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Biomedical subjects

P M Mertes

Publications and source records attributed to P M Mertes.

At least 19 recordsLinked to original sources
PubMed2006

Sequential measurements of troponin Ic values in brain-dead patients considered as potential heart donors.

It was suggested that a single value of normal or increased plasma cardiac troponin T or I (cTnT or cTnI) concentration could contribute to estimate donor myocardial damage and function in brain-dead patients. In patients with acute coronary syndromes, an initial normal value of troponin must be confirmed several hours later but no such recommendations exist for brain-dead patients. We investigated the relationship between two sequential (6 h interval) measurements of plasma cTnI concentrations in brain-dead patients considered as potential heart donors. The first and the second TnIc values were correlated with an adjusted r2 value of 0.92 (p<0.001). Our results suggest therefore that it is not necessary to repeat the measurements, when the value of plasma cTnI concentration is taken into consideration in the algorithm for cardiac harvesting.

Biomarkers↗
PubMed2006

Anaphylactic reaction to patent blue V after sentinel lymph node biopsy.

BACKGROUND: We report a documented grade III IgE-mediated hypersensitivity reaction associated with the use of 2.5% patent blue V dye for sentinel lymph node biopsy during breast cancer surgery. METHODS: Immediately after the reaction, when hemodynamic stability was obtained, plasma histamine was measured whereas serum tryptase was not. Six weeks later, with the patient's consent, cutaneous tests to patent blue V dye, methylene blue dye, latex and all drugs used during surgery were performed according to standardized procedures. RESULTS AND CONCLUSION: Clinical symptoms, biological assessment results and cutaneous tests positivity confirmed the onset of an anaphylactic reaction due to patent blue V. Of interest, the positivity of the cutaneous tests observed with patent blue V was not found with methylene blue which might be proposed for further investigations in our patient. This case report confirms the need for systematic allergological investigation of all drugs and substances administered during the peri-operative period in case of an immediate hypersensitivity reaction occurring during anesthesia.

Anaphylaxis↗
PubMed2006

Recovery after prolonged anaesthesia for acoustic neuroma surgery: desflurane versus isoflurane.

In this study, 33 patients were randomly assigned to receive desflurane (D) or isoflurane (I) for acoustic neuroma surgery. The time from end of the procedure to spontaneous breathing, extubation, eye-opening, hand-squeezing to command, and ability to state name, birthdate and phone number were recorded. The Steward recovery score was also recorded every five minutes during the first 20 minutes postoperatively and then every 10 to 15 minutes. Groups were similar regarding patient characteristics, depth of anaesthesia, sufentanil total dose, anaesthesia duration (D: 349.1 +/- 19.1 min; I: 349.2 +/- 22.9 min), haemodynamic/respiratory parameters, and surgical conditions (assessed by a bleeding score). The emergence time in the D group was significantly faster than the I group (D: 14.9 +/- 2.4 min vs I: 29.2 +/- 2.4 min for eye-opening). Full recovery also occurred earlier in the D group (D: 22.1 +/- 3.1 min vs I: 37.6 +/- 4.0 min, P<0.005 for stating name). Steward recovery scores were also better during the first postoperative hour in the D group (D: 40 min vs I: 90 min, P<0.005 for 100% of patients with Steward score of 6). The results indicate that desflurane is associated with similar operating conditions and faster postoperative recovery following acoustic neuroma surgery. The faster recovery following desflurane may be desirable after long surgical procedures, enabling the patient's full cooperation and facilitating early diagnosis of any potential neurological deficit.

Anesthesia Recovery Period↗
PubMed2005

Liposuction and extravasation injuries in ICU.

Liposuction is a minimally invasive surgical technique, occasionally used to minimize the risk of devastating soft tissue necrosis following extravasation of noxious substances. Anaesthetists and intensive care physicians frequently use agents that may cause serious tissue injury if extravasated. Therefore, knowledge on how to manage this complication is important. We present two cases of percutaneous extravasation of noxious agents in intensive care patients and discuss their subsequent management.

Adolescent↗
PubMed2005

Reducing the risk of anaphylaxis during anaesthesia: guidelines for clinical practice.

These guidelines represent a consensus of experts in the field of immediate hypersensitivity reactions occurring during anaesthesia. They were based on international science, and implemented in France under the auspices of the French Society for Anaesthesia and Intensive Care (SFAR: Société Française d'Anesthésie et de Reanimation). Their aim was to provide the most valid, widely accepted, effective and easily teachable guidelines that current knowledge, research and experience can provide. This paper presents the main extracts of these recommendations with the most relevant clinical implications.

Anaphylaxis↗
PubMed2004

Allergy and anaphylaxis in anaesthesia.

Immediate hypersensitivity reactions to anaesthetic and associated agents used during the perioperative period have been reported with increasing frequency in most developed countries. Most reactions are of immunologic origin (IgE mediated, anaphylaxis) or related to direct stimulation of histamine release (anaphylactoid reactions). The incidence of anaphylaxis is estimated between 1 in 10000 and 1 in 20000 anaesthesia, and any drug administered in the perioperative period can potentially produce life-threatening immune-mediated hypersensitivity reactions. Neuromuscular blocking agents (NMBAs), latex and antibiotics represent the most frequently involved substances. However, anaphylactic reactions cannot be clinically distinguished from non-immune mediated reactions which account for 30% to 40% of hypersensitivity reactions. Therefore, any suspected anaphylactic reaction must be extensively investigated using combined peroperative and postoperative testing to confirm the nature of the reaction, the responsibility of suspected drugs and to provide precise recommendations for future anaesthetic procedures. These investigations include plasma histamine, tryptase and specific IgE concentration determination at the time of the reaction, and skin tests 6 weeks later. In addition, since no specific treatment has been shown to reliably prevent the occurrence of anaphylaxis, allergy assessment must be performed in all high-risk patients. The need for proper epidemiological studies and the relative complexity of allergy investigation should be underscored. They represent an incentive for further development of allergo-anaesthesiology clinical networks to provide expert advice for anaesthetists and allergologists.

Anaphylaxis↗
PubMed2002

Allergic reactions occurring during anaesthesia.

Anaphylactic reactions to anaesthetic and associated agents used during the perioperative period have been reported with increasing frequency in most developed countries. Any drug administered in the perioperative period can potentially produce life-threatening immune-mediated anaphylaxis. Most published reports on the incidence of anaphylaxis come from France, Australia, the UK and New Zealand. These reflect an active policy of systematic clinical and/or laboratory investigation of suspected immune-mediated reactions. The estimated incidence of anaphylaxis ranges from 1:10,000 to 1:20,000. Muscle relaxants (69.1%) and latex (12.1%) were the most frequently involved drugs according to the most recent French epidemiological survey. Clinical symptoms do not afford an easy distinction between immune-mediated anaphylactic reactions and anaphylactoid reactions resulting from direct non-specific histamine release. Moreover, when restricted to a single clinical symptom, anaphylaxis can easily be misdiagnosed. Pre- and postoperative investigation must be performed to confirm the nature of the reaction, the responsibility of the suspected drugs and to provide precise recommendations for future anaesthetic procedures. These include plasma histamine, tryptase and specific IgE concentration determination at the time of the reaction and at skin tests 6 weeks later. In addition, since no specific treatment has been shown reliably to prevent the occurrence of anaphylaxis, allergy assessment must be performed in all high-risk patients. Treatment of anaphylaxis is aimed at interrupting contact with the responsible antigen, inhibiting mediator production and release, and modulating the effects of released mediators. It must be initiated as quickly as possible and relies on widely accepted principles. Finally, the need for proper epidemiological studies and the relative complexity of allergy investigation should be underscored. They represent an incentive for further development of allergo-anaesthesiology clinical networks to provide expert advice for anaesthetists and allergologists.

Anaphylaxis↗
PubMed2002

Butyrate affects differentiation, maturation and function of human monocyte-derived dendritic cells and macrophages.

We studied the in vitro effects of butyric acid on differentiation, maturation and function of dendritic cells (DC) and macrophages (M(Phi)) generated from human monocytes. A non-toxic dose of butyrate was shown to alter the phenotypic differentiation process of DC as assessed by a persistence of CD14, and a decreased CD54, CD86 and HLA class II expression. The more immature differentiation stage of treated cells was confirmed further by their increased phagocytic capability, their altered capacity to produce IL-10 and IL-12, and their weak allostimulatory abilities. Butyrate also altered DC terminal maturation, regardless of the maturation inducer, as demonstrated by a strong down-regulation of CD83, a decreased expression of CD40, CD86 and HLA class II. Similarly, butyrate altered M(Phi) differentiation, down-regulating the expression of the restricted membrane antigens and reducing the phagocytic capacity of treated cells. To investigate further the mechanism by which butyrate hampers the monocyte dual differentiation pathway, we studied the effects of 1,25(OH)2D3 alone or in combination with butyrate on the phenotypic features of DC. Unlike 1,25(OH)2D3, butyrate inhibited DC -differentiation without redirecting it towards M(Phi). Combined treatment gave rise to a new cell subset (CD14(high), CD86 and HLA-DR(low)) phenotypically distinct from monocytes. These results reveal an alternative mechanism of inhibition of DC and M(Phi) differentiation. Altogether, our data demonstrate a novel immune suppression property of butyrate that may modulate both inflammatory and immune responses and support further the interest for butyrate and its derivatives as new immunotherapeutic agents.

Antigen Presentation↗
PubMed2001

Lipopolysaccharide-induced increase of prostaglandin E(2) is mediated by inducible nitric oxide synthase activation of the constitutive cyclooxygenase and induction of membrane-associated prostaglandin E synthase.

NO produced by the inducible NO synthase (NOS2) and prostanoids generated by the cyclooxygenase (COX) isoforms and terminal prostanoid synthases are major components of the host innate immune and inflammatory response. Evidence exists that pharmacological manipulation of one pathway could result in cross-modulation of the other, but the sense, amplitude, and relevance of these interactions are controversial, especially in vivo. Administration of 6 mg/kg LPS to rats i.p. resulted 6 h later in induction of NOS2 and the membrane-associated PGE synthase (mPGES) expression, and decreased constitutive COX (COX-1) expression. Low level inducible COX (COX-2) mRNA with absent COX-2 protein expression was observed. The NOS2 inhibitor aminoguanidine (50 and 100 mg/kg i.p.) dose dependently decreased both NO and prostanoid production. The LPS-induced increase in PGE(2) concentration was mediated by NOS2-derived NO-dependent activation of COX-1 pathway and by induction of mPGES. Despite absent COX-2 protein, SC-236, a putative COX-2-specific inhibitor, decreased mPGES RNA expression and PGE(2) concentration. Ketoprofen, a nonspecific COX inhibitor, and SC-236 had no effect on the NOS2 pathway. Our results suggest that in a model of systemic inflammation characterized by the absence of COX-2 protein expression, NOS2-derived NO activates COX-1 pathway, and inhibitors of COX isoforms have no effect on NOS2 or NOS3 (endothelial NOS) pathways. These results could explain, at least in part, the deleterious effects of NOS2 inhibitors in some experimental and clinical settings, and could imply that there is a major conceptual limitation to the use of NOS2 inhibitors during systemic inflammation.

Animals↗
PubMed2001

Evidence of functional myocardial ischemia associated with myocardial dysfunction in brain-dead pigs.

BACKGROUND: Cardiac dysfunction after brain death has been documented, but its mechanisms remain unclear. Myocardial ischemia has been suggested as a possible cause. The aim of the present study was to investigate the existence of an imbalance between myocardial oxygen delivery and demand as a possible cause of myocardial dysfunction in brain-dead pigs. METHODS AND RESULTS: Interstitial myocardial lactate and adenosine concentrations were assessed with cardiac microdialysis in 2 groups of animals: brain-dead pigs (n=7) and brain-dead pigs treated with labetalol (10+/-3 mg/kg) (n=7). Heart rate (HR), left ventricular (LV) dP/dt(max), rate-pressure product (RPP), cardiac output (CO), and left anterior descending coronary artery blood flow (QLAD) were continuously monitored. Brain-dead pigs exhibited a transient significant increase in HR, LV dP/dt(max), RPP, and CO and a limited increase in QLAD. This resulted in functional myocardial ischemia attested to by the significantly increased adenosine and lactate microdialysate concentrations. In brain-dead pigs treated with labetalol, there was a moderate increase in HR, QLAD, and adenosine microdialysate concentrations; LV dP/dt(max), RPP, CO, and myocardial lactate concentrations remained stable, confirming the preservation of aerobic metabolism. CONCLUSIONS: Brain death was associated with an increase in myocardial interstitial adenosine and lactate concentrations, as well as with myocardial dysfunction; all were attenuated by labetalol, suggesting an imbalance between oxygen consumption and oxygen delivery as a possible cause of myocardial dysfunction after brain death.

Adenosine↗
PubMed2001

Retinoic acid attenuates inducible nitric oxide synthase (NOS2) activation in cultured rat cardiac myocytes and microvascular endothelial cells.

S. Grosjean, Y. Devaux, C. Seguin, C. Meistelman, F. Zannad, P.-M. Mertes, R. A. Kelly and D. Ungureanu-Longrois. Retinoic Acid Attenuates Inducible Nitric Oxide Synthase (NOS2) Activation in Cultured Rat Cardiac Myocytes and Microvascular Endothelial Cells. Journal of Molecular and Cellular Cardiology (2001) 33, 933-945. The inducible NO synthase (NOS2) in cardiac tissue contributes to myocardial and coronary inflammation and dysfunction. Several natural (endogenous) hormones such as retinoic acid, the active metabolite of vitamin A, have the ability to attenuate NOS2 activation in inflammatory cells. The aim of this study was to investigate the effect of RA on NOS2 activation in cultured cardiac microvascular endothelial cells (CMEC) and adult rat ventricular myocytes (ARVM). CMEC were stimulated either with a combination of 10 microg/ml lipopolysaccharide (LPS) and 50 IU/ml interferon- gamma (IFN- gamma) or with a combination of 1 ng/ml interleukin-1 beta (IL-1 beta)+IFN- gamma whereas ARVM were stimulated with 1 ng/ml IL-1 beta and 50 IU/ml IFN- gamma in the absence or presence of all-trans retinoic acid (atRA). Activation of the NOS2 pathway was estimated by measurement of mRNA (Northern blot) and protein (Western blot) expression, enzyme activity by conversion of [(3)H]L -arginine to [(3)H]L -citrulline, and nitrite accumulation. NOS2 mRNA half-life was studied in CMEC and ARVM in the presence of actinomycin D. In CMEC and ARVM stimulated with a combination of LPS and/or cytokines, atRA (10(-6), 10(-5)M) significantly (P<0.05) attenuated NOS2 mRNA and protein expression, enzymatic activity and reduced supernatant nitrite concentration. Upon stimulation with LPS/IFN- gamma, atRA significantly decreased NOS2 mRNA half-life. This was not seen after stimulation with IL-1 beta/IFN- gamma. These results document for the first time an effect of RA on NOS2 activation in cardiac cells. They may contribute to the characterization of the immunomodulatory effects of retinoids in myocardial and coronary inflammatory disorders.

Animals↗
PubMed2001

Anaphylaxis during anaesthesia. Results of a two-year survey in France.

Between January 1, 1997 and December 31, 1998, 467 patients were referred to one of the allergo-anaesthesia centres of the French GERAP (Groupe d'Etudes des Réactions Anaphylactoïdes Peranesthésiques) network and were diagnosed as having anaphylaxis during anaesthesia. Diagnosis was established on the basis of clinical history, skin tests and/or a specific IgE assay. The most frequent cause of anaphylaxis was a neuromuscular blocking agent (69.2%). Latex was less frequently incriminated (12.1%) than in previous reports. A significant difference was observed between the incidence of anaphylactic reactions observed with each neuromuscular blocking agent and the number of patients who received each drug during anaesthesia in France throughout the study period (P<0.0001). Succinylcholine and rocuronium were most frequently incriminated. Clinical reactions to neuromuscular blocking drugs were more severe than to latex. The diagnostic value of specific IgE assays was confirmed. These results are consistent with changes in the epidemiology of anaphylaxis related to anaesthesia and are an incentive for the further development of allergo-anaesthesia clinical networks.

Adolescent↗