Biomedical subjects

P Escourrou

Publications and source records attributed to P Escourrou.

At least 37 records · Page 2Linked to original sources

PubMed1997

Muscle chemoreflex alters carotid sinus baroreflex response in humans.

The arterial baroreflex opposes pressor responses to muscle ischemia (muscle chemoreflex). Our experiments sought to quantify the unknown effects of muscle chemoreflex on carotid sinus baroreflex (CSB) sensitivity. We generated CSB stimulus-response (S-R) curves by pulsatile application (triggered by each electrocardiogram R wave) of positive and negative neck pressure (from 60 to -80 mmHg in 20-mmHg steps of 20 s each) in seven normal young men. S-R curves were obtained at rest (upright), during the last 3 min of upright cycle ergometer exercise (150 W), and at the first minute of postexercise recovery with leg circulation free (control). A second study repeated the same procedures, except that leg circulation was occluded 20 s before the end of exercise to elicit muscle chemoreflex, and occlusion was maintained during recovery measurements (approximately 3- to 4-min duration). S-R curves for CSB were shifted upward and rightward (25 mmHg) to higher arterial blood pressure (BP) by exercise and less so (10 mmHg) in recovery (free leg flow). Postexercise occlusion (muscle chemoreflex) raised BP and shifted S-R curves above exercise curves. CSB gain rose from -0.26 +/- 0.06 (control) to -0.44 +/- 0.08 (occlusion) during positive neck pressure application and was reduced from -0.14 +/- 0.04 to zero (-0.04 +/- 0.03) during negative neck pressure. Heart rate responses during postexercise muscle chemoreflex were not significantly different from control. Results reveal a nonlinear summation of CSB and muscle chemoreflex effects on BP. BP-raising capability of muscle chemoreflex enhances CSB responses to hypotension but overpowers baroreflex opposition to hypertension.

Adolescent↗

PubMed1996

Ambulatory monitoring of blood pressure disturbs sleep and raises systolic pressure at night in patients suspected of suffering from sleep-disordered breathing.

1. The aim of the study was to assess the effect of ambulatory monitoring of blood pressure on sleep and on blood pressure in middle-aged patients. 2. Nine consecutive patients (seven men, two women; mean age 57 years) complaining of snoring and various degrees of excessive daytime somnolence were studied. Five patients were normotensive and four were being treated for hypertension. During one night standard laboratory polysomnography was performed with monitoring of blood pressure by a silent ambulatory monitor and continuous infrared blood pressure by photoplethysmography. 3. Ambulatory blood pressure significantly disturbs sleep architecture, causing EEG arousals in 64% of measurements, and induces a significant rise in blood pressure during systolic pressure measurement by the ambulatory monitor (rise in systolic pressure, 13.7 +/- 15.9 mmHg, P < 0.001; rise in diastolic pressure, 3.7 +/- 8.2 mmHg, P < 0.01). At the time of diastolic measurement, blood pressure had returned to the preinflation value. The rise in systolic blood pressure was higher when an arousal was associated with cuff inflation (P < 0.001). This rise in blood pressure is probably the consequence of sympathetic nervous system activation. 4. We conclude that ambulatory blood pressure recordings of systolic blood pressure during sleep should be interpreted with caution as systolic blood pressure may be significantly increased in patients suspected of suffering from sleep-disordered breathing.

Adult↗

PubMed1996

Role of the autonomic nervous system in the acute blood pressure elevation during repetitive hypoxic and hypercapnic breathing in rats.

Acute intermittent repetitive hypoxia simulating sleep apnoea syndrome is responsible for acute rises in blood pressure (BP). In the rat, the BP rises are enhanced by added hypercapnia. To investigate the role of the autonomic nervous system (ANS) in acute hypertension during repetitive hypoxia alone, FiO2 (inspiratory fractional concentration of oxygen) 2 to 5%, or combined with hypercapnia FiCO2 (inspiratory fractional concentration of carbon dioxide) 2 to 5%, we used autonomic blockade by atropine (1 mg kg-1) + propranolol (1 mg kg-1)-phentolamine (1 mg kg-1). Seven Wistar male rats were chronically instrumented with two aortic and venous catheters. Repetitive administration of N2 and N2 + CO2 for 10s followed by 20s compressed air was repeated for 4-5 min before (control) and after autonomic blockade. After autonomic blockade there was no significant difference in mean blood pressure (MBP) during severe hypoxia (SHO) (14.9 +/- 0.5 mmHg) compared to control (10.5 +/- 0.9 mmHg), while MBP was significantly decreased in severe hypoxia + hypercapnia (SHOHC) (14.1 +/- 0.4 mmHg) compared to control (26.8 +/- 0.3 mmHg) (p < 0.001). We conclude that the acute BP rise observed during hypoxic breathing is not due to the activation of ANS, but when hypercapnia is added to the hypoxic stimulus about half of pressor response is caused by ANS.

Animals↗

PubMed1995

Induction of rapid eye movement sleep by carbachol infusion into the pontine reticular formation in the rat.

Cholinergic regulation of sleep and wakefulness was studied in freely moving rats locally infused with various doses of carbachol into the pontine reticular formation. Induction of REM sleep occurred when carbachol was infused specifically into the posterior oral pontine reticular nucleus (PnO). This effect was observed with 1-10 ng of carbachol, and lasted for at least 6 h. It was antagonized by atropine (100-200 ng) infused into the same site 15 min before carbachol (10 ng), indicating that REM sleep induction resulted from the stimulation of pontine muscarinic receptors. High doses of carbachol (500 ng) did not affect REM sleep but enhanced wakefulness. Cholinergic mechanisms within the PnO may play a critical role in the regulation of REM sleep in the rat.

Animals↗

PubMed1995

Long-term pulmonary functional outcome of bronchopulmonary dysplasia and premature birth.

Pulmonary function and exercise tolerance were evaluated in late childhood in two groups of prematurely born children: one group with bronchopulmonary dysplasia (BPD) [n = 15; gestational age at birth (GA): 29.6 +/- 2.8 weeks; birth weight (BW): 1,367 +/- 548 g; age at test: 7.9 +/- 0.6 years], and a second group without significant neonatal lung disease [pre-term (PT)] (n = 9; GA: 30.3 +/- 1.7 weeks; BW: 1,440 +/- 376 g; age at test: 7.8 +/- 0.22 years). The results were compared with a control group of children of similar ages and heights, born at term [term born (TB)]. We observed that total lung resistance (RL) was significantly higher in BPD (11 +/- 3 cmH2O/L/s), and in PT (9 +/- 2) than in TB [5 +/- 1; (P < 0.001 and P < 0.05, respectively)]. In BPD RL was higher than in PT (P < 0.05). Dynamic lung compliance (CLdyn) was decreased in BPD (43 +/- 11 mL/cmH2O) and in PT (56 +/- 17) compared with TB (76 +/- 20) (P < 0.001 and P < 0.05), and also in BPD compared with PT (P < 0.05). Forced expiratory volume in 1 second (FEV1) and FEV1/forced vital capacity (FVC) were lower in BPD (1.07 +/- 0.15 L and 72 +/- 7%) than in PT (1.29 +/- 0.23 L, and 80 +/- 7%) (P < 0.05). Exercise tests were performed in six boys with BPD. The ratio between minute ventilation at maximal workload (VEmax) and the predicted value of maximal voluntary ventilation (MVV) was elevated in the six BPD boys tested, compared with five boys of Group 2 and five TB boys (87 +/- 15% vs. 62 +/- 14% and 65 +/- 13%) (P < 0.05). We conclude that: 1) prematurity and BPD is followed by long-term airway obstruction and a mild degree of exercise intolerance and; 2) premature birth without BPD may be followed by a milder degree of airway obstruction in childhood than in infants who developed BPD during the neonatal period.

Analysis of Variance↗

PubMed1995

Non-invasive measurement of haemodynamics during sleep apnoea.

Sleep apnoeas are accompanied by large variations in heart rate (HR) and blood pressure (BP). This nocturnal variability in BP may be involved in the increased cardiovascular morbidity of these patients. Due to the complex interaction between asphyxia, intrathoracic pressure, cardiac function and autonomic activation, the exact haemodynamic mechanisms are unclear. To evaluate the components of the BP surges at resumption of breathing (RB) a non-invasive beat-to-beat measurement was taken of cardiac output (CO) by the pulse contour analysis of the Finapres signal. Six male normotensive patients, free of medication (37-60 y, BMI 26.5-43.0 kg m-2) were studied during polysomnography (apnoea index: 22-69 h-1). Systolic blood pressure rose from 126.5 +/- 1.3 mmHg at beginning apnoea (P1) to 140.4 +/- 1.3 at RB (P < 0.01, ANOVA). During sleep Stages 2 and 3, stroke volume decreased during RB to 96% of P1 value (NS). Due to an opposite change in HR, CO tended to rise at RB to 106% of P1. Computed total peripheral resistance rose during RB to 105% of P1 value (P < 0.011. Therefore, it is concluded that the surge in BP at RB after apnoea is due to concomitant increases in CO and in TPR. Both rises are presumably a consequence of sympathetic nervous activation by the arterial chemoreceptors.

Journal Article↗

PubMed1995

Cardiovascular changes during acute episodic repetitive hypoxic and hypercapnic breathing in rats.

It has been shown that chronic repetitive ambient hypoxia, simulating pulmonary gas disturbances observed in apnoea, leads to systemic hypertension in rats. However, the relative roles of hypoxia (HO), hypercapnia (HC), gas stress and vigilance on the cardiovascular changes have not yet been demonstrated. The aim of this study was to investigate the acute haemodynamic changes observed during the repetitive inhalation of various gas mixtures in rats for HO alone and HO+HC, and to analyse the effects of vigilance and of the stress of gas administration. We studied 6 unanaesthetized Wistar rats chronically instrumented with an aortic catheter. Nitrogen, nitrogen+CO2 mixtures and compressed air were randomly administered in a Plexiglass chamber for 10 s and then flushed by compressed air for 20 s. Two cycles were repeated every min for 10 to 12 min. The inhaled gas fractions (FI,O2,FI,CO2) were monitored by O2 and CO2 analysers. Blood pressure (BP) was measured by a P23XL transducer. The blood gases were analysed by a 1306 IL meter. In control experiments, with compressed air alone, there were no significant acute changes in heart rate (HR) and BP. During HO there were no changes in HR or BP at FI,O2 values from 0.05-0.14, whilst at FI,O2 values from 0-0.05 systolic blood pressure (SBP) rose significantly (+25.3 +/- 25.7 (SD) mmHg) and HR decreased (-93.8 +/- 124.1 bpm). During HOHC, SBP rose (+35.1 +/- 26.4 mmHg) and HR decreased (-139.3 +/- 75.7 bpm), significantly more than in HO alone. SBP was linearly correlated with Pa,O2 during HO (r = 0.53) and also during HOHC (r = 0.44) and was not directly related to Pa,CO2 which has, nevertheless, an additive effect to HO. SBP rose with each challenge significantly more when the rats were awake than when asleep (behavioural sleep). We conclude that in this acute repetitive inhalation model, the rise in SBP is not related to gas stress or to Pa,CO2 but to a decrease in Pa,O2 and is enhanced by wakefulness.

Acute Disease↗

PubMed1995

Effect of autonomic blockade on heart rate and blood pressure in sleep apnea syndrome.

To determine the impact of the autonomic nervous system on hemodynamic responses to sleep apnea we studied 7 male patients (48 +/- 6 years, BMI = 29.7 +/- 2.9 kg/m2) with an apnea index = 33 + 11/h. In two hypertensives, therapy was withdrawn 2 weeks before the study. During a full night polysomnography EEG, EOG, EMG, respiration, oximetry, heart rate (HR) and blood pressure (BP) (Finapres 23OOE) were recorded. Placebo and 3 short-acting autonomic blockers were randomly i.v. administered: antimuscarinic (atropine 1 mg, A), beta 1 blocker (esmolol 40 mg, E), alpha blocker (nicergoline 2.5 mg, N). A total of 367 obstructive apneas in NREM sleep were studied. With atropine, HR was increased at the beginning of apnea (P1)(74.5 +/- 2 bpm vs 65.4 +/- 2 bpm with placebo) and at the end apnea (P3) (76.6 +/- 1.9 bpm vs 67.1 +/- 1.76 bpm). At the resumption of breathing (RB), HR still increased (83.5 +/- 1.5 bpm vs 80.1 +/- bpm). Nicergoline had no significant effect on HR but significantly decreased SBP (117.8 +/- 1.4 mmHg vs 127 +/- 1.6 with placebo, p < 0.001). Nevertheless, the rise in BP from P3 to RB remained significant (p < 0.001). Esmolol significantly decreased HR at P1 (68.1 +/- 1.9 bpm vs 73.9 +/- 1.9 bpm) and at RB (75.9 +/- 1.9 vs 81.6 +/- 1.8). With A, the rise in HR at end-apnea (P3) suggests a vagal hyperactivity during this phase which is blunted at resumption when HR is unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Antagonists↗

PubMed1994

Carotid baroreflex control of blood pressure and heart rate in men during dynamic exercise.

The degree of control of blood pressure (BP) and heart rate (HR) by arterial baroreflex during exercise is still controversial. We studied baroreflex control of BP and HR in seven normal young men by a noninvasive procedure employing a neck suction chamber that delivers pulsatile positive and negative pressures to the carotid sinus (CS). Pressures applied to the CS ranged from -80 to +60 Torr in steps of 20 Torr. Pressure stimuli were triggered by electrocardiogram R wave, and each pressure step was maintained for 20 s in a continuous sequence. One baroreflex-response curve was obtained during the last 3 min of each 6-min period of exercise. The four levels of upright (cycle) exercise were 60, 120, 180, and 240 W, the highest requiring approximately 75% of maximal O2 uptake. The sensitivity of the HR baroreflex response assessed by linear regression of HR vs. CS pressure (CSP) did not significantly decrease from rest (-0.09 +/- 0.053 beat/Torr) to 240 W (-0.06 +/- 0.025 beat/Torr). The BP above or below which CSP was increased or decreased by neck collar pressure was significantly increased from rest (76 +/- 6.5 Torr) to 240 W (111.2 +/- 4.0 Torr). The sensitivity of baroreflex response was assessed by linear regression of BP vs. CSP and was not significantly different from rest (-0.29 +/- 0.054 Torr/Torr) up to exercise at 240 W (-0.29 +/- 0.048 Torr/Torr). We conclude that mild to severe exercise does not reduce the gain of the CS reflex below resting values.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1993

Effect of breathing pattern on blood pressure and heart rate oscillations in humans.

1. The relationships of respiratory sinus arrhythmia (RSA) and respiratory changes in systolic blood pressure (SBP) to tidal volume (VT) and breathing frequency (BF), were quantified during voluntary control of VT and BF in healthy subjects. 2. Respiration was measured non-invasively with a respiratory inductive plethysmograph, which was calibrated prior to each study while breathing through a pneumotachygraph. Finger arterial blood pressure was measured non-invasively by the Finapres. 3. Heart rate (HR) increased during inspiration, with a nearly fixed time delay for most VT and BF approximating 0.9 s. The magnitude of RSA increased with increases in VT and with decreases in BF. SBP decreased during inspiration, with a time delay which increased as BF decreased, resulting in a phase delay approximating 160 degrees. The magnitude of the inspiratory fall in SBP increased with increases in VT. Increased amplitudes of RSA and SBP variation occurred at the lowest BF, consistent with the possibility of interactions between respiratory-related influences and those due to 'slow waves' of vasomotor tone. 4. The present results are consistent with the conclusion that respiratory effects on SBP are caused by a mechanism other that simply changes in HR.

Adult↗

PubMed1993

Cardiopulmonary and carotid baroreflex control of splanchnic and forearm circulations.

The objective was to determine whether a rise in carotid sinus transmural pressure by neck suction (NS) would counteract vasoconstriction secondary to inhibition of discharge of arterial and cardiopulmonary baroreceptors by simultaneous lower body negative pressure (LBNP). NS alone was applied to seven normal human subjects at -40 mmHg for 400-600 ms at each heartbeat during a 6-min period. NS reduced mean arterial pressure (MAP) from 94 +/- 6 to 86 +/- 9 mmHg and heart rate (HR) from 64 +/- 5 to 60 +/- 4.7 beats/min but did not affect vascular resistance in the splanchnic region (flow by constant infusion of indocyanine green; assumed constant extraction) or in the forearm (venous occlusion plethysmography). The same NS stimulus was applied during 23 min of continuous LBNP at -40 mmHg. LBNP alone before NS significantly reduced central venous pressure (CVP) from 5 +/- 0.3 to 1 +/- 0.5 mmHg and raised splanchnic (+34%) and forearm (+70%) vascular resistances and HR (from 64 to 74 beats/min) without reducing MAP. NS plus LBNP reduced MAP from 103 +/- 8 to 95 +/- 6 mmHg and HR from 74 +/- 6 to 67 +/- 5 beats/min without changing CVP but did not alter vascular resistances, which remained elevated and constant throughout LBNP before and after NS. Increments in plasma concentrations of renin (240%), aldosterone (70%), epinephrine (112%), and norepinephrine (46%) accompanied LBNP and NS; a separate influence of NS was not discernible. We conclude that vasoconstriction in response to combined cardiopulmonary and aortic inhibition is not overpowered by carotid sinus stimulation.

Adult↗

PubMed1993

Influence of pulmonary blood flow on gas exchange in piglets.

We previously reported that O2 diffusion was limited in piglets. To test the hypothesis of an inadequacy between diffusion and perfusion in piglets (< 4 wk) vs. older pigs (> 8 wk), we compared in these two age groups the effect of an increase (by opening an arteriovenous fistula) or a decrease (by inflating a balloon in the inferior vena cava) in cardiac output (Q) on gas exchange and on the O2 equilibration coefficient D/Q beta [ratio of the diffusion capacity of O2 (D) to the product of Q and the capacitance coefficient of blood (beta)]. In piglets but not in older pigs, a decrease in Q improved the alveolar-arterial Po2 difference (P < 0.05) and D/Q beta (P < 0.05), whereas an increase in Q had the opposite effect. Changes in the alveolar-arterial O2 difference and D/Q beta were linearly correlated with Q (r = 0.75, P < 0.01 and r = 0.88, P < 0.01, respectively). We suggest that the impaired O2 diffusion in piglets was due to inadequate diffusion-perfusion equilibrium of O2.

Aging↗

PubMed1993

[Risk factors for gastroesophageal reflux in chronic asthma].

In order to study risk factors for gastroesophageal reflux (RGO), we have analysed the clinical particulars, the spirometry and the different therapies of chronic asthmatics with and without RGO. RGO has been studied using 24 hour pH manometry in 53 patients suffering from chronic asthma. 70% of these patients had RGO, defined as oesophageal pH below 4, for 4.2% or more of the total time. The only predictive factor for the presence of RGO (log regression) was the dose of theophylline (P is equal to 0.02) whose average dose was higher in cases of RGO (9.1 plus or minus 2.3 mg/kg against 6.3 plus or minus 1.7 mg/kg, P is less than 0.03). Although the severity of the asthma and the spirometric parameters were similar. On the other hand, the severity of RGO, assessed as the percentage of the total time passed with a pH below 4 or correlated (multiple regression) with longevity of the disease (P is equal to 0.02) and the dose of theophylline (P is equal to 0.001). These results suggest that the treatment with theophylline and the duration of the asthma could constitute risk factors for RGO in chronic asthma.

Adolescent↗

PubMed1992

Cardiac, respiratory, and arousal responses to an esophageal acid infusion test in near-term infants during active sleep.

This study was designed to determine the cardiac, respiratory, and arousal responses to an esophageal acid infusion test in near-term infants free from neurological, gastroesophageal, and cardiopulmonary disease at time of testing during active sleep. Eight infants (gestational age 28-37.5 weeks, postconceptional age 36-40 weeks) were tested. Using standardized procedures and timing, we compared the cardiac, respiratory and arousal responses during a control period and during distal esophageal saline and acid infusion periods. The duration of each of these periods was 5 min. The pH of the acid infusion was 2.2. We found that this mild distal esophageal acid infusion test induced significant prolongation of the interval between successive electrocardiogram R waves compared with control and saline infusion periods (806.5 +/- 145.7 ms, 478.8 +/- 49.4 ms, and 468.8 +/- 37.2 ms, respectively; p less than 0.01) and of the duration of the respiratory cycle (2.9 +/- 0.7 s, 1.5 +/- 0.3 s, and 1.5 +/- 0.2 s, respectively; p less than 0.01). Esophageal acid infusion elicited significant electroencephalogram (EEG) arousal responses. The number of the EEG arousals was significantly increased during the acid period as compared with control and saline infusion periods (2.9 +/- 1.4, 0.5 +/- 0.5, and 0.4 +/- 0.5, respectively; p less than 0.01). Total arousal duration was significantly increased during acid as compared with control and saline infusion periods (42 +/- 17.5 s, 4.5 +/- 5.1 s, and 3.5 +/- 5.0 s, respectively; p less than 0.01). We conclude that distal esophageal acid stimulation elicits significant cardiac, respiratory, and EEG arousal responses in near-term infants during active sleep.

Administration, Oral↗

PubMed1992

Neonatal pattern of breathing during active and quiet sleep after maternal administration of meperidine.

The aim of this study was to reappraise the effects of maternal meperidine administration on breathing pattern during the first hours of life taking into account the state of alertness. Because breathing instability is more pronounced during active sleep, we hypothesized that meperidine administration might create a greater risk for respiratory instability during active sleep, the prominent sleep state in newborns. We studied eight full-term, healthy newborns whose mothers had received a continuous i.v. infusion of meperidine (81 +/- 9 mg) that was terminated 5.5 +/- 2.1 h before delivery. These infants were compared with a control group of eight full-term newborns whose mothers did not receive any opioids. In both groups, all babies were delivered vaginally after a normal labor and had Apgar scores of 9 or 10 at 1 and 5 min. Neonatal gastric secretion and maternal venous and umbilical venous blood were sampled at delivery for determination of meperidine concentration. From 60 to 300 min after delivery, behavioral sleep states and thoracic and abdominal movement as well as transcutaneous arterial oxygen saturation (SaO2) were monitored continuously. The number of apneic spells lasting more than 3 s during 100 min of recording and the percentage of time with SaO2 below 90% in each sleep state were recorded. During quiet sleep, all respiratory variables were similar in both groups. During active sleep, there were significantly more apneic episodes (37.1 +/- 25.1 versus 11.2 +/- 13.9) and a higher percentage of time with SaO2 less than 90% (14.3 +/- 16.7% versus 1.3 +/- 1.5%) in the meperidine group than in the control group (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Female↗

PubMed1992

Accuracy of respiratory inductive plethysmography during wakefulness and sleep in patients with obstructive sleep apnea.

To assess the accuracy of the respiratory inductive plethysmograph (RIP) during sleep in obese patients with obstructive sleep apnea (OSA), we monitored 13 patients with OSA during wakefulness and nocturnal sleep with simultaneous measurements of tidal volume from RIP and integrated airflow. Patients wore a tightly fitting face mask with pneumotachograph during wakefulness and sleep. Calibrations were performed during wakefulness prior to sleep and compared with subsequent wakeful calibrations at the end of the study. Patients maintained the same posture during sleep (supine, 11; lateral, two) as during calibrations. There were no significant differences in calibrations before sleep and after awakening. The mean error in 13 patients undergoing RIP measurements of tidal volume during wakefulness was -0.7 +/- 3.4 percent while that during sleep was 2.1 +/- 14.9 percent (p < 0.001). The standard deviation (SD) of the differences between individual breaths measured by RIP and integrated airflow was 9.8 +/- 5.5 percent during wakefulness and 25.5 +/- 18.6 percent during sleep (p < 0.001). During both wakefulness and sleep, errors in RIP tidal volume were not significantly correlated with body mass index. In 12 patients with at least 10 percent time in each of stages 1 and 2 sleep, SD was greater in stage 2 sleep compared with wakefulness and stage 1 (p < 0.001). In three patients who manifested all stages of sleep, SD was greater in REM sleep than in wakefulness and all stages of non-REM sleep (p < 0.001). In three patients who manifested all stages of sleep, SD was greater in REM sleep than in wakefulness and all stages of non REM sleep (p < 0.001). This was associated with paradoxic motion of the rib cage in two patients during REM. We conclude that, despite increased errors in individual breath measurements during sleep, more marked during stages 2 and REM sleep, RIP is clinically useful to measure ventilation quantitatively in obese patients with sleep apnea. The criterion of a decrease of 50 percent in tidal volume assessed by RIP is appropriate to define hypopneas in such patients.

Adult↗

PubMed1991

[Effects of respiratory physical therapy and nasopharyngeal suction on gastroesophageal reflux in infants less than a year of age, with or without abnormal reflux].

The purpose of this study was to analyse the effects on gastro-oesophageal reflux (GOR) of the different manipulations used during pulmonary physical therapy (nasal suctions, oropharyngeal suctions, acceleration of expiratory flow). 115 children less than 1 year old, were divided into two groups according to the results of oesophageal pH monitoring: 44 with and 61 without pathological GOR. Nasal suctions did not significantly increase GOR in children without pathological GOR. Oropharyngeal suctions increased GOR significantly more than nasal suctions (*p = 0.031). The technique of acceleration of expiratory flow, used in 35 degrees verticalized position and supine position, increased the index of reflux and the time with oesophageal pH below 4 in children with pathological GOR. However it did not increase reflux in normal children. The index of induced reflux in the whole population was increased in the horizontal position (4.81 +/- 0.88 reflux/hour) as compared with 35 degrees verticalized (2.92 +/- 0.79 reflux/hour). These oesophageal pH measurements confirm the clinical observations often made during physical therapy (vomiting, regurgitations, reflex cough). This statistical study suggests that one should take into account the adverse factor of GOR secondary to pulmonary physical therapy. It seems better to use nasal rather than oropharyngeal suctions and also to use the acceleration of expiratory flow technique in the 35 degrees verticalized rather than in the supine position, even more so if a pathological reflux does exist.

Gastroesophageal Reflux↗

PubMed1991

[Nocturnal continuous measurement of blood pressure in sleep apnea syndromes. Comparison between normotensive and hypertensive patients].

Sleep apnea syndrome and systemic hypertension are frequently associated but their causal relationship is unclear. We compared the oscillations of systemic blood pressure and heart rate during polysomnography in 8 normotensive subjects (2 females) and 5 hypertensive (supine awake blood pressure: 165 +/- 7/96 +/- 5 mmHg) without treatment. Their ages (normotensive: 52.1 +/- 11.0 yrs, hypertensive: 51.2 +/- 6.4 yrs) and body mass indices (32.6 +/- 9.6 kg/m2 vs 33.2 +/- 5.2 kg/m2 respectively) were not statistically different. Systemic blood pressure was continuously monitored by a non invasive digital plethysmography (Finapres). Both groups had similar respiratory events indices (normotensive: 45.2 +/- 18.1/hr, hypertensive: 48.4 +/- 20.5/hr) and minimal oxygen saturations (79.4 +/- 9.1% vs 82.4 +/- 7.0% respectively). During apneas in slow-wave sleep were observed the minimal values for systolic and diastolic pressures which were significantly higher in hypertensive than in normotensive (138.2 +/- 9.6/83.2 +/- 16.1 mmHg vs 105.9 +/- 11.1/60.5 +/- 10.9 mmHg respectively). During resumption of ventilation maximal blood values were recorded which were also higher in hypertensive than in normotensive (185.0 +/- 13.8/113.2 +/- 21.5 mmHg vs 155.9 +/- 19.8/88.7 +/- 17.1 mmHg respectively) (p less than 0.05). Although absolute variations of blood pressure were similar, relative changes in systolic pressure were significantly higher in normotensive (p less than 0.05). Maximal heart rate was 76.8 +/- 6.2 bpm in normotensive and 76.6 +/- 3.9 bpm in hypertensive during resumption of ventilation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗