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Biomedical subjects

Y Cormier

Publications and source records attributed to Y Cormier.

At least 109 records · Page 6Linked to original sources
PubMed1990

Influence of passive changes of lung volume on upper airways.

The total upper airway resistances are modified during active changes in lung volume. We studied nine normal subjects to assess the influence of passive thoracopulmonary inflation and deflation on nasal and pharyngeal resistances. With the subjects lying in an iron lung, lung volumes were changed by application of an extrathoracic pressure (Pet) from 0 to 20 (+Pet) or -20 cmH2O (-Pet) in 5-cmH2O steps. Upper airway pressures were measured with two low-bias flow catheters, one at the tip of the epiglottis and the other in the posterior nasopharynx. Breath-by-breath resistance measurements were made at an inspiratory flow rate of 300 ml/s at each Pet step. Total upper airway, nasal, and pharyngeal resistances increased with +Pet [i.e., nasal resistance = 139.6 +/- 14.4% (SE) of base-line and pharyngeal resistances = 189.7 +/- 21.1% at 10 cmH2O of +Pet]. During -Pet there were no significant changes in nasal resistance, whereas pharyngeal resistance decreased significantly (pharyngeal resistance = 73.4 +/- 7.4% at -10 cmH2O). We conclude that upper airway resistance, particularly the pharyngeal resistance, is influenced by passive changes in lung volumes, especially pulmonary deflation.

Adult↗
PubMed1990

Influence of apnea type and sleep stage on nocturnal postapneic desaturation.

We examined the influence of apnea type and sleep stage on the severity of apnea-induced desaturations in 32 patients with a sleep apnea syndrome. The individual postapneic desaturations were evaluated by a desaturation curve; this curve was built by plotting the fall in SaO2 after an apnea against this apnea's length for each apneic event during the whole night recording. We considered only apneas where the preapneic SaO2 was greater than 90% and the lowest SaO2 value after the apnea was equal to or greater than 60% (limit of linearity of our oximeter). From the desaturation curve, we determined a desaturation surface defined as the area under the curve between 10s and a variable apnea duration. The upper bound used for the determination of the desaturation curve and the desaturation surface was the maximal length of apnea type with the shortest apnea duration between non-REM obstructive apnea and the other apnea types (i.e., obstructive and central apnea, obstructive and mixed apnea, etc.). The desaturation surface was determined separately for non-REM sleep apneas (obstructive apneas, mixed apneas, central apneas, and obstructive apneas with persistent expiratory flow) and REM sleep apnea (all obstructive in type). Non-REM obstructive apneas served as reference to evaluate the severity of apnea-induced desaturations of the other apneas. We found that the desaturation surface of obstructive apnea (OA) with expiratory flow and of REM sleep OA were significantly greater than for OA in non-REM sleep (p less than or equal to 0.005). The OA-related desaturation was significantly greater than those of central apneas (p = 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)

Female↗
PubMed1990

Phase II study of amonafide: results of treatment and lessons learned from the study of an investigational agent in previously untreated patients with extensive small-cell lung cancer.

Thirteen previously untreated patients with extensive small-cell lung cancer (SCLC) were treated with the investigational agent amonafide in a dose of 300 mg/m2 intravenously (IV) over 1 hour daily for 5 consecutive days. No responses were seen in 12 eligible patients. Myelosuppression was only occasionally seen. Other toxicities included diaphoresis, chest pain, local irritation at the injection site, arthralgias, nausea and vomiting, and neuromuscular problems. There were two early deaths, both attributable to tumor progression with resultant obstruction of a vital structure. Ten patients crossed over to alternate active therapy (etoposide [VP-16]-cisplatin) and five responded. The median survival time (MST) of the whole group of treated patients was 31 weeks. In future trials of investigational new drugs in previously untreated SCLC, we recommend that patients with the following characteristics be excluded: Eastern Cooperative Oncology Group (ECOG) performance status 2, 3, and 4; superior vena cava (SVC) obstruction; any major paraneoplastic syndrome; serious comorbid illness; and extensive hepatic involvement by tumor. The trial design should include prompt crossover to active alternative therapy, such as VP-16 and cisplatin, for disease progression or for failure to respond after two treatment cycles. Also, the trial design should use an early stopping rule based on interest in identifying only very active agents with a minimum response rate of 30%.

Adenine↗
PubMed1990

Sequential bronchoalveolar lavages by endotracheal intubation in guineapigs.

We examined the feasibility of performing repeated bronchoalveolar lavage (BAL) on guineapigs. We also determined the influence of lavage volume on cell recovery in these animals, verified if the free cell populations were altered by repeated lavage, and compared the results with those obtained after euthanasia. Live animals were intubated orotracheally by direct vision laryngoscopy and lavaged, except for the last BAL which was done on isolated lungs after euthanasia. Each animal was lavaged weekly for 8 weeks: weeks 1-5 lavages were done with 5 aliquots of 2 ml of normal saline, week 6 with 3 aliquots of 1 ml, week 7 with 3 aliquots of 2 ml, and week 8 with 5 aliquots of 2 ml after euthanasia. The first 5 BAL gave similar results in volumes recovered, total number of cells, cell viability and differentials. The total cell yield of lavages 6 and 7 was less than that of the first 5 BAL and BAL 8; cell differentials with these smaller lavages were similar except for the percentage of neutrophils which was slightly higher than with the 10 ml lavage at week 3. The final lavage gave similar results as the first 5 BAL in terms of total cells recovered, cell viability, and differentials. We conclude that repeated BAL is feasible in live guineapigs, and that it gives a similar cells yield as lung lavage obtained after euthanasia.

Animals↗
PubMed1990

Blood hypereosinophilia in the course of posttraumatic pleural effusion.

We report four cases of posttraumatic pleural effusion associated with blood hypereosinophilia. Three men and one woman were examined at our institution for pleural effusion between 21 and 50 days after a minor thoracic trauma. At their initial examination, the pleural fluid analysis showed, for each subject, a high eosinophilic count (54, 45, 25, and 45 percent, respectively). Blood analysis taken at that time revealed a concomitant increase in the number of peripheral eosinophils (1,078, 3,894, 900, and 2,128 eosinophils per cubic millimeter, respectively). For each subject, there was no evidence of past or current allergy or of systemic disease that could be associated with hypereosinophilia. We observed a parallel regression of the pleural effusion and of the number of blood eosinophils in each case. Only when the pleural effusion completely cleared did the blood eosinophilia return to normal. We conclude that posttraumatic pleural effusion may cause a striking blood eosinophilia and that a persistently elevated number of blood eosinophils suggests the nonresolution of the pleural effusion.

Adult↗
PubMed1990

Mechanisms of hyperinflation in asthma.

We studied 11 mild asthmatics to verify whether the mechanisms of hyperinflation in asthma could be inhibited or overcome by passively changing lung volumes. On day 1, we induced a fall in forced expiratory volume in one second (FEV1) of 30-60% by methacholine inhalation and measured the resulting increase in FRC (delta FRC). The delta FRC was 729 +/- 378 ml (mean +/- SD). On day 2, with the subject supine in an iron lung, we measured oesophageal (Poes), gastric (Pgas) and transdiaphragmatic (Pdi) pressures, and changes in functional residual capacity (FRC) (delta V) induced by extrathoracic pressures from -20 to +20 cmH2O before and after bronchoprovocation. With positive pressures, the FRC decreased and reached a plateau at 10 cmH2O pressure or higher. This plateau was at a mean FRC of 839 ml higher after the bronchoprovocation than before. Pdi at FRC varied in the same direction as the extrathoracic pressure and was not modified by the bronchospasm. Peak inspiratory Pdi, without pressure applied in the iron lung, increased from 13.6 +/- 5.4 to 28.1 +/- 13.5 cmH2O after methacholine; extrathoracic pressure of -20 cmH2O decreased this latter value to 15.4 +/- 7.3 cmH2O (p less than 0.01). The increased lung volume and the displaced chest wall recoil curve after provocation were not inhibited by positive or negative extrathoracic pressures. Our data show that the mechanisms of hyperinflation are not eliminated or overcome by passively changing lung volumes and support the hypothesis that persisting activity of inspiratory muscles other than the diaphragm during expiration and perhaps a prolonged expiratory time constant are responsible for hyperinflation in asthma.

Asthma↗
PubMed1989

Influence of lung volume in sleep apnoea.

The influence of a constant increase in functional residual capacity on apnoea characteristics was studied in patients with the sleep apnoea syndrome. Pulmonary inflation was achieved by applying a continuous negative extrathoracic pressure into a Poncho type respirator. Nine patients slept in the Poncho for two consecutive nights, negative extrathoracic pressure being applied during the second night. There was no difference in the total sleep time, its composition within the different sleep stages, the apnoea and apnoea-hypopnoea indices, or the sleep time spent in apnoea between the two nights. The mean (SD) apnoea duration increased with negative extrathoracic pressure from 25.3 (2) to 30.5 (3) seconds (p = 0.003) and time spent in obstructive apnoea (percentage of apnoea time) from 56 (13) to 75 (8) (p = 0.02). The mixed apnoea time (%) decreased from 37 (7) to 21 (7) (p = 0.02). Despite the increase in apnoea duration, less time was spent below each oxygen saturation value during negative extrathoracic pressure. The results were similar for apnoeic episodes during non-REM (non-rapid eye movement) sleep, whereas no significant modifications were seen during REM sleep. It is concluded that the composition of apnoea time and resulting oxygen desaturation are influenced by lung volume.

Humans↗
PubMed1989

Changes in day and night time oxygenation with protriptyline in patients with chronic obstructive lung disease.

The effect of protriptyline, a tricyclic antidepressant, on sleep architecture, nocturnal arterial oxygen desaturation, pulmonary function, and diurnal arterial blood gases was investigated in an open study of 14 patients with stable chronic obstructive lung disease. Daytime and overnight measurements were made before and 2 and 10 weeks after they started protriptyline (20 mg daily at bedtime). Two patients had to be excluded before the second visit and one before the third visit because of changes in treatment for their chest disease. Protriptyline caused mouth dryness in all patients and dysuria in six men. With protriptyline there were no significant changes in total sleep time, sleep period time, or the percentages of total sleep time occupied by stage I-II and stage III-IV sleep. The mean (SEM) percentage of total sleep time spent in rapid eye movement (REM) sleep decreased from 11.1 (1.7) to 4.6 (0.7) at two weeks and to 4.2 (1.0) at 10 weeks. After protriptyline the time spent during sleep with an arterial oxygen saturation (SaO2) below each 5% increment above 65% was less than the baseline time; the lowest SaO2 (%) reached during sleep increased from 64.5 (1.7) to 72.7 (2.1) at 2 weeks and to 77.4 (2.1) at 10 weeks. Lung volumes and expiratory flows were unchanged during the study. Daytime arterial oxygen tension (PaO2) increased from 57 (1.4) mm Hg before treatment to 62 (1.9) mm Hg at 2 weeks and to 66 (1.9) mm Hg at 10 weeks (7.6 (0.2), 8.3 (0.3), 8.8 (0.3) kPa). Carbon dioxide tension fell from 52 (2.3) mm Hg to 49 (1.4) mm Hg at 2 weeks and to 48 (2.0) mm Hg at 10 weeks (6.9 (0.3), 6.5 (0.2), 6.4 (0.3) kPa), but these changes were not significant. These results suggest that protriptyline may benefit patients with chronic obstructive lung disease by reducing the sleep induced falls in SaO2 and improving diurnal PaO2; a controlled trial is now required.

Aged↗
PubMed1989

The fluctuant nature of precipitating antibodies in dairy farmers.

Four hundred and forty five of 888 dairy farmers studied in an epidemiological survey four years previously were restudied to determine change in precipitins and in clinical features. Subjects answered the same questionnaire, which was filled in by the same nurse in the same winter months, and had blood withdrawn for precipitin analysis (double diffusion technique). Of the 445 subjects retested, 48 (10.8%) had been precipitin positive at the first study; of these, 34 remained positive four years later and 14 had reverted to negative. Twenty eight subjects previously negative for precipitins had become positive, so that 62 subjects in all were precipitin positive when restudied (13.9%). Of the 445 farmers, 369 were precipitin negative at both studies. The prevalence of symptoms, including cough, sputum production, wheezing, dyspnoea, and fever and chills, was similar for subjects who were consistently negative for precipitins and consistently positive and for those who changed from one to the other. Only one subject developed farmer's lung; he had precipitins in both studies. This study shows a fluctuation in the precipitin state of dairy farmers, suggesting that more farmers have precipitins at least once in their lifetime than are identified by screening at a single point in time. Relatively few develop farmer's lung or other respiratory symptoms. The presence of precipitins in a symptomless farmer appears to have no clinical importance.

Adolescent↗
PubMed1989

Influence of respiratory drive on upper airway resistance in normal men.

The variations in nasal and pharyngeal resistance induced by changes in the central inspiratory drive were studied in 10 normal men. To calculate resistances we measured upper airway pressures with two low-bias flow catheters; one was placed at the tip of the epiglottis and the other in the posterior nasopharynx, and we measured flow with a Fleisch no. 3 pneumotachograph connected to a tightly fitting mask. Both resistances were obtained continuously during CO2 rebreathing (Read's method) and during the 2 min after a 1-min voluntary maximal hyperventilation. The inspiratory drive was estimated by measurements of inspiratory pressure generated at 0.1 s after the onset of inspiration (P0.1) and by the mean inspiratory flow (VT/TI). In each subject both resistances decreased during CO2 rebreathing; these decreases were correlated with the increase in P0.1. During the posthyperventilation period, ventilation fell below base line in seven subjects; this was accompanied by an increase in both nasal and pharyngeal resistances. These resistances increased exponentially as VT/TI decreased. Parallel changes in nasal and pharyngeal resistances were seen during CO2 stimulus and during the period after the hyperventilation. We conclude that 1) the indexes quantifying the inspiratory drive reflect the activation of nasopharyngeal dilator muscles (as assessed by the changes in upper airway resistance) and 2) both nasal and pharyngeal resistances are similarly influenced by changes in the respiratory drive.

Adult↗
PubMed1989

Effects of respiratory drive on upper airways in sleep apnea patients and normal subjects.

We compared the changes in nasal and pharyngeal resistance induced by modifications in the central respiratory drive in 8 patients with sleep apnea syndrome (SAS) with the results of 10 normal men. Upper airway pressures were measured with two low-bias flow catheters; one was placed at the tip of the epiglottis and the other above the uvula. Nasal and pharyngeal resistances were calculated at isoflow. During CO2 rebreathing and during the 2 min after maximal voluntary hyperventilation, we continuously recorded upper airway pressures, airflow, end-tidal CO2, and the mean inspiratory flow (VT/TI); inspiratory pressure generated at 0.1 s after the onset of inspiration (P0.1) was measured every 15-20 s. In both groups upper airway resistance decreased as P0.1 increased during CO2 rebreathing. When P0.1 increased by 500%, pharyngeal resistance decreased to 17.8 +/- 3.1% of base-line values in SAS patients and to 34.9 +/- 3.4% in normal subjects (mean +/- SE). During the posthyperventilation period the VT/TI fell below the base-line level in seven SAS patients and in seven normal subjects. The decrease in VT/TI was accompanied by an increase in upper airway resistance. When the VT/TI decreased by 30% of its base-line level, pharyngeal resistance increased to 319.1 +/- 50.9% in SAS and 138.5 +/- 4.7% in normal subjects (P less than 0.05). We conclude that 1) in SAS patients, as in normal subjects, the activation of upper airway dilators is reflected by indexes that quantify the central inspiratory drive and 2) the pharyngeal patency is more sensitive to the decrease of the central respiratory drive in SAS patients than in normal subjects.

Adult↗
PubMed1989

Predictive value of bronchoalveolar lavage cells and serum precipitins in asymptomatic dairy farmers.

In 1981 to 1982, we reported that many (19/43) asymptomatic dairy farmers, especially those with positive serum precipitins, had a lymphocytic alveolitis. We reevaluated, six and seven years later, 33 of the initial 43 farmers to verify their outcome. The restudied group included 31 men and 2 women between 24 and 67 years of age. In both studies, 24 were nonsmokers and 9 were exsmokers. Each farmer answered a questionnaire, had a physical examination, blood withdrawal for precipitin analysis, a chest roentgenogram, and pulmonary function tests (forced expiratory flows and diffusion capacity). At restudy, one subject had developed symptoms suggestive of sub-acute farmer's lung and now had inspiratory crackles; six had chronic morning cough and sputum production. Serum precipitins were positive in 10 subjects, whereas 16 had been positive at the initial study. Precipitins reverted from positive to negative in eight subjects and from negative to positive in six. Chest roentgenograms were normal in 23 subjects, while discrete interstitial abnormalities were noted in nine. One subject had significant pulmonary infiltrates. Results of current pulmonary function tests were (% predicted, mean +/- SEM) DL(CO) 114.8 +/- 3.0, FEV1 108.1 +/- 2.4, FVC 105.4 +/- 1.1. No correlations were found between these data and the lymphocytes or mast cells found in the bronchoalveolar lavage (BAL) at the initial study of 1981 and 1982. We conclude that bronchoalveolar lavage cell counts of asymptomatic farmers have no long-term clinical significance.

Adult↗
PubMed1989

Diffuse malignant mesothelioma of the pleura in Ontario and Quebec: a retrospective study of 332 patients.

Three-hundred thirty-two cases of pleural diffuse malignant mesothelioma (DMM) seen at large centers in Ontario and Quebec from 1965 to 1984 were reviewed retrospectively. Previous asbestos exposure was found in 44% of patients. Diagnosis was most often made by exploratory thoracotomy; pleural biopsy or cytology were rarely contributory. The delay in diagnosis was often long (median time, 3.5 months) and thrombocytosis (platelets greater than or equal to 400,000/microL) was common (41% of cases). The median survival (MS) was only 9 months. Eleven clinical variables were analyzed for prognostic significance. The three most important prognostic factors using a univariate analysis were stage, weight loss, and histologic type. For 118 patients with complete data, multivariate analysis showed that the stage of disease, high platelet count, and asbestos exposure were the most important prognostic factors. There was no cure of DMM, and we did not find any drastic differences in survival among groups of patients subjected to the different therapeutic measures. Radical surgery and radiotherapy were ineffective and we confirmed the low response rate to chemotherapeutic agents. This large retrospective trial can serve as a baseline for future studies in this field. In particular, it provides the basis for appropriate stratification variables to be used in future therapeutic trials.

Adult↗
PubMed1989

Bronchocutaneous fistula in dogs: influence of fistula size and ventilatory mode on airleak.

Bronchocutaneous fistula (BCF) can originate at different levels, from the major airways to the peripheral lung. Little is published on the influence of the fistula origin or the ventilatory effect of the airleak. This study evaluates relative CO2 elimination via fistulas of various size and how different ventilatory modes influence both the quantity and quality, i.e., oxygen and CO2 content, of the airleak. We created BCF with five polyethylene tubings of different diameters (tube 1, 3.0 mm; tube 2, 4.0 mm; tube 3, 5.1 mm; tube 4, 6.4 mm; tube 5, 9.8 mm) in nine dogs. Six modes of ventilation were used with each tubing: spontaneous breathing (SB), pressure support (PS), high frequency (HF), assisted controlled with inspiration set at 20% (AC20) and at 67% (AC67) of the respiratory cycle, and AC20 with an end-expiratory pressure of +10 cm H2O (PEEP). For each ventilatory mode, the fistula air flow (Vf), CO2, and oxygen partial pressure of fistula air (PfCO2 and PfO2) and arterial blood were measured. Vf was measured for all tubes, while gas analysis was done for tubes 1, 3, and 5 only. As expected, Vf increased with tubing size. Vf was higher with AC67 and PEEP than with the other ventilatory modes. PfCO2 was not significantly influenced by the tube size and Vf. Fistula air alveolization was increased only with HF ventilation. Air leaked via the fistula contributed significantly to gas exchange; even when expiration was totally via the fistula, the arterial gases remained unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

[Physiopathology of obstructive sleep apneas].

The syndrome of obstructive sleep apnoea is associated with an increased morbidity (the consequence of diurnal hypersomnolence and cardiovascular complications). The contraction of the dilator muscles of the upper airways (nose and pharynx) allows their patency at the time of inspiration. The obstruction of the airways resulted in a disequilibrium between the forces which tend to their collapse (negative inspiratory transpharyngeal pressure gradient) and those which contribute to their opening (muscle contraction). The mechanisms which underlie the triggering of obstructive apnoea are multiple including a reduction in the calibre of the superior airways, an increase in their compliance, and a reduction in the activity of the muscle dilators. This latter is intimately linked to the respiratory muscles and these muscles respond in a similar manner to a stimulation or a depression of the respiratory centre. The ventilatory fluctuations observed during sleep (alternately hyper and hypo ventilation of periodic respiration) thus favours an instability of the superior airways and the occurrence of oropharyngeal obstruction. The depth of post-apnoeic desaturation depends on the value of the arterial oxygen saturation at the beginning of apnoea, the duration of the period of apnoea and the pulmonary volume as the period of apnoea passes off. The cardiovascular consequences of apnoea include disorders of rhythm (bradycardia, auriculoventricular block, ventricular extrasystoles) and haemodynamic (pulmonary and systemic hypertension). This results in a stimulatory metabolic and mechanical effect on the autonomic nervous system. The electroencephalographic awakening which precedes the easing of obstruction of the upper airways is responsible for the fragmentation of sleep. The factors implicated in the cessation of the apnoea include hypoxia and hypercapnia but one also invokes a role for the negative pressure generated during the course of the apnoea.

Airway Resistance↗
PubMed1989

Role of lung volumes in sleep apnoea-related oxygen desaturation.

We studied the influence of lung volumes on apnoea-induced desaturation in ten subjects with sleep apnoea syndrome. Lung volumes were measured by helium dilution in the sitting and supine position and closing volume with the single-breath nitrogen washout test. To characterize the severity of apnoea-induced desaturations, we determined a desaturation curve for each patient. This curve was obtained by plotting the fall in arterial oxygen saturation (SaO2) reached at the end of each apnoea against the apnoea duration. From this curve we selected two indices: 1) the SaO2 fall following 30 s of obstructive apnoea (delta SaO2 30); and 2) the desaturation surface between 10-30 s of obstructive apnoea (DS 10-30). Both the delta SaO2 30 and the DS 10-30 were significantly correlated with the expiratory reserve volume (ERV), measured in the sitting (r = 0.77 and 0.65, respectively; p less than 0.05) and the supine positions (r = 0.96 and 0.87; p less than 0.005). A strong correlation was also observed with the difference between the supine ERV and the seated closing volume CV) (r = 0.99 with delta SaO2 30 and 0.89 with DS 10-30; p less than 0.005). Obesity influenced sitting and supine ERV values. We conclude that, among lung volumes, supine ERV and supine ERV-seated CV are the best indicators of the severity of apnoea-induced desaturation.

Humans↗
PubMed1988

Sequential bronchoalveolar lavage in experimental extrinsic allergic alveolitis. The influence of cigarette smoking.

We studied the alterations induced by acute experimental extrinsic allergic alveolitis (EAA) on bronchoalveolar cell population in smoking and nonsmoking guinea pigs. Sixty-two animals divided into 3 groups were studied: Group 1 (17 animals), controls; Group 2 (21 animals), extrinsic alveolitis; Group 3 (24 animals), cigarette smoking and alveolitis. Bronchoalveolar lavages (BAL) were performed on Days 1, 19, and 44 for all animals. Group 3 animals had a fourth lavage before starting cigarette smoking, that is, 28 days before the beginning of the antigen injections. The other lavages were as for the other groups. BAL results on Day 1 were similar for each group. Cigarette smoking per se did not modify BAL in Group 3. EAA induction resulted in a large increase in all BAL cells, especially neutrophils of recovered fluid, which increased from 38 x 10(3) to 1,474 x 10(3) ml-1 (p less than 0.01) in Group 2 and from 58 x 10(3) to 740 x 10(3) in Group 3 (p less than 0.01). After maintenance, BAL neutrophils.ml-1 decreased to 444 x 10(3) in Group 2 (p less than 0.01), but stayed the same in Group 3: 973 x 10(3). After EAA induction, BAL neutrophils.ml-1 were higher in Group 2 than in Group 3 (p = 0.039); however, Group 2 had less neutrophils.ml-1 than Group 3 (p = 0.035) after EAA maintenance. We conclude that EAA results in a neutrophilic alveolitis and which can be evaluated by sequential BAL, and that cigarette smoking decreases the initial neutrophilic response and retards the eventual recovery during maintenance injections.

Acute Disease↗