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Biomedical subjects

M Lamy

Publications and source records attributed to M Lamy.

At least 127 records · Page 7Linked to original sources
PubMed1994

Are similar inflammatory factors involved in strenuous exercise and sepsis?

An increasing body of data suggest that strenuous exercise triggers an inflammatory response having some similarity with those occurring in sepsis. Indices of this inflammatory response to exercise (IRE) especially include leukocytosis, release of inflammatory mediators and acute phase reactants, tissue damage, priming of various white blood cell lines, production of free radicals; activation of complement, coagulation and fibrinolytic cascades. Inflammatory responses to strenuous exercise and sepsis could in part be due to the release of endotoxin in blood as common triggering factor, but it seems that tissue damage and/or contact system activation are more important triggering mechanisms in exercising subjects. While the magnitude and duration of cellular and humoral changes associated with IRE are quite different from those observed in sepsis, recent human studies suggested that chronic and/or excessive IRE could have adverse effects. Among the possible consequences of acute and chronic IRE are delayed onset muscular soreness and loss of force, cardiovascular complications, intravascular hemolysis, hypoferraemia and increased susceptibility to infection.

Blood Coagulation↗
PubMed1994

Report of the American-European Consensus conference on acute respiratory distress syndrome: definitions, mechanisms, relevant outcomes, and clinical trial coordination. Consensus Committee.

The acute respiratory distress syndrome (ARDS), a process of nonhydrostatic pulmonary edema and hypoxemia associated with a variety of etiologies, carries a high morbidity rate, mortality rate (10% to 90%), and financial cost. The reported annual incidence in the United States is 150,000 cases, but this figure has been challenged and may be different in Europe. Part of the reason for these uncertainties is the heterogeneity of diseases underlying ARDS and the lack of uniform definitions for ARDS. Thus, those who wish to know the true incidence and outcome of this clinical syndrome are stymied. The European American Consensus Committee on ARDS was formed to focus on these issues and on the pathophysiologic mechanisms of the process. It was felt that international coordination between North America and Europe in clinical studies of ARDS was becoming increasingly important to address the recent plethora of potential therapeutic agents for the prevention and treatment of ARDS.

Clinical Trials as Topic↗
PubMed1994

Direct evidence of free radical production after ischaemia and reperfusion and protective effect of desferrioxamine: ESR and vitamin E studies.

After surgical renal revascularisation, warm renal ischaemia due to renal artery cross-clamping contributes to postoperative renal dysfunction. After reperfusion, free radicals are thought to be a significant cause of injury. Nevertheless, indisputable proof of free radical production is scarce, partly because of their transient nature. In this study, electron paramagnetic resonance and vitamin E levels were used to demonstrate the free radical production after renal ischaemia and reperfusion. Rabbit kidneys were submitted either to 15 or 60 minutes of ischaemia followed by reperfusion. A spin trap agent (alpha-phenyl-N-tert-butyl nitrone (PBN), 20mg/ml, 1 ml/min) was infused during reperfusion directly into the left renal artery via an aortic catheter before declamping. Blood samples were selectively drawn from the left renal vein for ESR analysis (Varian spectrometer E109) of lipidic residues extracted from blood samples. The vitamin E content of the left renal cortex was determined by HPLC procedure. The right renal cortex was used as a control for the vitamin E values. In the venous effluent, ESR analysis revealed the formation of a spectrum consisting of a triplet of asymmetric doublets. This signal resulted from the spin trapping by PBN of a mixture of both oxygen- and carbon- centred lipidic radicals. The amplitude of the signal which is proportional to the amount of free radicals was significantly higher after 60 minutes ischaemia than after 15 minutes.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Anaphylatoxin C5a production during short-term submaximal dynamic exercise in man.

We studied the effects of short-term submaximal exercise on the plasma levels of myeloperoxidase ([MPO]) and C5a anaphylatoxin ([C5a]), taken as specific markers of polymorphonuclear neutrophil (PMN) and complement activation, respectively. Eleven young, healthy male volunteers were subjected to a constant-load concentric exercise on a cycle ergometer (20 min at 80% maximal oxygen uptake). Mean resting MPO and C5a concentrations were 437 +/- 113 and 0.47 +/- 0.21 ng/ml, respectively. During exercise, [MPO] and [C5a] increased significantly (p < 0.001) towards respective peak values of 649 +/- 131 and 1.3 +/- 0.6 ng/ml. A rapid decrease of both [MPO] and [C5a] was observed during recovery. The similar time course of [MPO] and [C5a] changes and the highly significant relationship between these two variables (r = 0.651; p < 0.001) argues for the possible involvement of the complement anaphylatoxin C5a in the process of PMN degranulation. During exercise, the number of circulating PMN increased (+80%; p < 0.001) and remained practically unchanged up to 20 minutes of recovery. As [MPO] and PMN count were not significantly related (r = 0.2; p < 0.1), we concluded that the activation of PMN was independent of their mobilization.

Adult↗
PubMed1994

High-dose aprotinin reduces blood loss in patients undergoing total hip replacement surgery.

BACKGROUND: Aprotinin, a proteinase inhibitor, has been reported to reduce blood loss significantly during cardiac surgery. The mechanisms of this effect remain unclear. We studied the effect of aprotinin on blood loss and transfusion requirement during total hip replacement. Potential mechanisms of action and side effects also were investigated. METHODS: Forty patients scheduled for primary total hip replacement were randomized to receive, in double-blind fashion, either aprotinin given as a bolus of 2 x 10(6) kallikrein inactivator units (KIU) followed by an infusion of 5 x 10(5) KIU/h until the end of surgery or an equivalent volume of normal saline. Anesthesia and surgical techniques were standardized and systematic deep venous thrombosis prophylaxis was used. Peri- and postoperative blood loss and transfusion were measured. Fibrinolysis, coagulation pathways, and platelet function were assessed. Renal and hepatic function as well as the incidence of deep venous thrombosis also were assessed. RESULTS: Aprotinin reduced total blood loss from 1,943 +/- 700 ml to 1,446 +/- 514 ml (P < 0.05). This reduction of blood loss occurred during surgery (P < 0.05) and postoperatively (P < 0.001). Total amounts of blood transfused were 3.4 +/- 1.3 units/patient in the control group and 1.8 +/- 1.2 units/patient in the aprotinin group (P < 0.001). The activated partial thromboplastin time was significantly prolonged by aprotinin immediately after surgery, at 50.6 +/- 12.4 versus 32.3 +/- 4.6 s in control patients (P < 0.001), but results of the other coagulation tests were not different between the two groups. No side effects were observed in the aprotinin group. The incidence of deep venous thrombosis in the two groups was not significantly different. CONCLUSIONS: The use of high-dose aprotinin during total hip replacement results in a reduction in both blood loss and the amount of blood transfused. Aprotinin's mode of action, however, remains to be elucidated.

Aged↗
PubMed1994

Epidural anesthesia impairs both central and peripheral thermoregulatory control during general anesthesia.

BACKGROUND: The authors tested the hypotheses that: (1) the vasoconstriction threshold during combined epidural/general anesthesia is less than that during general anesthesia alone; and (2) after vasoconstriction, core cooling rates during combined epidural/general anesthesia are greater than those during general anesthesia alone. Vasoconstriction thresholds and heat balance were evaluated under controlled circumstances in volunteers, whereas the clinical importance of intraoperative thermoregulatory vasoconstriction was evaluated in patients. METHODS: Five volunteers were each evaluated twice. On one of the randomly ordered days, epidural anesthesia (approximately T9 dermatomal level) was induced and maintained with 2-chloroprocaine. On both study days, general anesthesia was induced and maintained with isoflurane (0.7% end-tidal concentration), and core hypothermia was induced by surface cooling and continued for at least 1 h after fingertip vasoconstriction was observed. Patients undergoing colorectal surgery were randomly assigned to combined epidural/enflurane anesthesia (n = 13) or enflurane alone (n = 13). In appropriate patients, epidural anesthesia was maintained by an infusion of bupivacaine. The core temperature that triggered fingertip vasoconstriction identified the threshold. RESULTS: In the volunteers, the vasoconstriction threshold was 36.0 +/- 0.2 degrees C during isoflurane anesthesia alone, but significantly less, 35.1 +/- 0.7 degrees C, during combined epidural/isoflurane anesthesia. Cutaneous heat loss and the rates of core cooling were similar 30 min before vasoconstriction with and without epidural anesthesia. In the 30 min after vasoconstriction, heat loss decreased 33 +/- 13 W when the volunteers were given isoflurane alone, but only 8 +/- 16 W during combined epidural/isoflurane anesthesia. Similarly, the core cooling rates in the 30 min after vasoconstriction were significantly greater during combined epidural/isoflurane anesthesia (0.8 +/- 0.2 degrees C/h) than during isoflurane alone (0.2 +/- 0.1 degrees C/h). In the patients, end-tidal enflurane concentrations were slightly, but significantly, less in the patients given combined epidural/enflurane anesthesia (0.6 +/- 0.2% vs. 0.8 +/- 0.2%). Nonetheless, the vasoconstriction threshold was 34.5 +/- 0.6 degrees C in the epidural/enflurane group, which was significantly less than that in the other patients, 35.6 +/- 0.8 degrees C. When the study ended after 3 h of anesthesia, patients given combined epidural/enflurane anesthesia were 1.2 degrees C more hypothermic than those given general anesthesia alone. The rate of core cooling during the last hour of the study was 0.4 +/- 0.2 degrees C/h during combined epidural/enflurane anesthesia, but only 0.1 +/- 0.3 degrees C/h during enflurane alone. CONCLUSIONS: These data indicate that epidural anesthesia reduces the vasoconstriction threshold during general anesthesia. Furthermore, the markedly reduced rate of core cooling during general anesthesia alone illustrates the importance of leg vasoconstriction in maintaining core temperature.

Adolescent↗
PubMed1994

The American-European Consensus Conference on ARDS. Definitions, mechanisms, relevant outcomes, and clinical trial coordination.

The acute respiratory distress syndrome (ARDS), a process of nonhydrostatic pulmonary edema and hypoxemia associated with a variety of etiologies, carries a high morbidity, mortality (10 to 90%), and financial cost. The reported annual incidence in the United States is 150,000 cases, but this figure has been challenged, and it may be different in Europe. Part of the reason for these uncertainties are the heterogeneity of diseases underlying ARDS and the lack of uniform definitions for ARDS. Thus, those who wish to know the true incidence and outcome of this clinical syndrome are stymied. The American-European Consensus Committee on ARDS was formed to focus on these issues and on the pathophysiologic mechanisms of the process. It was felt that international coordination between North America and Europe in clinical studies of ARDS was becoming increasingly important in order to address the recent plethora of potential therapeutic agents for the prevention and treatment of ARDS.

Americas↗
PubMed1994

Massive ketonuria during sedation with propofol in a 12 year old girl with severe head trauma.

Severe ketonuria developed during sedation with propofol in a 12 year old girl with brain injury. Deep sedation with propofol (5.1 mg/kg/h) was required because of agitation and severe intracranial hypertension; as a part of our management protocol, glucose intake was restricted to 5 Kcal/h. After 18 hours of propofol infusion there was intense ketonuria (8+ by Ketostix) without any evidence of metabolic acidosis (pH, HCO3- and anion gap were within normal values). At this time, indirect calorimetry (Deltatrac) confirmed that energy expenditure was principally based on fat consumption (70% of energy expenditure). Lowering the propofol infusion rate and increasing glucose intake reduced fat consumption to 39% within 8 hours: at this time, Ketostix was negative for ketone bodies. This case illustrates a potential risk of ketonuria during prolonged sedation with propofol (a 10% solution of intralipid), particularly if glucose intake is restricted. Monitoring urinary ketone bodies is recommended under these circumstances.

Brain Injuries↗
PubMed1994

Malignant hyperthermia and severe hypoglycemia after reexposure to halothane.

A four year child presented with an episode of malignant hyperthermia induced by reexposure to halothane. The episode was associated with early onset of a severe hypoglycemia and liver enzymatic perturbances. Etiology of these perturbances is hard to state precisely in this clinical context, but a hepatic toxicity of halothane and/or by dantrolene is considered.

Child, Preschool↗
PubMed1993

[Other mediators of inflammation and sepsis].

During sepsis, the systemic inflammatory response is characterized by the release of numerous mediators supporting and dispersing inflammation. In Gram negative sepsis, the endotoxins play a starting role, while in other sepsis, the triggering mediators or mechanisms are unknown but lead to a similar inflammatory reaction. Coagulation and complement cascades are activated, with the release of chemoattractive substances, mediators and proteases and the activation of phagocytic cells. Macrophages/monocytes and polymorphonuclear leucocytes produce then active oxygen species and cytokines; they degranulate (releasing active enzymes such as myeloperoxidase), they express an increasing number of membrane receptors able to interact with endothelial cells and release a supplementary lot of inflammatory mediators (prostanoids, platelet activating factor, leukotrienes ... ). Platelets, also activated, produce the same mediators (TXA2, PAF ...) or specific ones such as serotonine, platelet factor 4, growth factors. Last, but not least, the endothelial cells are stimulated, directly (by endotoxins) or undirectly (by cytokines, C5a, PAF ...). These cells play then a main role by their own phagocytic activity, by alteration of their antithrombotic and fibrinolytic potential, by their secretion of inflammatory mediators and by an increased expression of receptors of adhesivity for the activated phagocytes or platelets, what leads to endothelium injury with membrane permeability alterations. These cascades of activation, these extensions of the inflammatory reaction by the mediators and by the phagocytes and platelets can explain the frequency of multiple organ failure during sepsis as well as the difficulty of an adequate pharmacological therapy.

Blood Coagulation↗
PubMed1993

Comparison between alprazolam and hydroxyzine for oral premedication.

The safety and efficacy of alprazolam and hydroxyzine administered orally as surgical premedicants were compared in a double-blind controlled study. Sixty-five patients were given either alprazolam 1 mg or hydroxyzine 75 mg, one to two hours before surgery. Anxiety was assessed by both the patient and the anaesthetist, the patient using a visual analogue scale, the anaesthetist employing both analogue and ordinal ratings. Sedation was assessed by the anaesthetist only, using the same two methods. Amnesia was appraised with a simple memory test. Safety was assessed by recording adverse effects and measuring haemodynamic variables. Premedication with alprazolam produced a modest reduction in anxiety (28%) (P < 0.01) while hydroxyzine had no detectable effect. The comparison of the sedation level and of the memory test revealed no difference between the two premedicants. Minor side effects were only observed in the hydroxyzine group. Changes in blood pressure were more pronounced in the hydroxyzine group. This study shows that alprazolam and hydroxyzine are safe and efficient oral premedicants. However, alprazolam is preferable to hydroxyzine in terms of anxiolytic and adverse effects.

Administration, Oral↗
PubMed1993

Evidence for free radical formation during human kidney transplantation.

Fourteen patients undergoing kidney transplantation were studied for evidence of the production of free radicals as assessed by the measurement of vitamin E (an index of lipid peroxidation) and of myeloperoxidase (a marker of neutrophil activation) in the systemic blood. Early (2 min) and late revascularization (30 min) of the kidney were respectively associated with a significant decrease of 35.5 and 40% of the initial level of plasma vitamin E. This consumption paralleled to the decrease of the vitamin E/total lipids ratio, a better indicator of vitamin E status. Heparin administration preceding renal artery clamping resulted in a twofold significant increase of baseline plasma myeloperoxidase (MPO) level (523 +/- 214 ng/ml). At kidney reperfusion, MPO concentration rose again and reached a maximum value of 1,653 +/- 882 ng/ml, indicating the presence of considerable neutrophil activation. A return to the baseline value was observed after 30 min of reperfusion. A short discussion about the possible origin of this MPO increase is given. Taken together, these data strongly suggest that free radical production, leading to lipid peroxidation phenomena, can occur within the early phase of kidney revascularization. Preliminary data using electron spin resonance with the spin-trapping technique strengthen this hypothesis.

Adult↗
PubMed1993

Production of active oxygen species by isolated human chondrocytes.

The ability of isolated human chondrocytes to produce active oxygen species has been investigated. The two methods for determining H2O2 and hydroxyl radicals (.OH) production were, by a fluorimetric method (production of dichlorofluorescein from a precursor in the presence of horseradish peroxidase and H2O2) and by a chromatographic method (measurement of ethylene production from gamma-methiol-keto-butyric acid after .OH attack). Chondrocytes were tested, both with and without activation by phorbol myristate acetate (PMA: 10(-6) M), in the presence of Ca2+ (1 x 10(-4) M) and Mg2+ (2 x 10(-4) M) or after variable periods of anoxia under nitrogen (4 to 12 h) followed by reoxygenation (with 95% O2, 5% CO2). Under these experimental conditions, the PMA-excited chondrocytes produced from 80 to 180 nmol of hydrogen peroxide per 1 x 10(6) cells and chondrocytes subjected to anoxia-reoxygenation produced up to 1700 nmol H2O2 per 1 x 10(6) cells. The hydroxyl radical production by PMA or anoxia-reoxygenation excited cells reached 600% of the production of non-excited cells and 1300% when they were subjected to successive stimulations by PMA and anoxia-reoxygenation. The possible pathological significance of these observations is discussed. The results indicate that stimulated human chondrocytes are capable of producing active oxygen species which could play a major role in joint inflammation and cartilage damage.

Adolescent↗
PubMed1993

Clonidine and ketanserin both are effective treatment for postanesthetic shivering.

BACKGROUND: Although meperidine is an effective treatment of postanesthetic shivering, its mechanism of action remains unknown. Investigation of other drugs might help clarify the mechanisms by which shivering can be controlled. Accordingly, we investigated the efficacy of clonidine, an alpha 2-adrenergic agonist, and ketanserin, a 5-hydroxytryptamine antagonist, in treating postanesthetic shivering. METHODS: First, 54 patients shivering after general anesthesia were allocated randomly to receive an intravenous bolus of saline, 150 micrograms clonidine, or 10 mg ketanserin. A second study explored the dose-dependence of clonidine. Forty shivering patients were given saline or clonidine, 37.5, 75, or 150 micrograms. RESULTS: The duration of shivering was significantly shorter in those given clonidine (2.1 +/- 0.9 min) than in the other two groups and shorter in the ketanserin group (4.3 +/- 0.9 min) than in the saline group (12.0 +/- 1.6 min). Clonidine and ketanserin significantly decreased systolic arterial blood pressure when compared to saline. Core rewarming was significantly slower in the clonidine group. In the second study, 37.5 micrograms clonidine was no more effective than saline. Two minutes after treatment, 150 micrograms obliterated shivering in all patients. Five minutes after treatment, all patients given 75 micrograms had stopped shivering. Systolic arterial pressure and heart rate decreased significantly in patients given 75 and 150 micrograms clonidine. CONCLUSIONS: Clonidine (150 micrograms) and ketanserin (10 mg) both are effective treatment for postanesthetic shivering. The effect of clonidine on shivering is dose-dependent: whereas 37.5 micrograms had no effect, 75 micrograms clonidine stopped shivering within 5 min.

Adult↗
PubMed1993

Sequential anti-core glycolipid immunoglobulin antibody activities in patients with and without septic shock and their relation to outcome.

OBJECTIVE: This study follows the sequential changes in anti-lipopolysaccharide antibodies in infected patients with and without septic shock. SUMMARY BACKGROUND DATA: A relation between high endogenous levels of anti-LPS antibodies and protection against bacteremia and septic shock in at-risk patient groups has been observed. However, information on the daily follow-up and kinetics of apparition or disappearance of anti-LPS antibody activities and their relations with the protective properties of the different immunoglobulin classes has not been clearly investigated. METHODS: Two hundred and five septic surgical patients were studied during their stay in the intensive care unit during a period of 3 years. Among these patients, septic shock developed in 54 and 47 died. A sensitive ELISA was used to study circulating IgM and IgG antibodies to the core glycolipid (CGL) region of Salmonella minnesota R595. The activities were measured each day when sepsis occurred and every hour during septic shock. RESULTS: Anti-CGL IgM activity was found in 32% of the septic patients. This response, however, most often appeared to be transient. A strong correlation was observed between the occurrence of septic shock and the absence of anti-CGL IgM activity on admission to the ICU (p < 0.02). Anti-CGL IgG activity was detected in 82% of the patients and better correlated with outcome for patients with high or rising activities during their hospitalization (p < 0.0005). In patients with septic shock or irreversible organ failure, a fall in the anti-CGL IgG activity was observed before death, suggesting that the IgG antibodies were consumed during this acute event. Therefore, the anti-CGL IgG activity measured by ELISA could be used as a marker of the evolution of the illness. CONCLUSIONS: Our observations demonstrate the interest to follow-up the evolution of the anti-CGL antibodies during sepsis. The fall of these antibodies during septic shock and in patients who died was an additional argument to perform, as an additive form, passive antibody therapy to decrease lethality in this group of patients.

Bacterial Infections↗