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Biomedical subjects

P Escourrou

Publications and source records attributed to P Escourrou.

At least 19 recordsLinked to original sources
PubMed2006

Outcome of acetylcholinesterase deficiency for neuromuscular functioning.

Acetylcholinesterase (AChE) plays an essential role in neuromuscular transmission, therefore it is surprising that AChE knockout (KO) mice could live to the adulthood. Neuromuscular functioning in KO and normal (wild type, WT) mice were studied, at different age (1.5-, 4- and 9-month-old). Hindlimb muscle force productions in response to nerve or muscle electric stimulation were recorded in situ and in vitro. Our results show that contrary to WT mice, 1.5-, 4- and 9-month-old KO mice exhibited a decreased in tetanic force during short periods (500 ms) of repetitive nerve stimulations (tetanic fade). Nevertheless submaximal muscle forces in response to single or repetitive nerve stimulation were increased (potentiation) in 1.5-, 4- and 9-month-old KO mice as compared to WT mice (p<0.05). Tetanic fade and potentiation were absent when muscles were directly stimulated, indicating neuromuscular transmission alterations in KO mice. Contrary to younger mice, muscle weight and maximal tetanic force in response to repetitive nerve stimulation were not reduced in 4- and 9-month-old KO mice as compared to WT mice (p>0.05). In conclusion AChE deficit leads to marked neuromuscular alterations in hind limb muscle functioning and a prominent symptom is the lack of resistance to fatigue.

Acetylcholine↗
PubMed2005

Compliance with and effectiveness of adaptive servoventilation versus continuous positive airway pressure in the treatment of Cheyne-Stokes respiration in heart failure over a six month period.

OBJECTIVE: To compare compliance with and effectiveness of adaptive servoventilation (ASV) versus continuous positive airway pressure (CPAP) in patients with the central sleep apnoea syndrome (CSA) with Cheyne-Stokes respiration (CSR) and with congestive heart failure in terms of the apnoea-hypopnoea index (AHI), quality of life, and left ventricular ejection fraction (LVEF) over six months. METHODS: 25 patients (age 28-80 years, New York Heart Association (NYHA) class II-IV) with stable congestive heart failure and CSA-CSR were randomly assigned to either CPAP or ASV. At inclusion, both groups were comparable for NYHA class, LVEF, medical treatment, body mass index, and CSA-CSR. RESULTS: Both ASV and CPAP decreased the AHI but, noticeably, only ASV completely corrected CSA-CSR, with AHI below 10/h. At three months, compliance was comparable between ASV and CPAP; however, at six months compliance with CPAP was significantly less than with ASV. At six months, the improvement in quality of life was higher with ASV and only ASV induced a significant increase in LVEF. CONCLUSION: These results suggest that patients with CSA-CSR may receive greater benefit from treatment with ASV than with CPAP.

Adult↗
PubMed2004

Increased ventilation and CO2 chemosensitivity in acetylcholinesterase knockout mice.

To investigate the effects of a permanent excess of acetylcholine (AChE) on respiration, breathing and chemosensitivity were analyzed from birth to adulthood in mice lacking the AChE gene (AChE-/-), in heterozygotes, and in control wild-type (AChE+/+) littermates. Breathing at rest and ventilatory responses to brief exposures to hypoxia (10% O2) and hypercapnia (3-5% CO2) were measured by whole-body plethysmography. At rest AChE-/- mice show larger tidal volumes (VT, + 96% in adults), overall ventilation (VE, + 70%), and mean inspiratory flow (+270%) than wild-type mice, with no change in breathing frequency (fR). AChE-/- mice have a slightly blunted response to hypoxia, but increased VE and fR responses to hypercapnia. Heterozygous animals present no consistent alterations of breathing at rest and chemosensitivity is normal. Adult AChE-/- mice have an increased VE/VO2 and a marginally higher normalized VO2. The results suggest that the hyperventilation and altered chemosensitivity in AChE-/- mice largely reflect alterations of central respiratory control.

Acetylcholinesterase↗
PubMed2004

Bench testing of auto-adjusting positive airway pressure devices.

Continuous positive airway pressure devices are routinely used to treat sleep breathing disorders. Automated devices that adjust the therapeutic pressure have recently been proposed. The utility of such devices is still controversial, as rigorous clinical comparisons are difficult to perform as a result of patient and device differences. The current authors studied automated devices in a respiratory model that was able to mimic upper airway mechanics and to interact with pressure adjustment in a closed loop. Five auto-adjusted devices were submitted to this model, in order to determine their ability to detect respiratory events and adjust pressure accordingly. All apnoeas were suppressed, whilst the reaction to repetitive hypopnoeas was dependent on the airflow shape. In some devices, repetitive hypopnoeas were changed to flow limitation. Artificial snoring caused a pressure increase in four devices, and constant mask leak was not systematically compensated. Only one device did not raise pressure in response to central apnoeas with opened upper airways. These findings show that, in some devices, event classification failed and normal airflow was not fully restored, resulting in elevated residual event indices. In conclusion, this model is useful in order to reproducibly compare diagnostic and therapeutic capacities of commercial devices as a first step, before costly clinical studies.

Continuous Positive Airway Pressure↗
PubMed2003

[Nasal obstruction and compliance to nasal positive airway pressure].

UNLABELLED: Obstructive sleep apnea syndrome is a very common disease. Nasal continuous positive airway pressure is a useful and efficient treatment but compliance depends on several factors including the degree of nasal obstruction. OBJECTIVES: The aim of this study was to evaluate the effects of surgical correction of nasal obstruction on compliance to nasal continuous positive airway pressure in obstructive sleep apnea syndrome. MATERIAL AND METHODS: This retrospective study (from March 1998 to March 2000) included ten patients suffering from a severe obstructive sleep apnea syndrome (apnea-hypopnea index greater than 30 per hour) treated by nasal continuous positive airway pressure for at least three months and presenting an anatomic nasal obstruction limiting the use of nasal continuous positive airway pressure. Surgical procedures included one septoplasty, two inferior turbinectomies and seven septoplasties with turbinectomies. RESULTS: The post-operative polysomnography showed that surgical correction of nasal obstruction had no effect on obstructive sleep apnea syndrome severity (no significative change of apnea hypopnea index after surgery) but allowed the use of lower nasal continuous positive airway pressure levels (7.1 mmHg after surgery versus 10 mmHg before) and improved compliance to treatment (six compliant patients after surgery versus no compliant patient before). These results were compared with those published in the literature. CONCLUSION: An examination of the nose has to be performed before initiating nasal continuous positive airway pressure. If nasal continuous positive airway pressure cannot be tolerated because of nasal obstruction, surgery is required to improve compliance and tolerance to treatment.

Humans↗
PubMed2002

Autonomic control of the cardiovascular system during sleep in normal subjects.

The autonomic control of heart rate and blood pressure during sleep is controversial: although it has been reported that vagal activity is more often lower in rapid eye movement sleep (REM) than in other stages of sleep (non-REM, NREM), the opposite has also been described. Initially, it was reported that baroreflex sensitivity (BRS) increases during sleep (REM and NREM), but in later studies, this was only partially confirmed. We therefore studied autonomic control of the cardiovascular (CV) system during sleep in 12 normal adults. The spectral components of the heart rate R-R interval, blood pressure (BP), and BRS were computed at low (LF) and actual breathing frequency (high frequency, HF). Analysis of sleep stage and a cycle-by-cycle stage II analysis were performed. CV variability is affected largely by sleep-stage and sleep-cycle organisation: NREM and the last cycle exhibit the greatest vagal activity and the lowest sympathetic activity. BRS estimation for both the LF and HF bands confirmed previous results obtained by pharmacological and spontaneous slope methods: BRS is greater during sleep than during nocturnal wake periods, and further increased in REM. BRS is frequency dependent: in NREM, the higher value of HF BRS compared to LF BRS favours the HF control of BP variability, whereas higher BRS HF and LF components contribute to the strongest control in REM. BRS variability exhibits no significant pattern during the night. Our results suggest that both sleep-cycle organisation and BRS estimation in the LF and HF bands should be considered in sleep studies of autonomic CV control.

Adult↗
PubMed2002

[Heart failure and respiratory sleep disorders].

Chronic cardiac failure is often associated with sleep respiratory disorders. These abnormalities are often unrecognised and represent a marker of the severity of cardiac failure and carry a poor prognosis. The mechanism of apnoea is either central, resulting in periodic nocturnal Cheyne-Stokes respiration, or peripheral by obstruction of the upper respiratory tract. Both mechanisms may be observed in the same patient. Oxygen desaturation, fragmentation of sleep and inspiratory depression lead to sympathetic activation and an increase in let ventricular afterload which can aggravate the cardiac failure. Treatment by continuous positive pressure with a nasal mask can help some patients. It is therefore important to diagnoses these nocturnal disorders using simplified polysomnographic recordings.

Cheyne-Stokes Respiration↗
PubMed2001

Hypoxia-hypotension decreases pressor responsiveness to exogenous catecholamines after severe traumatic brain injury in rats.

OBJECTIVE: To quantify the phenylephrine pressor responsiveness after severe brain injury combined with hypoxia-hypotension, and to study the respective roles of brain injury and hypoxia-hypotension in the observed alteration. DESIGN: Randomized study. SETTING: Accredited animal laboratory. SUBJECTS: Adult Sprague Dawley rats. INTERVENTIONS: Anesthetized animals were assigned to control, brain injury, hypoxia-hypotension, and brain injury combined with hypoxia-hypotension groups. Brain injury was induced with an impact-acceleration device. During the 15-min hypoxia-hypotension, arterial oxygen pressure was decreased to 40 torr (5.3 kPa) and mean arterial pressure to 30 mm Hg. Thirty-six of the 53 included rats were alive at the end of hypoxia-hypotension (nine animals per group). In an additional group (Hypo, n = 8), mean arterial pressure was lowered to the level observed in brain injury combined with hypoxia-hypotension with pentobarbital infusion. Sixty minutes after injuries (T60), animals received 0.1, 1, and 10 microg/kg phenylephrine in a random order. Pressor responsiveness to phenylephrine was defined as maximal postinjection minus preinjection mean arterial pressure. MEASUREMENTS AND MAIN RESULTS: During hypoxia-hypotension, mortality was higher and residual restored blood volume was lower (p <.01) in the animals with brain injury and hypoxia-hypotension compared with hypoxia-hypotension alone. At T60, mean arterial pressure (mm Hg) was lower (p <.01) in the brain injury group (83 +/- 22) compared with controls (110 +/- 10) and in brain injury combined with hypoxia-hypotension (76 +/- 18) compared with controls and hypoxia-hypotension (107 +/- 14). Pressor responsiveness (mm Hg) to 1 and 10 microg/kg phenylephrine was less (p <.05) in brain injury combined with hypoxia-hypotension (15 +/- 6 and 44 +/- 8) and hypoxia-hypotension (15 +/- 3 and 44 +/- 8) compared with controls (26 +/- 2 and 57 +/- 11). No significant difference was observed for phenylephrine pressor responsiveness between controls and the Hypo group (25 +/- 5 and 66 +/- 7). CONCLUSIONS: Combination of brain injury and hypoxia-hypotension induces a severe hemodynamic alteration associated with a decreased pressor responsiveness to phenylephrine. Transient hypoxia-hypotension is responsible for the depressed alpha-1 adrenergic reactivity.

Adrenergic alpha-Agonists↗
PubMed2001

[Obstructive sleep apnea syndrome and heart failure].

Heart failure has an increasing prevalence in middle age adults. The prognosis is very poor even with improved medical therapy and heart transplants. The outcome is related to the neurohumoral disease resulting from heart failure which leads to sympathetic activation that in turns worsens the prognosis. About half of the patients have sleep breathing disorders with variable proportions of central and obstructive apneas. Obstructive apneas are acutely deleterious to ventricular function. On the long run, they may be responsible for a worsening of the disease due to the permanent sympathetic activation seen in obstructive sleep apnea. It is therefore important to detect sleep apnea in patients and to apply a treatment. The best therapeutic procedure in obstructive events appears to be CPAP, provided hemodynamic status is closely monitored.

Aged↗
PubMed2000

Muscarinic and PACAP receptor interactions at pontine level in the rat: significance for REM sleep regulation.

Cholinergic and PACAPergic systems within the oral pontine reticular nucleus (PnO) play a critical role in REM sleep generation in rats. In this present work, we have investigated whether REM sleep enhancement induced by carbachol (a cholinergic agonist) or PACAP, depends on an interaction between muscarinic and PACAP receptors. This hypothesis was tested by recording sleep-wake cycles in freely moving rats injected into the PnO with PACAP in combination with the muscarinic receptor antagonist atropine, or with carbachol in combination with the PACAP receptor antagonist PACAP6-27. When administered alone, PACAP (3 pmol) or carbachol (110 pmol) induced an enhancement of REM sleep during 8 h (+61%, n = 8; +70%, n = 5), which was totally prevented by infusion of atropine (290 pmol) for PACAP, or of PACAP6-27 (3 pmol) for carbachol. Quantitative autoradiographic studies indicated that (i) PACAP (10-9-10-7 M) induced in the PnO an increase (+35%) of the specific binding of the muscarinic antagonist [3H]quinuclidinyl benzylate, which could be completely prevented by PACAP6-27 (IC50 = 8 x 10-8 M) and (ii) both carbachol and PACAP enhanced [35S]GTP-gamma-S binding in a concentration-dependent manner in the PnO. The maximal increase due to carbachol was significantly higher in the presence (+126%) than in the absence (+102%) of PACAP (0.1 microM). These data showed that interactions between muscarinic and PACAP receptors do exist within the PnO and play a role in the local mechanisms of REM sleep control in the rat.

Animals↗
PubMed2000

[Heart failure and sleep respiratory disorders. Prevalence, physiopathology and treatment].

Cheyne-Stokes respiration occurs during sleep in 40-45% of patients with NYHA class III and IV heart failure. Such patients experience repeated episodes of progressively diminishing ventilation associated with desaturation followed by periods of increasing-amplitude ventilation. The mechanism appears to be related to hyperventilation leading to hypocapnia which occurs near a critical threshold of apnea during sleep stages I and stage II and interrupts central ventilatory control. The total duration of the periodic respiration cycle would depend on the increased circulation time subsequent to lowered cardiac output. Brief periods of waking provoked by Cheyne-Stokes respiration, accentuating sympathetic nervous system activity, are an unfavorable prognostic factor in heart failure. Activation of the sympathetic system may be corrected by CPAP although the long-term effect on heart failure remains controversial. Other treatments, such as oxygen therapy or theophylline, combined with optimized treatment of heart failure, have been proposed.

Cardiac Output↗
PubMed2000

[Short term evaluation of a new treatment method for primary snoring: radiofrequency energy].

The usual treatments for primary snoring are uvulopalatopharyngoplasty (UPPPP) and laser assisted uvulopalatoplasty, their morbidity is known, particularly considerable postoperative pain. We have performed a prospective study on a population of 23 patients with primary snoring (respiratory disturbance index =6 +/- 1) to 1) evaluates by means of questionnaires the short term (2 month) efficacy of the application of radiofrequency energy at the level of the soft palate, and 2) assess the morbidity associated with this treatment in this population. In the group of patients receiving treatment at three sites in a maximum of three sessions, the short term satisfaction rate was 75 %. The postoperative pain was of minor importance and the use of major analgesics was necessary in 2 cases only. We conclude that this treatment with radiofrequency energy seems to be an effective treatment for primary snoring at short term. The morbidity, specially the pain seems to be distinctly inferior compared to UPPP or laser treatment. Further prospective studies on a larger number of patients and with a longer follow-up are absolutely necessary to confirm these results.

Catheter Ablation↗
PubMed2000

The sleep data transfer between remote and central sites.

Sleep laboratory have long waiting lists due to the high prevalence of sleep disorders and the low availability of centers. One possibility for improving patient care is an ambulatory recording at home or in a distributed center. Then the data recorded must be transferred for analysis in the specialized center. Similarly, an application is needed for the transfer of raw data when the recordings are made by a health care provider sending sleep technologists to set-up the equipment in the patient's home. It is ethically preferable that the analysis be made by a physician from an independent organization from the provider to avoid any conflict of commercial interest with the provider whose main purpose is delivering therapeutic equipment (CPAP, oxygen...). The objectives were to set-up and test the transfer of sleep data files by ISDN lines between a health care provider and an expert sleep center. The application had to take into account a wide geographical dispersion of patients, general practitioners and medical experts. For that reason, it was decided to use existing Internet Web technology to facilitate portability and interoperability, reduce design time and costs and speed up deployment. The healthcare provider is the collecting site of ambulatory sleep recordings performed at the patient's home by the sleep technician of the provider. The raw data are sent to the sleep center for expert analysis. The methods used were: a PC set-up with a Gazel pro 2B PCI board, a commercially available file transfer software (DT Winstutel from ORSENNA) and an ISDN connection at 128 Kbps. The transfer security needs a set-up to maintain the confidentiality of the personal data transmitted: this is ensured through an identification sequence with several encrypted passwords. The duration of the transfer between Paris and Clamart has been tested for a 44 Moctets file: it took 66 min instead of a theoretical duration of 50 min. This difference was explained by a slower transfer rate (93 Kbps) instead of 128 Kbps. The cost of the transfer has been estimated at 5.4 Euro. This cost can be reduced by subscribing higher transfer tariffs. It amounts to 4.5% of the total cost of the ambulatory procedure at a value of 0.12 Euro per Moctet.

Computer Security↗
PubMed2000

Needs and costs of sleep monitoring.

Sleep disorders have a high prevalence in the general population: insomnia (10-20% of adults), sleep apnoea syndromes (4-6%). They are responsible for high costs of investigations and treatment modalities. The investigations are usually done in sleep laboratories at the expense of cost in personnel and long waiting lists. Remote monitoring could be an alternative to sleep laboratory studies. The first aim was to determine the need for sleep remote recording in sleep medicine in Europe, to improve health delivery and to reduce investigation costs. An enquiry was sent to 500 sleep medicine providers in Europe. Response rate was 11%. Analysis showed that the main diagnosis is obstructive sleep apnoea in adults. Currently 2/3 of sleep studies are performed in laboratory: In-lab studies: Average cost for the health care is 390 EURO/study. The range is from 700 in Finland and Germany and 180 in Greece, Belgium and Sweden are around the mean. Ambulatory studies with EEG: Average cost is around 120 EURO/study i.e. 30% of in-lab cost. The range is from 180 EURO in Portugal to 70 EURO in Germany. 50% of users are not satisfied with their current practice of ambulatory monitoring although they have a clear need for this technique to increase monitoring capacity (88%), reduce cost of investigation (85%), improve sleep quality (60%), and obtain better acceptance from the patient (76%). The expectations from ambulatory monitoring are: high diagnostic sensitivity (86%) high reliability of equipment (92%) low interference with patient's habits (94%) It is worth noting that 74% of users do not expect a fully automated interpretation of data. The indications cited are screening and follow-up of SAS, epilepsy, Periodic Leg Movements and also insomnia and narcolepsy. As a second aim, a validation study has been set-up for an ambulatory recorder. The reproducibility of the system has been evaluated in 14 patients by 2 consecutive home recordings and was satisfactory in terms of total sleep time and apnoea-hypopnea index. Nevertheless a failure rate of 7% was observed which should be improved by a better ergonomy of the system. The third aim was a socio-economical analysis in Paris, in order to define the actual standard mean cost of a polysomnography in the lab (500 EURO) and in ambulatory (238 EURO) i.e. less than one half of the laboratory cost. The monography of the health care process for sleep medicine in Paris showed a delay of more than 10 years for diagnosis of SAS in 25% of the patients and up to 5 physicians visited before referral to the sleep lab. In 48% of the cases the primary physician visited is a GP. In conclusion, there is a clear need for ambulatory monitoring of sleep disorders to decrease the burden of cost and long waiting lists which is not well satisfied with the current health care system and commercially available equipment.

Adult↗
PubMed1999

Effects of exercise load and breathing frequency on heart rate and blood pressure variability during dynamic exercise.

It is known that heart rate (HR) variability decreases with dynamic exercise, but there are only few studies on blood pressure (BP) variability with exercise loads and the effect of breathing pattern has never been investigated. Thus, we studied HR and systolic blood pressure (SBP) signals by spectral analysis (FFT), in 9 healthy subjects, at different breathing frequencies (0.15, 0.2, 0.3, 0.4, 0.5, 0.6 Hz), at rest and during 3 exercise loads (25, 50 and 75% VO2max). BP was measured with a non-invasive device (Finapres) and continuously recorded. The power spectrum of R-R period significantly decreased with exercise loads in the low frequency band (LF: 0.04-0.128 Hz) and in the high frequency band (HF: 0.128-0.65 Hz), but with breathing frequency only in the HF part of the spectrum. The power spectrum of SBP significantly increased with exercise loads in LF and HF bands, and decreased in HF band with increasing breathing frequency. R-R and SBP HF peaks were centered on breathing frequency peaks. Therefore, spectral analysis of HR and SBP confirm the withdrawal of vagal control during exercise, while mechanical effect of respiration on SBP persists. LF/HF ratio of R-R spectral components decreased with increasing load, whereas cardiovascular sympathetic activity is known to rise, suggesting that this ratio is not a good indicator of cardiovascular autonomic modulation during exercise.

Adolescent↗
PubMed1999

[Sleep-related cardiac insufficiency and respiratory disorders. Prevalence, physiopathology, and treatment].

Cheyne-Stokes respiration occurs during sleep in 40-45% of patients with NYHA class III and IV heart failure. Such patients experience repeated episodes of progressively diminishing ventilation associated with desaturation followed by periods of increasing-amplitude ventilation. The mechanism appears to be related to hyperventilation leading to hypocapnia which occurs near a critical threshold of apnea during sleep stages I and stage II and interrupts central ventilatory control. The total duration of the periodic respiration cycle would depend on the increased circulation time subsequent to lowered cardiac output. Brief periods of waking provoked by Cheyne-Stokes respiration, accentuating sympathetic nervous system activity, are an unfavorable prognostic factor in heart failure. Activation of the sympathetic system may be corrected by CPAP although the long-term effect on heart failure remains controversial. Other treatments, such as oxygen therapy or theophylline, combined with optimized treatment of heart failure, have been proposed.

Adolescent↗
PubMed1997

Vasoactive intestinal polypeptide microinjections into the oral pontine tegmentum enhance rapid eye movement sleep in the rat.

Rapid eye movement sleep can be elicited in the rat by microinjection of the cholinergic agonist carbachol into the oral pontine reticular nucleus. Intracerebroventricular administration, during the light period, of vasoactive intestinal peptide enhances rapid eye movement sleep in several species. Since this peptide is co-localized with acetylcholine in many neurons in the central nervous system, it was assumed that the oral pontine tegmentum could also be one target for vasoactive intestinal peptide to induce rapid eye movement sleep. This hypothesis was tested by recording the sleep-wakefulness cycle in freely-moving rats injected with vasoactive intestinal peptide or its fragments (1-12 and 10-28) directly into the oral pontine reticular nucleus. when administered into the posterior part of this nucleus, vasoactive intestinal peptide at 1 and 10 ng (in 0.1 microliter of saline), but not its fragments, induced a 2-fold enhancement of rapid eye movement sleep during 4 h, at the expense of wakefulness. At the dose of 10 ng, a significant increase in rapid eye movement sleep persisted for up to 8 h. Moreover, when the peptide was injected into the centre of the positive zone, rapid eye movement sleep was enhanced during three to eight consecutive days. These data provide the first evidence that rapid eye movement sleep can be elicited at both short- and long-term by a single intracerebral microinjection of vasoactive intestinal peptide. Peptidergic mechanisms, possibly in association with cholinergic mechanisms, within the caudal part of the oral pontine reticular nucleus may play a critical role in the long-term regulation of rapid eye movement sleep in rats.

Animals↗