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Biomedical subjects

B Lambermont

Publications and source records attributed to B Lambermont.

At least 19 recordsLinked to original sources
PubMed2003

BM-573, a dual thromboxane synthase inhibitor and thromboxane receptor antagonist, prevents pig myocardial infarction induced by coronary thrombosis.

The aim of this study was to characterize the effects of BM-573 [N-terbutyl-N'-[2-(4'-methylphenylamino)-5-nitro-benzenesulfonyl] urea], a novel dual thromboxane A2 receptor antagonist and thromboxane synthase inhibitor, on myocardial infarction induced by topical ferric chloride (FeCl3) application to the left anterior descending (LAD) coronary artery in anesthetized pigs. All control animals (n = 6) developed an occlusive thrombus in the LAD coronary artery. The mean infarct size, revealed by triphenyl tetrazolium chloride (TTC), and the area at risk, evidenced by Evans blue, corresponded to 35.3 +/- 2.2 and 36.9 +/- 2.1% of the left ventricular mass, respectively. In the BM-573-treated group (n = 6), a drug infusion (10 mg. kg-1. h-1) started 30 min before FeCl3 application and continued throughout the experimentation. Among the BM-573-treated group, four pigs did not develop coronary artery thrombus and their myocardium appeared healthy. Histopathological examination of FeCl3-injured coronary artery revealed an occlusive and adherent thrombus in control group, while pretreatment with BM-573 prevented thrombus formation. In infarcted zones, lack of desmin staining and muscle structure disorganization were obvious. Depletion of myocardial ATP content was observed in the myocardial necrotic region of the control group, but not in myocardial samples of BM-573-treated pigs that did not develop myocardial infarction. When BM-573 prevented LAD artery occlusion, the area under the curve of plasmatic troponin T was reduced by 77% over 6 h. These data suggest that BM-573 could be useful for the prevention of myocardial infarction.

Animals↗
PubMed2003

[Comparison of a nurse-directed weight-based heparin nomogram with standard empirical doctor-based heparin dosage].

OBJECTIVE: To assess efficiency of a nurse directed weight-based nomogram (NWN) for heparin dosage without training. STUDY DESIGN: Prospective, comparative, before/after intervention study. PATIENTS AND METHODS: In a university medical intensive care unit, 19 patients receiving unfractionned intravenous heparin, following standard medical prescriptions (SHT), were compared to 19 patients submitted to NWN (80 U kg(-1) bolus, starting infusion at 18 U kg(-1) h(-1) and secondary dosage adaptations following a specific nomogram). RESULTS: Dose of heparin bolus and starting dose infusion were significantly greater in NWN group than in the SHT group. The delay in achieving a predetermined therapeutic APTT level of at least 60 s was 6 (1-76) hours in the SHT group and 4 (3- 32) hours in the NWN group. The target APTT (60-85 s) was obtained after 13.5 (1-76) hours and 9.5 (3-32) hours in the two groups, respectively. Although reduction in delay seemed to favour anticoagulation dictated by the NWN protocol, the difference failed to reach statistical significance. Percentage of target APTT over total number of APTT values per patient was significantly higher in the NWN group (41 [0-87] vs. 31% [0-54]) in the SHT group. Strict observance of anticoagulation by using NWN tended to be better than that in SHT group. CONCLUSIONS: NWN protocol was easy to use without previous training. NWN was associated with the best anticoagulation state although its superiority was less evident than expected.

Aged↗
PubMed2003

Effects of U-46619 on pulmonary hemodynamics before and after administration of BM-573, a novel thromboxane A2 inhibitor.

We studied the effects on pulmonary hemodynamics of U-46619, a thromboxane A2 (TXA2) agonist, before and after administration of a novel TXA2 receptor antagonist and synthase inhibitor (BM-573). Six anesthetized pigs (Ago group) received 6 consecutive injections of U-46619 at 30-min interval and were compared with six anesthetized pigs (Anta group) which received an increasing dosage regimen of BM-573 10 min before each U-46619 injection. Consecutive changes in pulmonary hemodynamics, including characteristic resistance, vascular compliance, and peripheral vascular resistance, were continuously assessed during the experimental protocol using a four-element Windkessel model. At 2 mg/kg, BM-573 completely blocked pulmonary hypertensive effects of U-46619 but pulmonary vascular compliance still decreased. This residual effect can probably be explained by a persistent increase in the tonus of the pulmonary vascular wall smooth muscles sufficient to decrease vascular compliance but not vessel lumen diameter. Such molecule could be a promising therapeutic approach in TXA2 mediated pulmonary hypertension as it is the case in pulmonary embolism, hyperacute lung rejection and endotoxinic shock.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed2003

Effects of BM-573, a novel thromboxane A2 inhibitor, on pulmonary hemodynamics in endotoxic shock.

Thromboxane A2 is considered to be partially responsible for the increase in pulmonary vascular resistance observed after endotoxin administration and to participate in proinflammatory reactions. The effects of a novel dual TXA2 synthase inhibitor and TXA2 receptor antagonist (BM-573) on pulmonary hemodynamics were investigated in endotoxic shock. 30 mins before the start of a 0.5 mg/kg endotoxin infusion, 6 pigs (Endo group) received a placebo infusion and 6 other pigs (Anta group) received a BM-573 infusion. In Endo group, pulmonary artery pressure increased from 25 +/- 1.8 (T0) to 42 +/- 2.3 mmHg (T60) (p < 0.05) after endotoxin infusion while, in Anta group, it increased from 23 +/- 1.6 (T0) to 25 +/- 1.5 mmHg (T60). This difference is due to a reduction in pulmonary vascular resistance in Anta group while pulmonary arterial compliance changes in Endo group remained comparable with the evolution in Anta group. In Endo group, PaO2 decreased from 131 +/- 21 (T0) to 74 +/- 12 mmHg (T300) (p < 0.05), while in Anta group, PaO2 was 241 +/- 31 mmHg at the end of the experimental period (T300). These results demonstrate that TXA2 plays a major role in pulmonary vascular changes during endotoxin insult. Concomitant inhibition of TXA2 synthesis and of TXA2 receptors by BM-573 inhibited the pulmonary vasopressive response during the early phase of endotoxin shock as well as the deterioration in arterial oxygenation.

Animals↗
PubMed2003

Effect of hemodiafiltration on pulmonary hemodynamics in endotoxic shock.

Hemofiltration can improve pulmonary hemodynamics during septic shock. The main objective of the study was to determine whether hemodiafiltration (HDF) would also have beneficial effects on pulmonary hemodynamics during septic shock. In the Endo group, six anesthetized pigs received a 0.5 mg/kg endotoxin infusion over 30 min. In the HDF group (n = 6), HDF was started 30 min after the end of the endotoxin infusion, while in the Control group (n = 4) they received HDF but no endotoxin infusion. Pulmonary hemodynamics were analyzed in detail with a four-element windkessel model. Although in the Control group, HDF did not alter pulmonary hemodynamic parameters, in the HDF group, it was responsible for an amplification of the deleterious pulmonary vascular response to endotoxin insult. Our results show that HDF must be used cautiously in septic shock since it can precipitate right heart failure by increasing pulmonary vascular resistance.

Animals↗
PubMed2003

Alteration of left ventriculo-arterial coupling and mechanical efficiency during acute myocardial ischemia.

AIM: Myocardial revascularisation being frequently performed during acute myocardial ischemia, in a hostile hemodynamic environment, we evaluated left ventriculo-arterial (VA) coupling, left ventricular (LV) mechanical efficiency, and the mechanical properties of the systemic vasculature during acute myocardial ischemia. METHODS: In 6 pigs, vascular properties [characteristic impedance (R(1)), peripheral resistance (R(2)), compliance (C), inductance (L), arterial elastance (E(a))] were estimated with a windkessel model. LV function was assessed by the slope (E(es)) of end-systolic pressure-volume relationship (ESPVR), and stroke work (SW) - end-diastolic volume (EDV) relation. Pressure-volume area (PVA) was referred to as myocardial oxygen consumption. VA coupling was defined as E(es)/E(a), and mechanical efficiency as SW/PVA. After baseline recordings, the left anterior descending coronary artery was ligated and hemodynamic measures obtained every 30 minutes for 3 hours. Data are expressed as mean (SEM). RESULTS: Coronary occlusion induced an ESPVR rightward shift, and decreased E(es) from 3.67 (0.33) to 1.92 (0.20) mmHg/ml and the slope of the SW - EDV relationship from 72.3 (3.4) to 40.4 (4.5) mmHg (p<0.001), while E(a) increased from 3.33 (0.56) to 4.65 (0.29) mmHg/ml (p<0.005). This was responsible for a dramatic alteration of VA coupling from 1.22 (0.11) to 0.44 (0.07), (p<0.001). While R2 increased from 1.72 (0.30) to 2.38 (0.16) mmHg x s x ml(-1) (p<0.05) and C decreased from 0.78 (0.16) to 0.46 (0.08) ml/mmHg (p<0.05), R(1) and L were unchanged. Coronary occlusion decreased SW from 4056 (223) to 2580 (122) mmHg.ml (p<0.001), while PVA and SW/PVA decreased from 5575 (514) to 4813 (317) mmHg x ml (NS), and from 0.76 (0.04) to 0.57 (0.03) (p<0.001), respectively. CONCLUSION: Acute myocardial ischemia severely altered left ventriculo-arterial coupling and LV mechanical efficiency. Impaired left VA coupling was due to a combination of augmented arterial elastance, secondary to early vasoconstriction later associated with decreased arterial compliance, and decreased LV contractility.

Animals↗
PubMed2002

[Dog bite in a splenectomized patient].

We present a case of Capnocytophaga canimorsus fulminant infection linked to a dog bite in a splenectomized patient. Capnocytophaga canimorsus is a gram-negative rod that typically causes septicaemia with disseminated intravascular coagulation in both immunocompromised and immunocompetent hosts. It is associated with high mortality. We also reviewed the literature and provide some recommendations on the management of bite wound as well as on both prevention and treatment of infection in asplenic state.

Adult↗
PubMed2002

Cortical processing of noxious somatosensory stimuli in the persistent vegetative state.

The persistent vegetative state (PVS) is a devastating medical condition characterized by preserved wakefulness contrasting with absent voluntary interaction with the environment. We used positron emission tomography to assess the central processing of noxious somatosensory stimuli in the PVS. Changes in regional cerebral blood flow were measured during high-intensity electrical stimulation of the median nerve compared with rest in 15 nonsedated patients and in 15 healthy controls. Evoked potentials were recorded simultaneously. The stimuli were experienced as highly unpleasant to painful in controls. Brain glucose metabolism was also studied with [(18)F]fluorodeoxyglucose in resting conditions. In PVS patients, overall cerebral metabolism was 40% of normal values. Nevertheless, noxious somatosensory stimulation-activated midbrain, contralateral thalamus, and primary somatosensory cortex in each and every PVS patient, even in the absence of detectable cortical evoked potentials. Secondary somatosensory, bilateral insular, posterior parietal, and anterior cingulate cortices did not show activation in any patient. Moreover, in PVS patients, the activated primary somatosensory cortex was functionally disconnected from secondary somatosensory, bilateral posterior parietal, premotor, polysensory superior temporal, and prefrontal cortices. In conclusion, somatosensory stimulation of PVS patients, at intensities that elicited pain in controls, resulted in increased neuronal activity in primary somatosensory cortex, even if resting brain metabolism was severely impaired. However, this activation of primary cortex seems to be isolated and dissociated from higher-order associative cortices.

Adult↗
PubMed2001

[Venous and arterial thromboembolism in a patient with factor V R506Q Leiden mutation and heparin-induced immuno-allergic reaction].

A forty-six-year old in-patient was treated with heparin for massive pulmonary embolism. During the hospitalization, the clinical evolution was unusual and characterised as follows: a) the extent of pulmonary embolism justified a thrombolysis by streptokinase; b) an acute thrombocytopenia occurred a few days later, preceded by a slower, but significant decrease of platelet count; c) a non-occlusive aortic thrombosis developed, distal to renal arteries, causing distal embolisation, successfully treated by local fibrinolysis. The prompt correction of platelet count after interruption of heparin therapy confirmed the diagnosis, before the detection of antibodies against heparin-PF4 complexes. Heparin was immediately replaced by another direct anticoagulant, recombinant hirudin (lépirudine-Refludan), initially given alone and progressively replaced by an antivitamin K (Sintrom). The occurrence of distal embolism from aortic thrombosis, developed during the critical period, characterizes this syndrome, which appears rare but whose incidence is probably underestimated. A subsequent investigation for risk factors for venous thromboembolism in this patient revealed a heterozygous mutation of the Leiden type factor V in our patient, and also in others family members.

Anticoagulants↗
PubMed2001

[Clinical case of the month. Porto-pulmonary hypertension syndrome associated with severe hypoxemia].

We report the case of a patient with liver cirrhosis who was admitted to the emergency room for rapid occurrence of dyspnea and severe hypoxemia at rest. Lung CT-scan and echocardiography did not disclose any right-to-left shunt and right-sided heart catheterization evidenced major precapillary pulmonary hypertension. The present feature supports the hypothesis that the pulmonary complications of cirrhosis, the hepatopulmonary syndrome and the portopulmonary hypertension, which are usually considered as mutually exclusive, may coexist. In such circumstances, the right failing heart is the major determinant to the immediate prognosis.

Female↗
PubMed2000

Effects of cold and warm ischemia on the mitochondrial oxidative phosphorylation of swine lung.

BACKGROUND: The aim of the study was to investigate the consequence of warm and cold ischemia on lung mitochondria in order to define bioenergetic limits within lung could be suitable for pulmonary transplantation. METHODS: Twenty-two pigs underwent lung harvesting after lung flush with Euro-Collins solution. Mitochondria were isolated from fresh lungs, from lungs submitted to 24 or 48 hr of cold ischemia, to 30 or 45 min of warm ischemia, and to 30 min of warm ischemia followed by 24 or 48 hr of cold ischemia. Mitochondrial oxidative phosphorylation parameters were determined in isolated mitochondria by in vitro measurement of oxygen consumption. RESULTS: Relative to controls, mitochondria submitted to cold ischemia showed an alteration in the oxidoreductase activities of the respiratory chain but no membrane permeability alteration. After 48 hr of cold ischemia, there was a decrease in the yield of the oxidative phosphorylation. Thirty minutes of warm ischemia did not alter the mitochondrial respiratory parameters. However, lung submitted to 45 min of warm ischemia showed mitochondrial damage as a decrease in the oxidative phosphorylation efficiency and ADP availability but no change in the oxidoreductase activities. Relative to cold ischemia alone, 30 min of warm ischemia preceding cold ischemia promoted no significant change in the respiratory parameters. CONCLUSIONS: On bioenergetic basis, lung submitted to warm ischemia could be suitable for transplantation if the warm ischemia duration does not exceed 30 min. This could be a major concern in lung procurement from non-heart beating donors.

Animals↗
PubMed2000

[Application of the Simplified Acute Physiology Score II (SAPS II) in a medical intensive care unit].

OBJECTIVE: Our study was to assess the validity of SAPS II (New Simplified Acute Physiology Score) to predict the probability of in hospital mortality, in a cohort of patient admitted to a medical intensive care unit. STUDY DESIGN: Prospective study. PATIENTS AND METHODS: Out of 467 the 525 patients admitted were included. SAPS score and in hospital mortality prediction were calculated for each of them. RESULTS: In this group, SAPS II offered a satisfactory discrimination power with an area under the curve of 0.843. However, calibration showed a lack of fit (chi 2 = 28.5, P < 0.001), with an overall under prediction of mortality (observed versus expected ratio of 1.12). CONCLUSION: This SAPS II lower predicting accuracy in a specific population and for individual outcome prediction may reduce its interest in clinical decision-making.

Area Under Curve↗
PubMed2000

Increased aortic compliance maintains left ventricular performance at lower energetic cost.

OBJECTIVE: The aim of this study was to investigate left ventricular contractility and energetic cost of cardiac ejection under conditions of acute increase in aortic compliance. METHODS: In six anaesthetized pigs, ascending aortic compliance was increased by adding a volume chamber in parallel to the ascending aorta. Systemic vascular parameters, including characteristic impedance, peripheral resistance, total vascular compliance, and inertance, were estimated with a four-element windkessel model. Arterial elastance was derived from these parameters. Left ventricular systolic function was assessed by end-systolic pressure-volume relationship (end-systolic elastance), and stroke work. Pressure-volume area was used as a measure of myocardial oxygen consumption. Heart rate remained constant during the experimentation. RESULTS: Adding the aortic volume chamber significantly increased vascular compliance from 0. 95+/-0.08 to 1.17+/-0.06 ml/mmHg (P<0.01), while inductance, characteristic impedance, peripheral resistance, and arterial elastance remained statistically at basal values, respectively 0. 0020+/-0.0003 mmHg.s(2)/ml, 0.105+/-0.009 mmHg.s/ml, 1.27+/-0.12 mmHg.s/ml, and 2.43+/-0.21 mmHg/ml. During the same interval, stroke work and pressure-volume area decreased respectively from 2700+/-242 to 2256+/-75 mmHg.ml (P<0.01), and from 3806+/-427 to 3179+/-167 mmHg.ml (P<0.01). Stroke work and pressure-volume area decreased at matched end-diastolic volumes. In contrast, end-systolic elastance, ejection fraction, and stroke volume remained statistically unchanged, respectively at 2.29+/-0.14 mmHg/ml, 48.1+/-2.1 %, and 32. 4+/-1.7 ml. CONCLUSIONS: These data suggest that, when facing an increased aortic compliance, the left ventricle displays unchanged contractility, but the energetic cost of cardiac ejection is significantly decreased. These data may be of clinical importance when choosing an artificial prosthesis for ascending aortic replacement.

Animals↗
PubMed2000

Auditory processing in the vegetative state.

H(2)(15)O-PET was used to investigate changes in regional cerebral blood flow in response to auditory stimulation in patients in the vegetative state. Five patients in a vegetative state of hypoxic origin were compared with 18 age-matched controls. In addition, the cerebral metabolism of these patients and 53 age-matched controls was studied using [(18)F]fluorodeoxyglucose. In control subjects, auditory click stimuli activated bilateral auditory cortices [Brodmann areas (BA) 41 and 42] and the contralateral auditory association cortices (BA 22). In the patients, although resting metabolism was decreased to 61% of normal values, bilateral auditory areas 41 and 42 showed activation as seen in the controls, but the temporoparietal junction cortex (BA 22) failed to be activated. Moreover, the auditory association cortex was functionally disconnected from the posterior parietal association area (BA 40), the anterior cingulate cortex (BA 24) and the hippocampus, as revealed by psychophysiological interaction analysis. Thus, despite altered resting metabolism, the auditory primary cortices were still activated during external stimulation, whereas hierarchically higher-order multi- modal association areas were not. Such a cascade of functional disconnections along the auditory cortical pathways, from the primary auditory areas to multimodal and limbic areas, suggests that the residual cortical processing observed in the vegetative state cannot lead to the integrative processes that are thought to be necessary for the attainment of the normal level of awareness.

Acoustic Stimulation↗
PubMed1999

Analysis of endotoxin effects on the intact pulmonary circulation.

OBJECTIVE: The mechanism of sustained alterations in pulmonary hemodynamics during endotoxin shock remains unclear. To gain more detailed knowledge we used the four-element windkessel model as a descriptor of the pulmonary circuit. METHODS: Consecutive changes in characteristic resistance (R1), vascular compliance (C), input resistance (R2) and inductance (L) were continuously assessed following injection of endotoxin in 6 anaesthetised pigs, and were compared with the corresponding values measured in a similar group of sham-operated animals. RESULTS: Endotoxin challenge resulted in a biphasic pulmonary artery pressure response. Blood flow decreased progressively from 2.8 +/- 0.2 l/min to 2 +/- 0.2 l/min. Ohmic pulmonary vascular resistance (PVR) increased gradually from 0.2 +/- 0.04 to 0.76 +/- 0.1 mm Hg s ml-1. The early increase in PAP (from 14 +/- 2 to 27 +/- 4 mm Hg) was mediated by changes in both R1 (from 0.04 +/- 0.01 to 0.06 +/- 0.01 mm Hg s ml-1) and R2 (from 0.16 +/- 0.04 to 0.61 +/- 0.2 mm Hg s ml-1). These responses, in turn, altered the proximal vascular compliance. A subsequent increase in PAP (from 27 +/- 2 to 32 +/- 3 mm Hg) paralleled the specific decline in distal pulmonary vasculature compliance from 0.84 +/- 0.1 to 0.65 +/- 0.1 ml/mmHg. Analysis of the time course of PVR did not allow us to distinguish between vasoconstriction and stiffening of the vascular tree as mechanisms accounting for PAP changes. CONCLUSIONS: Endotoxemia leads to pulmonary hypertension, which is a result of constriction of proximal pulmonary arteries during the early phase, whereas the late phase is characterised by a decline in distal pulmonary vasculature compliance.

Animals↗