharmacological inhibition of mPTP opening, added to basic life support, attenuates the post-CA syndrome and improves short-term outcomes in the rabbit model.European Heart Journal 01/2011; 32(2):226-35. · 10.48 Impact Factor -
Article: Management of metformin-associated lactic acidosis by continuous renal replacement therapy.
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ABSTRACT: Metformin-associated lactic acidosis (MALA) is a severe metabolic failure with high related mortality. Although its use is controversial, intermittent hemodialysis is reported to be the most frequently used treatment in conjunction with nonspecific supportive measures. Our aim was to report the evolution and outcome of cases managed by continuous renal replacement therapy (CRRT). Over a 3-year period, we retrospectively identified patients admitted to the intensive care unit for severe lactic acidosis caused by metformin. We included patients in our study who were treated with CRRT because of shock. We describe their clinical and biological features at admission and during renal support, as well as their evolution. We enrolled six patients with severe lactic acidosis; the mean pH and mean lactate was 6.92±0.20 and 14.4±5.1 mmol/l, respectively. Patients had high illness severity scores, including the Simplified Acute Physiology Score II (SAPS II) (average score 63±12 points). Early CRRT comprised either venovenous hemofiltration (n = 3) or hemodiafiltration (n = 3) with a mean effluent flow rate of 34±6 ml/kg/h. Metabolic acidosis control and metformin elimination was rapid and there was no rebound. Outcome was favorable in all cases. Standard use of CRRT efficiently treated MALA in association with symptomatic organ supportive therapies.PLoS ONE 01/2011; 6(8):e23200. · 4.09 Impact Factor -
Article: Postconditioning: from the bench to bedside.
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ABSTRACT: Infarct size is determined not only by the severity of ischemia but also by pathological processes initiated at reperfusion. Accumulating experimental evidence indicates that lethal reperfusion injury might account for up to half of the final size of the myocardial infarct. Ischemic postconditioning (brief repeated periods of ischemia-reperfusion applied at the onset of coronary reflow) has been recently described as a powerful cardioprotection mechanism that prevents lethal reperfusion injury. This is the first method proven to reduce the final infarct size by about 50% in several in vivo models and to be confirmed in recent preliminary human studies. The molecular pathways are incompletely mapped but they probably converge to a mitochondrial key target: the mitochondrial permeability transition pore (PTP) which opening during early reperfusion is an event that promotes myocardial cell death. In different animal models and experimental settings, pharmacological PTP inhibition at the onset of reperfusion reproduces all the cardioprotective effects of ischemic postconditioning. In a recent proof-of-concept trial, the administration (just before percutaneous coronary intervention) of cyclosporine A, a potent PTP inhibitor, was associated with smaller infarct size. This review will focus on the physiological preclinical data on both ischemic and pharmacological postconditioning that are relevant to their translation to clinical therapeutics.Journal of Cardiovascular Pharmacology and Therapeutics 10/2010; 16(2):117-30. · 1.75 Impact Factor -
Article: Bilevel positive airway pressure ventilation: factors influencing carbon dioxide rebreathing.
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ABSTRACT: Use of bilevel positive airway pressure (BLPAP) ventilators for noninvasive ventilation (NIV) is an established treatment for both acute and chronic ventilatory failure. Although BLPAP ventilator circuits are simpler than those of conventional ventilators, one drawback to their use is that they allow variable amounts of rebreathing to occur. The aim of this work is to measure the amount of CO(2) reinsufflated in relation to the BLPAP ventilator circuit in patients, and to determine predictive factors for rebreathing. Eighteen adult patients were ventilated on pressure support, either by intubation or with mask ventilation, during a weaning period. The mean inspiratory fraction of CO(2) (tidal FiCO(2)) reinsufflated from the circuit between the intentional leak and the ventilator was measured for each breath. The influence of end-tidal CO(2) concentration (ETCO(2)), respiratory rate (RR), percentage of inspiratory time (T (i)/T (TOT)), application of expiratory positive airway pressure (EPAP), and inspiratory tidal volume on magnitude of tidal FiCO(2), as well as the influence of intubation versus NIV, were studied by univariate comparisons and logistic regression analysis. In a total of 11,107 cycles, tidal FiCO(2) was 0.072 +/- 0.173%. Of fractions measured, 8,976 (81%) were under 0.10% and 2,131 (19%) were over 0.10%, with mean values of 0.026 +/- 0.027% and 0.239 +/- 0.326%, respectively. ETCO(2), EPAP, NIV versus intubation, and RR had significant predictive value for tidal FiCO(2) >0.10%. BLPAP ventilators present a specific rebreathing risk to patients. However, that risk remains modest, even in intubated patients, provided that EPAP is applied.European Journal of Intensive Care Medicine 02/2010; 36(4):688-91. · 5.17 Impact Factor -
Article: Second-generation sulfonylureas preserve inhibition of mitochondrial permeability transition by the mitochondrial K+(ATP) opener nicorandil in experimental myocardial infarction.
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ABSTRACT: Openers of K+(ATP) channels protect the myocardium from I/R injury. Sulfonylureas are known as potent blockers of K(ATP) channels. We investigated whether 1) mitochondrial permeability transition pore may be involved in the protection afforded by the mitoK+(ATP) opener nicorandil and 2) whether sulfonylureas may prevent this beneficial effect. Anesthetized New Zealand White rabbits underwent 30 min of coronary artery occlusion, followed by 60 (isolated mitochondria) or 240 min (infarct size) of reperfusion. They received an administration of either saline (control) or nicorandil (0.5 mg kg(-1), i.v.) 15 min before ischemia. Each control and nicorandil group was divided in four subgroups pretreated by either saline, glibenclamide (Glib; 1 mg kg(-1)), gliclazide (Glic; 1 mg kg(-1)), or glimepiride (Glim; 5 microg kg(-1)) 10 min before this. Infarct size was assessed by triphenyltetrazolium chloride staining. Mitochondria were isolated from the area at risk for further assessment of the calcium retention capacity. Glibenclamide (35 +/- 8), but neither Glic (61 +/- 9) nor Glim (48 +/- 7), reversed the improvement in calcium retention capacity due to nicorandil (58 +/- 10 vs. 27 +/- 8 nmoles CaCl2 mg(-1) proteins in control). Infarct size reduction by nicorandil (32% +/- 6% vs. 65% +/- 6% of area at risk) was abolished by Glib (55 +/- 5) but not by Glic (37 +/- 3) or Glim (31 +/- 5). These data suggest that 1) the protective effect of nicorandil involves the inhibition of the mitochondrial permeability transition pore and 2) that unlike Glib, second-generation sulfonylureas preserve this cardioprotection.Shock (Augusta, Ga.) 02/2009; 32(3):247-52. · 2.87 Impact Factor -
Article: [Fever as a prognostic factor for heat stroke].
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ABSTRACT: Classic heatstroke that is, due to very hot weather, rare in Europe. Its clinical characteristics and course in temperate zones are not well known. The objective of this study was to assess the influence of initial fever on prognosis in heatstroke. All patients admitted through the emergency department from 8-13 August 2003 for heatstroke (defined by fever > or = 40 degrees C, with neurologic symptoms in the absence of sepsis) were included in the study. Patients' clinical and laboratory indicators were recorded at admission. Follow-up took place at D28 and 1 year. The influence of fever on survival was assessed with the Kaplan-Meier method. During the study period, 63 patients, aged 78+/-9 years, were admitted for heatstroke, with a SAPS II (Simplified Acute Physiology Score) of 61+/-24. Core body temperature was 41.4+/-1.2 degrees C. Mortality was 59% at D28 and 67% at 1 year. Prognosis was influenced from admission by temperature, with a higher probability of survival for patients with temperature < 41 degrees C, compared with those whose temperature > or = 41 degrees C (log-rank test: p<0.001). Prognosis is poor for classic heatstroke. Rapid temperature reduction, especially when it exceeds > 41 degrees C, must be considered a priority. Fever > or = 41 degrees C at admission for heatstroke is a poor prognostic factor that is simple to identify and may modify treatment strategies in the future.La Presse Médicale 03/2008; 37(3 Pt 1):406-11. · 0.67 Impact Factor -
Article: Persistent inhibition of mitochondrial permeability transition by preconditioning during the first hours of reperfusion.
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ABSTRACT: Mitochondrial permeability transition pore (mPTP) opening is a crucial event in cardiomyocyte death after I/R. We questioned whether preconditioning (PC) may inhibit mPTP opening during ischemia and/or during reperfusion and whether this effect would persist as reperfusion evolves. Anesthetized New Zealand white rabbits underwent a test ischemia followed by reperfusion. Ischemia lasted either 10 or 30 min, whereas reperfusion duration varied from 5 to 20, 60 and up to 240 min. For each duration of ischemia and reperfusion, animals were randomized as either control or PC. Preconditioning was induced by 5 min of ischemia followed by 5 min of reperfusion. Mitochondria were isolated from myocardium at risk for assessment of the calcium retention capacity (CRC) (potentiometric technique) used here as an index of sensitivity of the mPTP to Ca2+ loading. In controls, the CRC was moderately reduced after ischemia alone, but reperfusion severely and time-dependently accelerated further CRC reduction. Preconditioning failed to modify mPTP opening during ischemia alone, but significantly improved CRC during reperfusion. This protective effect persisted as reperfusion evolved. These data suggest that (a) reperfusion strikingly increases the susceptibility to Ca2+-induced mPTP opening, and that (b) PC inhibits mPTP opening at reflow and throughout the first hours of reperfusion.Shock (Augusta, Ga.) 03/2008; 30(5):552-6. · 2.87 Impact Factor -
Article: Increased mitochondrial calcium coexists with decreased reperfusion injury in postconditioned (but not preconditioned) hearts.
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ABSTRACT: Ca(2+) is the main trigger for mitochondrial permeability transition pore opening, which plays a key role in cardiomyocyte death after ischemia-reperfusion. We investigated whether a reduced accumulation of mitochondrial Ca(2+) might explain the attenuation of lethal reperfusion injury by postconditioning. Anesthetized New Zealand White rabbits underwent 30 min of ischemia, followed by either 240 (infarct size protocol) or 60 (mitochondria protocol) min of reperfusion. They received either no intervention (control), preconditioning by 5-min ischemia and 5-min reperfusion, postconditioning by four cycles of 1-min reperfusion and 1-min ischemia at the onset of reflow, or pharmacological inhibition of the transition pore opening by N-methyl-4-isoleucine-cyclosporin (NIM811; 5 mg/kg iv) given at reperfusion. Area at risk and infarct size were assessed by blue dye injection and triphenyltetrazolium chloride staining. Mitochondria were isolated from the risk region for measurement of 1) Ca(2+) retention capacity (CRC), and 2) mitochondrial content of total (atomic absorption spectrometry) and ionized (potentiometric technique) calcium concentration. CRC averaged 0.73 +/- 0.16 in control vs. 4.23 +/- 0.17 mug Ca(2+)/mg proteins in shams (P < 0.05). Postconditioning, preconditioning, or NIM811 significantly increased CRC (P < 0.05 vs. control). In the control group, total and free mitochondrial calcium significantly increased to 2.39 +/- 0.43 and 0.61 +/- 0.10, respectively, vs. 1.42 +/- 0.09 and 0.16 +/- 0.01 mug Ca(2+)/mg in sham (P < 0.05). Surprisingly, whereas total and ionized mitochondrial Ca(2+) decreased in preconditioning, it significantly increased in postconditioning and NIM811 groups. These data suggest that retention of calcium within mitochondria may explain the decreased reperfusion injury in postconditioned (but not preconditioned) hearts.AJP Heart and Circulatory Physiology 01/2008; 294(1):H386-91. · 3.71 Impact Factor -
Article: Short- and long-term outcomes of heatstroke following the 2003 heat wave in Lyon, France.
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ABSTRACT: During August 2003, Europe sustained a severe heat wave that resulted in 14 800 heat-related deaths in France. Most of these excess deaths occurred in urban areas, where maximal temperatures broke all records. Heatstroke is the most severe form of heat-related illness. The clinical course of heatstroke in urban areas of temperate countries is poorly documented. During the French heat wave (August 1-20, 2003), we conducted a prospective study in a university hospital located in Lyon, one of the largest metropolitan areas in France. We evaluated survival and functional outcome for 2 years and looked for factors influencing the prognosis. A total of 83 patients presented with heatstroke. The 28-day and 2-year mortality rates were 58% and 71%, respectively. Mortality was influenced as early as admission by the level of fever and the number of organ dysfunctions. Multivariate analysis revealed an independent contribution to mortality if patients came from an institution (hazard ratio [HR], 1.98; 95% confidence interval [CI], 1.05-3.71), used long-term antihypertensive medication (HR, 2.17; 95% CI, 1.17-4.05), or presented at admission with anuria (HR, 5.24; 95% CI, 2.29-12.03), coma (HR, 2.95; 95% CI, 1.26-6.91), or cardiovascular failure (HR, 2.43; 95% CI, 1.14-5.17). Most surviving patients exhibited a dramatic alteration of their functional status at 1 and 2 years. Heatstroke is associated with poor outcomes in temperate urban areas. This could be explained at least in part by our lack of experience. Western temperate countries need to be more prepared for future heat waves.Archives of Internal Medicine 12/2007; 167(20):2177-83. · 11.46 Impact Factor -
Article: Non-invasive positive ventilation in the treatment of sleep-related breathing disorders.
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ABSTRACT: This chapter addresses the use of long-term non-invasive positive pressure ventilation (NIPPV) (to the exclusion of continuous positive airway pressure) in the different clinical settings in which it is currently proposed: principally in diseases responsible for hypoventilation characterized by elevated PaCO(2). Nasal masks are predominantly used, followed by nasal pillow and facial masks. Mouthpieces are essentially indicated in case daytime ventilation is needed. Many clinicians currently prefer pressure-preset ventilator in assist mode as the first choice for the majority of the patients with the view of offering better synchronization. Nevertheless, assist-control mode with volume-preset ventilator is also efficient. The settings of the ventilator must insure adequate ventilation assessed by continuous nocturnal records of at least oxygen saturation of haemoglobin-measured by pulse oximetry. The main categories of relevant diseases include different types of neuromuscular disorders, chest-wall deformities and even lung diseases. Depending on the underlying diseases and on individual cases, two schematic situations may be individualized. Either intermittent positive pressure ventilation (IPPV) is continuously mandatory to avoid death in the case of complete or quasi-complete paralysis or is used every day for several hours, typically during sleep, producing enough improvement to allow free time during the daylight in spontaneous breathing while hypoventilation and related symptoms are improved. In case of complete or quasi-complete need of mechanical assistance, a tracheostomy may become an alternative to non-invasive access. In neuromuscular diseases, in kyphosis and in sequela of tuberculosis patients, NIPPV always significantly increases survival. Conversely, no data support a positive effect on survival in chronic obstructive pulmonary disease.Sleep Medicine 07/2007; 8(4):441-52. · 3.40 Impact Factor -
Article: Clinical review: long-term noninvasive ventilation.
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ABSTRACT: Noninvasive positive ventilation has undergone a remarkable evolution over the past decades and is assuming an important role in the management of both acute and chronic respiratory failure. Long-term ventilatory support should be considered a standard of care to treat selected patients following an intensive care unit (ICU) stay. In this setting, appropriate use of noninvasive ventilation can be expected to improve patient outcomes, reduce ICU admission, enhance patient comfort, and increase the efficiency of health care resource utilization. Current literature indicates that noninvasive ventilation improves and stabilizes the clinical course of many patients with chronic ventilatory failure. Noninvasive ventilation also permits long-term mechanical ventilation to be an acceptable option for patients who otherwise would not have been treated if tracheostomy were the only alternative. Nevertheless, these results appear to be better in patients with neuromuscular/-parietal disorders than in chronic obstructive pulmonary disease. This clinical review will address the use of noninvasive ventilation (not including continuous positive airway pressure) mainly in diseases responsible for chronic hypoventilation (that is, restrictive disorders, including neuromuscular disease and lung disease) and incidentally in others such as obstructive sleep apnea or problems of central drive.Critical care (London, England) 02/2007; 11(2):210. · 4.61 Impact Factor -
Article: Changeovers of vasoactive drug infusion pumps: impact of a quality improvement program.
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ABSTRACT: Hemodynamic instability following the changeover of vasoactive infusion pump (CVIP) is a common problem in the intensive care unit. Several empiric methods are used to achieve CVIP. We hypothesized that the variation in these procedures could generate some morbidity. We sought to assess the effects of the standardization of practice, as a quality improvement program, on the CVIP-induced incidents. We performed a prospective before-and-after intervention study including all adult patients with a diagnosis of cardiovascular failure who received a continuous infusion of vasoactive drugs or inotropic drugs. After a baseline preimplementation period (phase 1), a standardized 'quick change method' of CVIP using two syringe drivers was implemented in our intensive care unit (phase 2). Endpoints (rate and distribution of incidents: variations of systolic blood pressure >20 mmHg or heart rate >20 beats/min, and arrhythmias) were registered in both 3-month phases. We studied a total of 913 CVIP events (phase 1, 435 events; phase 2, 478 events) from 43 patients. Patient characteristics were not significantly different among phases, with a majority of the patients having septic shock. The frequency of incidents was significantly (P < 0.0001) reduced in phase 2 (5.9%, n = 28) versus phase 1 (17.8%, n = 78). This effect was observed whichever catecholamine was used. More than 98% of incidents were blood pressure variations, with a similar distribution of the nature of incidents in both phases. The present study illustrates that adverse events are common following CVIP, and illustrates the positive impact of a quality improvement program to enhance inpatient safety related to this current process of care.Critical care (London, England) 01/2007; 11(6):R133. · 4.61 Impact Factor -
Article: Mitochondrial permeability transition pore and postconditioning.
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ABSTRACT: Postconditioning has recently been described as a powerful cardioprotection that prevents lethal reperfusion injury. Growing evidence suggests that mitochondrial permeability transition may be a key event in postconditioning. This proposition arises from the complementary observations that: (1) conditions for the mitochondrial permeability transition pore (mPTP) opening are built up during early reperfusion, (2) mPTP opens at the time of reperfusion, (3) transgenic structural alteration of mPTP modifies its opening probability following ischemia-reperfusion, (4) mPTP plays a role in preconditioning, and (5) postconditioning attenuates lethal reperfusion injury. We review in this article current evidence for an important role of the mitochondrial transition pore in postconditioning.Cardiovascular Research 06/2006; 70(2):264-73. · 6.06 Impact Factor -
Article: Inactive tuberculosis cavity responsible for fatal cerebral air embolism.
Intensive Care Medicine 05/2006; 32(4):622-3. · 5.40 Impact Factor -
Article: Favourable issue of a fulminant hepatitis associated with sulfasalazine DRESS syndrome without liver transplantation.
Intensive Care Medicine 01/2006; 31(12):1727-8. · 5.40 Impact Factor -
Article: Trimetazidine inhibits mitochondrial permeability transition pore opening and prevents lethal ischemia-reperfusion injury.
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ABSTRACT: Trimetazidine (TMZ) affects mitochondrial function during ischemia. Mitochondrial permeability transition is a pivotal event in cardiomyocyte death following acute ischemia. The aim of the present study was to determine whether the anti-ischemic agent TMZ might modulate mitochondrial permeability transition pore (mPTP) opening and limit lethal ischemia-reperfusion injury. Anesthetized NZW rabbits underwent 30 min of coronary artery occlusion followed by 4 hours of reperfusion. Prior to this, they underwent either no intervention (control, C), ischemic preconditioning (PC), or an IV injection of 5 mg kg(-1) TMZ 10 min before ischemia (TMZ). Additional rabbits (Sham group) underwent no ischemia/reperfusion throughout the experiment. Infarct size was assessed by triphenyltetrazolium staining, and apoptosis via measurement of caspase 3 activity. Ca(2+)-induced mPTP opening was assessed in mitochondria isolated from ischemic myocardium. TMZ and PC significantly reduced infarct size that averaged 34 +/- 4% and 21 +/- 4% of the risk region respectively, versus 63 +/- 6% in controls (P<0.005). Caspase 3 activity was reduced in both TMZ and PC groups: 37 +/- 11 and 29 +/- 7 respectively, versus 68 +/- 9 nmol min(-1) mg(-1) mitochondrial protein in controls (P=0.01 versus TMZ and PC). In controls, Ca(2+) load required for mPTP opening averaged 11 +/- 4 microM mg(-1) mitochondrial protein versus 116 +/- 6 in shams (P<0.0001). Pre-treatment by TMZ or PC attenuated this, with Ca(2+) loads averaging 45 +/- 4 and 46 +/- 4 microM mg(-1) mitochondrial proteins, respectively (P<0.005 versus C). These data suggest that TMZ inhibits mPTP opening and protects the rabbit heart from prolonged ischemia-reperfusion injury.Journal of Molecular and Cellular Cardiology 12/2005; 39(6):893-9. · 5.17 Impact Factor -
Article: Specific inhibition of the mitochondrial permeability transition prevents lethal reperfusion injury.
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ABSTRACT: The aim of the present study was to determine whether specific inhibition of mitochondrial permeability transition (MPT) by NIM811 at the time of reperfusion following acute myocardial infarction may protect the heart. MPT pore opening appears to be a pivotal event in cell death following acute myocardial infarction. Recently, MPT pore opening has been involved in ischemic preconditioning. In protocol 1, NZW rabbits underwent either no intervention (sham) or 10 min of ischemia followed by 5 min of reperfusion, preceded (preconditioned, PC) or not (control, C) by 5 min of ischemia and 5 min of reperfusion. Additional rabbits were treated by cyclosporin A (CsA) or its non-immunosuppressive and more specific derivative (NIM811) (10 mg kg(-1), IV bolus), either 10 min before ischemia or 1 min before reperfusion. Hearts were excised and mitochondria isolated for further assessment of Ca(2+)-induced MPT. In protocol 2, animals were randomly assigned into similar experimental groups and underwent 30 min of ischemia and 4 h of reperfusion. Infarct size was assessed by TTC staining, and apoptosis by TUNEL assay. The Ca2+ overload required to induce MPT pore opening was significantly higher in NIM811, CsA and PC groups than in controls. Both necrotic and apoptotic cardiomyocyte death were significantly reduced by NIM811, CsA and PC. In both protocols, administration of NIM811 at reperfusion provided full protection. These data indicate that specific inhibition of MPT pore opening at reperfusion following acute myocardial infarction provides a powerful antinecrotic and antiapoptotic protection.Journal of Molecular and Cellular Cardiology 03/2005; 38(2):367-74. · 5.17 Impact Factor
Top co-authors
Top Journals
Institutions
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2003–2013
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CHU de Lyon - Groupement Hospitalier Edouard Herriot
Lyon, Rhone-Alpes, France
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2010
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Szpital Uniwersytecki nr 1 im. A. Jurasza w Bydgoszczy
Bydgoszcz, Kujawsko-Pomorskie, Poland -
INSERM, GIP CYCERON
Caen, Basse-Normandie, France
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2008–2009
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CHU de Lyon - Institut d'hématologie et d'oncologie pédiatrique
Lyon, Rhone-Alpes, France
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2004–2008
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Université Claude Bernard Lyon 1
Villeurbanne, Rhone-Alpes, France -
Centre Hospitalier Lyon Sud
Lyon, Rhone-Alpes, France
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2003–2004
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Institut national de la santé et de la recherche médicale
Paris, Ile-de-France, France
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