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M Dauzat

Publications and source records attributed to M Dauzat.

At least 19 recordsLinked to original sources
PubMed2006

Effects of high-altitude exercise training on contractile function of rat skinned cardiomyocyte.

OBJECTIVE: Previous studies have questioned whether there is an improved cardiac function after high-altitude training. Accordingly, the present study was designed specifically to test whether this apparent blunted response of the whole heart to training can be accounted for by altered mechanical properties at the cellular level. METHODS: Adult rats were trained for 5 weeks under normoxic (N, NT for sedentary and trained animals, respectively) or hypobaric hypoxic (H, HT) conditions. Cardiac morphology and function were evaluated by echocardiography. Calcium Ca2+ sensitivity of the contractile machinery was estimated in skinned cardiomyocytes isolated from the left ventricular (LV) sub-epicardium (Epi) and sub-endocardium (Endo) at short and long sarcomere lengths (SL). RESULTS: Cardiac remodelling was harmonious (increase in wall thickness with chamber dilatation) in NT rats and disharmonious (hypertrophy without chamber dilatation) in HT rats. Contrary to NT rats, HT rats did not exhibit enhancement in global cardiac performance evaluated by echocardiography. Stretch- dependent Ca2+ sensitization of the myofilaments (cellular index of the Frank-Starling mechanism) increased from Epi to Endo in N rats. Training in normoxic conditions further increased this stretch-dependent Ca2+ sensitization. Chronic hypoxia did not significantly affect myofibrilar Ca2+ sensitivity. In contrast, high-altitude training decreased Ca2+ sensitivity of the myofilaments at both SL, mostly in Endo cells, resulting in a loss of the transmural gradient of the stretch-dependent Ca2+ sensitization. Expression of myosin heavy chain isoforms was affected both by training and chronic hypoxia but did not correlate with mechanical data. CONCLUSIONS: Training at sea level increased the transmural gradient of stretch-dependent Ca2+ sensitization of the myofilaments, accounting for an improved Frank-Starling mechanism. High-altitude training depressed myofilament response to Ca2+, especially in the Endo layer. This led to a reduction in this transmural gradient that may contribute to the lack of improvement in LV function via the Frank-Starling mechanism.

Actin Cytoskeleton↗
PubMed2006

Chronic exercise does not prevent hypoxia-induced increased aortic sensitivity to endothelin in rats.

OBJECTIVES: We report in the present study the effect of regular exercise on vascular reactivity alterations to endothelin (ET-1) following prolonged exposure to hypoxic stress. METHODS: Male Dark Agouti rats were randomly assigned to N (sedentary rats), NCE (normoxic exercised rats), CH (chronic hypoxic sedentary rats) and CHCE (chronic hypoxic exercised rats) groups. The effects of ET-1 in the presence or not of the endothelium and/or of the specific inhibitor, bosentan, have been investigated in an isolated model of rat thoracic aorta. RESULTS: Prolonged exposure to hypoxia induced a significant increase in aortic sensitivity to ET-1 (-log ED50 in CH = 8.15 +/- 0.01 vs in N = 7.98 +/- 0.02, p < 0.05). Despite exercise training reduced the sensitivity to ET-1 in normoxic rats, it has no effects in hypoxic rats (-log ED50 in CH = 8.15 +/- 0.01 vs in CHCE = 8.19 +/- 0.01, NS). Moreover, although the removal of endothelium has no effect in N rats, it leads, in NCE rats, to a significant increase in sensitivity to ET-1 (-log ED50 in endothelium intact rings = 7.89 +/- 0.04 vs in denuded rings = 8.04 +/- 0.02, p < 0.05). The implication of ET-1 receptors on both endothelial and smooth muscle cells is confirmed by the significant reduced sensitivity to ET-1 in the four groups when bosentan is present in organ bath. CONCLUSION: Our study clearly suggests that part of the beneficial effect of chronic exercise could be mediated by enhancing endothelial function associated with endothelin reactivity in peripheric vessels. However, chronic exercise training does not seem to be able to limit the increased vasoconstriction to ET-1 stimulation induced by chronic hypoxia exposure.

Animals↗
PubMed2006

Protection against reactive oxygen species injuries in rat isolated perfused hearts: effect of LPBNAH, a new amphiphilic spin-trap derived from PBN.

Numerous strategies have been designed to protect the myocardium against reactive oxygen species (ROS). The present study was designed to test wether LPBNAH, a new amphiphilic spin-trap derived from PBN is able to protect isolated perfused rat hearts against ROS injuries. Following total glola ischemia (30 min), hearts were reperfused in the presence or not of LPBNAH (10 micromol/l), and left ventricular function was continuously monitored. The addition of LPBNAH led to a significant recovery in left ventricular developped pressure (LVDevP, control: 16.5+/- 7.5, p < 0.05). To conclude, the present results strongly suggest that the modification of previous wellknown molecules in order to facilitate their access to intracellular site of ROS production might be of interest to limit oxidative stresses.

Animals↗
PubMed2006

Reproducibility of automated pulse wave velocity measurement during exercise. Running head: pulse wave velocity during exercise.

Pulse wave velocity measurement is used as an index of arterial stiffness. The purpose was to evaluate the reproducibility of pulse wave velocity measurement at rest, during exercise and recovery from exercise, using an automated device. Twelve healthy young adults (mean age 22.0 +/- 3.1 yrs) underwent an upright submaximal cycle test on two separate occasions, one week apart. Pulse wave velocity, systolic and diastolic blood pressures and heart rate were assessed at rest, during the last 2 min of exercise and 10 min later. Pulse wave velocity was measured on the upper limb and the forearm by the cross-correlation function of photoplethysmography and Doppler signals. Brachial artery pulse wave velocity was calculated from upper limb and forearm pulse wave velocities. No significant difference was found on duplicate measurements of heart rate, systolic and diastolic blood pressures at rest, during exercise and recovery, showing that pulse wave velocity was measured under similar conditions. Coefficient of variation for upper limb and forearm pulse wave velocities ranged from 2.9 to 5.9% at rest and during recovery, and were respectively 2.9% and 8.3% during exercise. However, coefficient of variation for brachial pulse wave velocity was 7.7 and 10.3% at rest, 15.7% during exercise, and 5.8% during recovery. During exercise, pulse wave velocity measurements were satisfying, but indirect assessment of brachial artery pulse wave velocity showed poor reproducibility. Thus, upper limb and forearm pulse wave velocities may be used during exercise to assess the effect of training or drugs on arterial wall mechanical properties.

Adult↗
PubMed2005

Chronic hypoxia exposure depresses aortic endothelium-dependent vasorelaxation in both sedentary and trained rats: involvement of L-arginine.

This study was designed to test the hypothesis that the previously demonstrated training-induced improvement of the endothelium vasodilator function would be blunted under conditions of chronic hypoxia exposure as a result of deleterious effects of hypoxia per se on the nitric oxide pathway. Sea-level-native rats were randomly assigned to N (living in normoxia), NT (living and training 5 days/wk for 5 wk in normoxia), CH (living in hypoxia, 2,800 m), and CHT (living and training 5 days/wk for 5 wk in hypoxia, 2,800 m) groups. Concentration-response curves to acetylcholine (ACh; 10(-9) to 10(-4) M) with or without L-arginine (10(-3) to 10(-5) M) and/or nitro-L-arginine methyl ester (10(-5) M) were assessed on aortic isolated rings. The main finding was that chronic hypoxia severely depressed maximal ACh-responses of aortic rings in both sedentary and trained groups. However, chronic hypoxia did not interfere with training-induced increases in maximal ACh responses, considering that maximal ACh vasorelaxation was improved in CHT rats to the same extent as in NT rats when both groups were directly compared with their sedentary counterparts. It should be pointed out that the vasodilator response to ACh was restored in CH and CHT rats to the level obtained in N and NT rats, respectively, by an in vitro L-arginine addition. A hypoxia-induced decrease in L-arginine bioavailability resulting from acclimatization at altitude may be involved in this limitation of the NO pathway in CH and CHT rats. These results are of importance for aerobic performance as the specific vascular adaptations to training at altitude could contribute to limit peripheral vasodilatation and subsequently blood flow during exercise.

Adaptation, Physiological↗
PubMed2005

A numerical assessment of wall shear stress changes after endovascular stenting.

This theoretical/numerical study aims at assessing the haemodynamic changes induced by endovascular stenting. By using the classical one-dimensional linear pressure waves theory in elastic vessels, we first show that the modulus of the reflection coefficient induced by an endovascular prosthesis is most likely small since it is proportional to the stent-to-wavelength ratio. As a direct consequence, the wall motion of the elastic (stented) artery can be prescribed a priori and the coupled fluid-structure problem does not have to be solved for assessing the haemodynamic changes due to stenting. Several 2D axisymetric calculations are performed to solve the unsteady incompressible Navier-Stokes equations on moving meshes for different types of (stented) arteries. The numerical results suggest that endovascular stenting increases the systo-diastolic variations of the wall shear stress (by 35% at the middle of the stent, by almost 50% in the proximal transition region). Additional calculations show that over-dilated stents produce less haemodynamic perturbations. Indeed, the increase of the amplitude of the wall shear stress variations over the cardiac cycle is only 10% when the stent radius is equal to the radius of the elastic artery at systole (instead of being equal to the mean artery radius).

Elasticity↗
PubMed2005

[Spontaneous thrombosis of lesion-free carotid arteries: a retrospective analysis of eight patients].

Strokes are rarely secondary to spontaneous carotid artery thrombosis. The objectives of this retrospective analysis were to define characteristic features and the clinical course. The study population included eight patients (6 females/2 males) seen at six university neurological centers. Age of onset was 46.5 years (range 38-52). Half of the patients had no vascular risk factor. Symptoms were TIA (n=1), strokes (n=7). Echotomography revealed intraluminal thrombus, with occlusion in 2 cases. Thrombi were found in common carotid artery (n=3), carotid bifurcation (n=2) and internal carotid artery (n=3). The thrombus was mobile in 4 cases. Seven patients were treated by anticoagulation therapy, one by surgery because of recurrent TIA. Further echotomographic exams revealed total resolution (3 cases) or decrease of the thrombus (3 cases). Occlusion was definitive in one patient. A cause was identified in six patients: acute leukemia (n=1), thrombocytopenic purpura (n=1), iron deficiency anemia (n=4).

Adult↗
PubMed2005

Factor V Leiden and prothrombin G20210A polymorphisms as risk factors for miscarriage during a first intended pregnancy: the matched case-control 'NOHA first' study.

Factor V Leiden (FVL) and prothrombin G20210A (FIIG20210A) mutations are associated with a higher risk of miscarriage: we sought to understand whether this association differs by clinical time of unexplained miscarriage, and by ethnic origin, among women with no previous thrombotic episode, during the first intended pregnancy. We performed a case-control study nested in a cohort of 32 683 women. We analyzed 3496 pairs of women matched for classical confounding factors. The FVL and FIIG20210A mutations were associated with an increased risk of miscarriage in Caucasian women [odds ratio (OR) 3.19, 95% confidence interval (CI) 2.37-4.30, P < 0.001 and OR 2.36, 95% CI, 1.72-3.24, P < 0.001, respectively]. Among non-Caucasian women, the mutations were rare and the associations with risk of miscarriage less clear. FVL and FIIG20210A mutations were independent risk factors for miscarriages only for women with related clinical signs occurring from the 10th week of gestation on (OR 3.46, 95% CI 2.53-4.72, P < 0.001 and OR 2.60, 95% CI 1.86-3.64, P < 0.001, respectively). These results indicate that FVL and FIIG20210A mutations are associated with a significant risk of spontaneous abortion which clinical signs occur from the 10th week on of the first intended pregnancy.

Abortion, Spontaneous↗
PubMed2004

Cardiac remodeling and functional adaptations consecutive to altitude training in rats: implications for sea level aerobic performance.

This study questioned the effect of living and training at moderate altitude on cardiac morphological and functional adaptations and tested the incidences of potential specific adaptations compared with aerobic sea level training on maximal left ventricular performance. Sea level-native rats were randomly assigned to N (living in normoxia), NT (living and training 5 days/wk for 5 wk in normoxia), CH (living in hypoxia, 2,800 m), and CHT (living and training 5 days/wk for 5 wk in hypoxia, 2,800 m) groups. Cardiac adaptations were evaluated throughout the study period by Doppler echocardiography. Maximal stroke volume (LV(SVmax)) was measured during volume overloading before and after the study period. Finally, at the end of the study period, passive pressure-volume relationships on isolated heart and cardiac weighing were obtained. Altitude training resulted in a specific left ventricular (LV) remodeling compared with NT, characterized by an increase in wall thicknesses without any alteration in internal dimensions. These morphological adaptations associated with hypoxia-induced alterations in pulmonary outflow and preload conditions led to a decrease in LV filling and subsequently no improvement in LV performance during resting physiological conditions in CHT compared with NT. Such a lack of improvement was confirmed during volume overloading that simulated maximal effort (LV(SVmax) pretest: NT = 0.58 +/- 0.05, CHT = 0.57 +/- 0.08 ml; posttest: NT = 0.72 +/- 0.06, CHT = 0.58 +/- 0.07 ml; NT vs. CHT in posttest session, P < 0.05). Maximal aerobic velocities increased to the same extent in NT and CHT rats despite marked polycythemia in the latter. The lack of LV(SVmax) improvement resulting from altitude training-induced cardiac morphological and functional adaptations could be responsible for this phenomenon.

Adaptation, Physiological↗
PubMed2004

Three-dimensional computer-assisted reconstruction of ductal plate in the rat embryo (Carnegie stages 19-23).

In bile duct morphogenesis it has been established that the extrahepatic bile ducts in human originate from hepatic diverticulum while intrahepatic bile ducts arise from the ductal plate (DP), a network of primitive biliary epithelium that develops in the periportal connective tissue. The aim of this work was to reconstruct in rat embryos, stages 19-23, the three-dimensional (3D) distribution of the DP by means of a computer-assisted method. Six specimens, stages 19-23, fixed, dehydrated and paraffin-embedded, were submitted to serial histological sections and stained by hematoxylin-eosin and Heidenhain techniques. The images were directly digitalized with a CCD camera. The serial views were aligned anatomically by software and the data were analyzed following segmentation and thresholding. At stage 19, the DP was not yet organized. The periportal mesoderm (M) was gaining ground with some cords of cubic cells evoking primitive ductal cells. At stage 20, a row of ductal cubic cells went around the transverse portal sinus at the junction between M and liver cells. At stage 21, the DP developed at the periphery of periportal connective tissue and appeared in direct continuity with the hepatic duct (HDu). Four evaginations emerged from the DP and were growing up in the hepatic parenchyma. At stage 23, the DP appeared as a large network in continuity with the HDu located at the periphery of periportal M and presenting several evaginations radiating in the liver parenchyma. This work in the rat embryo permits the clear visualization of the development of the junctional zone in the hepatic hilum. Three phenomena are observed: (1) proximal left and right hepatic ducts and their segmental branches are derived from DP and not from the HDu; (2) the extrahepatic biliary system is in contact with the developing hilar ducts; (3) ductal maturation begins at the hilum and proceeds centrifugally. These observations are of great relevance in explaining pathological changes appearing at the hepatic hilum of neonates: hepatic polycystic disease, intrahepatic bile duct agenesis or atresia, and cyst of the extrahepatic bile duct.

Animals↗
PubMed2004

[Frequency of thrombosis in hemodialysis arteriovenous fistulas. Contribution of 2 surveillance methods: Doppler and dilution ultrasound techniques].

A correct access flow is one of the most important factors for dialysis efficiency. Clinical examination does not allow the detection of flow decrease. We conducted a prospective study comparing the dilution ultrasound system (Transonic) to duplex Doppler sonography (GE logiq 700 expert series) in two phases: Comparison of the access flow values obtained with both devices and discussion of their discrepancies. Scheduled survey of vascular access, analysis of its results regarding the rate of fistula thrombosis, then definition and achievement of a strategy of early preventive surgery. After two years, flow data were similar with both systems, provided that Transonic values were corrected by a constant coefficient. The use of both techniques during the scheduled survey of fistulas resulted in a 43% decrease of the rate of acute thrombosis (p < 0.05).

Adult↗
PubMed2003

Impairment of endothelial function in patients with spontaneous cervical artery dissection: evidence for a general arterial wall disease.

BACKGROUND AND PURPOSE: Cervical artery dissection (CAD) accounts for 10-20% of ischemic strokes in young adults. Although trauma and preexisting disorders of the arterial wall are the main predisposing factors, most CADs are considered 'spontaneous'. We hypothesized that CAD could originate in systemic vascular disease bound to the intima-media interface without clinical signs. If this hypothesis is true, endothelium-dependent vasodilation would be impaired in response to a physiological stimulus such as an increase in blood flow. METHODS: Flow-mediated arterial dilation was studied in 65 consecutive patients with spontaneous CAD: 26 with carotid artery dissection (ICAD), and 39 with vertebral artery dissection (VAD). CAD patients with vascular risk factors, trivial or obvious cervical trauma, or connective tissue disease were excluded. Twenty-three patients with ischemic stroke of unknown cause were included as controls. Using high-resolution ultrasonography, brachial artery diameter was measured at rest, during post-ischemic hyperemia (flow-mediated endothelium-dependent dilation), and after sublingual glyceryl trinitrate spray (endothelium-independent dilation). RESULTS: The mean +/- SD values of the flow-mediated vasodilation index were 5.7 +/- 6.2% in ICAD, 5.0 +/- 9.3% in VAD and 13.2 +/- 6.5% in controls (p < 0.0005), without any difference between ICAD and VAD. Endothelium-independent dilation mean values were 21.5 +/- 9.5% in ICAD, 25.1 +/- 12.5% in VAD, and 20.8 +/- 8.4% in controls, without a significant difference between groups (p = 0.49). CONCLUSIONS: These results give evidence of impaired endothelium-dependent vasodilation in CAD patients that is not the result of stroke, and suggest that an underlying abnormality of the arterial wall layers may predispose to CAD.

Adult↗
PubMed2003

Evaluation of cardiac troponin I and T levels as markers of myocardial damage in doxorubicin-induced cardiomyopathy rats, and their relationship with echocardiographic and histological findings.

BACKGROUND: Cardiac troponins I (cTnI) and T (cTnT) have been shown to be highly sensitive and specific markers of myocardial cell injury. We investigated the diagnostic value of cTnI and cTnT for the diagnosis of myocardial damage in a rat model of doxorubicin (DOX)-induced cardiomyopathy, and we examined the relationship between serial cTnI and cTnT with the development of cardiac disorders monitored by echocardiography and histological examinations in this model. METHODS: Thirty-five Wistar rats were given 1.5 mg/kg DOX, i.v., weekly for up to 8 weeks for a total cumulative dose of 12 mg/kg BW. Ten rats received saline as a control group. cTnI was measured with Access(R) (ng/ml) and a research immunoassay (pg/ml), and compared with cTnT, CK-MB mass and CK. By using transthoracic echocardiography, anterior and posterior wall thickness, LV diameters and LV fractional shortening (FS) were measured in all rats before DOX or saline, and at weeks 6 and 9 after treatment in all surviving rats. Histology was performed in DOX-rats at 6 and 9 weeks after the last DOX dose and in all controls. RESULTS: Eighteen of the DOX rats died prematurely of general toxicity during the 9-week period. End-diastolic (ED) and end-systolic (ES) LV diameters/BW significantly increased, whereas LV FS was decreased after 9 weeks in the DOX group (p<0.001). These parameters remained unchanged in controls. Histological evaluation of hearts from all rats given DOX revealed significant slight degrees of perivascular and interstitial fibrosis. In 7 of the 18 rats, degeneration and myocyte vacuolisation were found. Only five of the controls exhibited evidence of very slight perivascular fibrosis. A significant rise in cTnT was found in DOX rats after cumulative doses of 7.5 and 12 mg/kg in comparison with baseline (p<0.05). cTnT found in rats after 12 mg/kg were significantly greater than that found after 7.5 mg/kg DOX. Maximal cTnI (pg/ml) and cTnT levels were significantly increased in DOX rats compared with controls (p=0.006, 0.007). cTnI (ng/ml), CK-MB mass and CK remained unchanged in DOX rats compared with controls. All markers remained stable in controls. Analysis of data revealed a significant correlation between maximal cTnT and ED and ES LV diameters/BW (r=0.81 and 0.65; p<0.0001). A significant relationship was observed between maximal cTnT and the extent of myocardial morphological changes, and between LV diameters/BW and histological findings. CONCLUSIONS: Among markers of ischemic injury after DOX in rats, cTnT showed the greatest ability to detect myocardial damage assessed by echocardiographic detection and histological changes. Although there was a discrepancy between the amount of cTnI and cTnT after DOX, probably due to heterogeneity in cross-reactivities of mAbs to various cTnI and cTnT forms, it is likely that cTnT in rats after DOX indicates cell damage determined by the magnitude of injury induced and that cTnT should be a useful marker for the prediction of experimentally induced cardiotoxicity and possibly for cardioprotective experiments.

Blotting, Western↗
PubMed2003

Thrombophilic families with inheritably associated high levels of coagulation factors VIII, IX and XI.

We describe six families in which associated high levels of coagulation factors (F) XI, FIX and FVIII (each with a plasma concentration higher than the 95th percentile found in a control group of 500 asymptomatic individuals: respectively, 135, 145 and 155 IU dL-1) were inherited as a dominant autosomic genetic traits. In these six families, this syndrome is associated with venous thromboembolic events (Odds ratio 41 [4.9-353], P = 0.0006). It seems to predispose to idiopathic events and, as age increases, is often associated with recurrence. First thrombotic episodes occur in young patients (50% of the carriers are symptomatic at the age of 32 years) and in women, can be unmasked by hormonal treatments, mainly oral contraceptives. The association of high levels of coagulation FXI, FIX and FVIII is thus a new rare high-risk inherited thrombophilia syndrome.

Adolescent↗
PubMed2001

Tissue factor coagulation pathway and blood cells activation state in renal insufficiency.

INTRODUCTION: Atherosclerotic cardiovascular disease is the leading cause of the increased morbidity and mortality observed in uremic patients. Thrombosis is an important contributor to the evolution of atherosclerotic lesions. The physiologically-relevant blood clotting depends on binding of activated factor VII (FVIIa) to exposed tissue factor (TF) on activated/damaged cells. MATERIALS AND METHODS: A cross-sectional study was performed on three age- and sex-matched groups of individuals: one group of 50 patients on maintenance hemodialysis (D group), one of 50 patients with a non-dialysed renal insufficiency (ND group) and one of 50 healthy controls (HC group). We studied basal plasma concentrations of FVIIa, factor VII-related antigen (FVIIAg), soluble TF, tissue factor pathway inhibitor (TFPI), TF-dependent circulating monocytes procoagulant activity (TF-dMPA), tissue factor-dependent plasma reactivity to activated protein C (TF-aPC), D-dimers (D-Di), and circulating markers of cellular activation/injury: soluble thrombomodulin (sTM), circulating microparticles (microP), soluble leukocyte, endothelial and platelet selectins (sL-selectin, sE-selectin, sP-selectin), soluble intercellular adhesion molecule 1 and vascular cell adhesion molecule 1 (sICAM-1 and sVCAM-1). Their variations induced, in hemodialysis patients, by a dialysis run were thereafter studied RESULTS: Values of FVIIa, FVIIa/FVIIAg ratio, sTF, TFPI, TF-dMPA, D-Di, sTM, microP, sL, sE and sP selectins, sICAM-1 and sVCAM-1 increased all along the hierarchy HC group/ND group/D group. Microparticles were mainly of platelet origin, to a lesser extent of monocyte origin. Dialysis induced an increase of FVIIa, sTF, TF-dMPA and circulating markers of cellular activation/injury. Strong correlations were observed between FVIIa/FVIIAg ratio and serum creatinine levels, sTF, TF-dMPA, sTM, sE-selectin, sVCAM-1. The TF-aPC was impaired in the ND and the D group, and the lower values were, in the D group, associated with antecedents of vascular access thrombosis. CONCLUSION: Renal insufficiency is associated to an activation of the tissue factor coagulation pathway, to a platelet, monocyte and endothelial activation/injury and to a deficient tissue-factor induced response to activated protein C which culminate in end-stage disease and are increased by hemodialysis runs. This contributes to linked coagulation and cellular conditions for an enhanced atherosclerosis progression. Due to the TF pathway activation, the therapeutic use of recombinant TFPI should be evaluated.

Activated Protein C Resistance↗
PubMed2001

Diaphragm movement before and after cholecystectomy: a sonographic study.

UNLABELLED: Respiratory disorders after abdominal surgery are commonly explained by changes in diaphragmatic movement that are difficult to demonstrate and quantify. Our aim was thus to quantify these changes using a noninvasive method. We used M-mode sonography for the prospective study to measure diaphragmatic amplitude in 14 patients before and after cholecystectomy. During quiet breathing, the diaphragm inspiratory amplitude (DIA) was significantly decreased after surgery from 1.4 +/- 0.2 cm to 1 +/- 0.1 cm and from 1.6 +/- 0.3 cm to 1.2 +/- 0.3 cm in the Laparoscopic and Open Cholecystectomy groups, respectively. The total time cycle of diaphragmatic motion decreased significantly in the two groups. The DIA also decreased significantly during deep breathing after cholecystectomy from 6.0 +/- 0.8 cm to 3.0 +/- 1.8 cm and from 6.1 +/- 1.3 cm to 3.1 +/- 1.6 cm in the Laparoscopic and Open Cholecystectomy groups, respectively. The six patients who underwent spirometric examination showed, during quiet breathing, a significant decrease in DIA without change in tidal volume, i.e., 0.51 +/- 0.08 L to 0.45 +/- 0.08 L. We found a significant decrease in DIA after cholecystectomy and a significant interindividual correlation between DIA during deep inspiration and inspiratory capacity. Using M-mode sonography techniques, we were able to demonstrate changes in diaphragmatic mobility after laparoscopic or open cholecystectomy. IMPLICATIONS: Cholecystectomy at times results in impaired respiratory and diaphragmatic functions. The techniques currently used to study these repercussions are both laborious and invasive. Our sonographic technique is completely noninvasive and can be used to study diaphragm morphology and movement in real time.

Adult↗
PubMed2001

Changes in wall mechanics after endovascular stenting in the rabbit aorta: comparison of three stent designs.

OBJECTIVE: The aim of this study was to evaluate changes in the wall mechanics of small-diameter arteries after endovascular placement of three different stents. SUBJECTS AND METHODS: Five self-expandable stents (Wallstent), five balloon-expandable noncovered Palmaz stents, and three balloon-expandable covered stents (Jostent) were placed in the infrarenal aorta of 13 New Zealand white rabbits. Systolic blood pressure changes, blood-flow velocity, systolic diameter, and diameter changes were measured and used to calculate the diameter compliance, the distensibility coefficient, and the pulsatility index. RESULTS: Compliance (10(-3) mm kPa(-1)) was 75.3 +/- 20.1 before stenting and reached 94.7 +/- 42.2 upstream, 38.8 +/- 14.2 at the stent level (p < 0.05), and 70.8 +/- 23.2 downstream from the stent. Distensibility (10(-3) kPa(-1)) was 24.3 +/- 6.3 before stenting and reached 27.8 +/- 10.3 upstream, 10.5 +/- 4.4 at the stent level (p < 0.001), and 21.9 +/- 8.6 downstream from the stent. Compliance and distensibility were significantly lower at the stent level than upstream and downstream (p < 0.05). Aortic diameter increased significantly at the stent level from 3.11 +/- 0.40 mm before to 3.76 +/- 0.42 mm after stenting. No significant difference was found among the three stent designs for all the studied data. CONCLUSION: Regardless of the three tested stent designs, endovascular stenting produces a significant decrease in arterial wall compliance of the rabbit aorta.

Animals↗