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Biomedical subjects

D C Stănescu

Publications and source records attributed to D C Stănescu.

At least 19 recordsLinked to original sources
PubMed1992

Upper airway anesthesia induces airflow limitation in awake humans.

Upper airway receptors are thought to contribute to upper airway stability by reducing collapsing forces. Their activity can be abolished by topical anesthesia. We have measured in 16 healthy volunteers (mean +/- SD age, 23.7 +/- 1.6 yr) specific airway conductance (SGaw), maximal inspiratory (MIFR) and expiratory (MEFR) flow rates before and 15, 35, and 45 min after extensive upper airway anesthesia (UAA) with 10% lidocaine. Average values of MIFR decreased (p less than 0.01) 15 min after UAA, but they returned to or near to control values at 45 min: MIF25 (4.8 versus 6.0 L/s); MIF50 (5.1 versus 6.2 L/s); MIF75 (4.4 versus 5.3 L/s). Transient decreases in flow (V) rates, reaching zero flow in some subjects, were observed in 13 subjects during forced inspiratory vital capacity (FIVC) maneuvers and in seven subjects during forced expiratory vital capacity (FEVC) maneuvers. MEFR at 25, 50, and 75% FVC, SGaw, and FVC did not change after anesthesia. Simultaneous measurements of supraglottic pressure, V, and lung volume in 12 of the 16 subjects showed that the site of flow limitation was localized at the level of the glottis in all except one subject in whom there was both a glottic and a supraglottic obstruction. We conclude that extensive upper airway anesthesia induced a profound but transitory upper airway obstruction during FIVC and FEVC maneuvers. These findings are compatible with the concept of reflex regulation of upper airway caliber.

Adult↗
PubMed1991

Pattern of snoring in obstructive sleep apnea patients and in heavy snorers.

We measured respiratory mechanical characteristics during sleep in five heavy, nonapneic snorers (HS) and in five obstructive sleep apnea (OSA) patients. In two HS and in two OSA patients we obtained lateral pharyngeal cineradiographic images during sleep while snoring. Flow limitation preceded all snores in both HS and OSA. Pattern of snoring, hysteresis and temporal relationship between supraglottic pressure (Psg) and flow rate were different in HS and OSA. Maximal flow during snoring was less (p less than 0.05) in OSA (0.18 +/- 0.07 liter/second) than in HS (0.36 +/- 0.06 liter/second). Linear supraglottic resistance during inspiratory snoring was higher, though not significantly, in OSA patients (7.11 +/- 3.01 cm H2O/liter/second) than in HS (4.80 +/- 2.83 cm H2O/liter/second). We conclude that: 1) Snoring is characterized by high frequency oscillations of the soft palate, pharyngeal walls, epiglottis and tongue. 2) Flow limitation appears to be a sine qua non for snoring during sleep. 3) The pattern of snoring is different in OSA and HS. 4) Pharyngeal size during snoring is probably larger in HS than in OSA patients.

Adult↗
PubMed1988

Ventilatory and diaphragmatic EMG changes during negative-pressure ventilation in healthy subjects.

To evaluate the response of normal subjects to assisted ventilation, we studied 6 naive healthy subjects before and during negative-pressure ventilation (NPV) with "low" (-10 cmH2O) and "high" (-30 cmH2O) pressures in an Emerson tank respirator. Ventilation was measured with an inductive plethysmograph (Respitrace), and diaphragmatic electromyogram (DEMG) was studied with a bipolar esophageal electrode. During NPV a 1:1 phase lock was observed between subjects and iron lung frequency in all subjects. Tidal volume increased in most subjects, more with high than with low pressures (P less than 0.05), whereas DEMG increased, decreased, or showed no change. Postinspiratory inspiratory diaphragmatic activity (PIIA) significantly increased during high-pressure NPV and was accompanied by an increase in tonic DEMG in one-half of the subjects. Voluntary relaxation resulted in a decrease in DEMG and PIIA. We suggest that cortical activity can explain persistency of active breathing during negative-pressure ventilation.

Adult↗
PubMed1988

Ventilatory and diaphragmatic EMG responses to negative-pressure ventilation in airflow obstruction.

To assess the responses of patients with chronic obstructive lung disease (COLD) to negative-pressure ventilation (NPV), we studied eight naive patients with moderate to severe COLD before (control) and during NPV with "low" (-10-cmH2O) and "high" (-30-cmH2O) pressure swings in a Drinker tank respirator. Tidal volume (VT) and minute ventilation (VE) were recorded from a Respitrace and diaphragmatic electromyogram (DEMG) from a bipolar esophageal electrode. During short, 5-min runs of "low" and "high" NPV, VT did not change and VE increased in a borderline significant way at -30-cmH2O NPV. Peak integrated DEMG amplitude did not change with respect to control during short runs of NPV. However, when NPV was maintained for 20-60 min, a significant (though small, 20%) decrease in peak DEMG amplitude was observed with respect to control. By contrast, in a ninth patient habituated to NPV, the decrease in peak DEMG amplitude during a 5-min run of NPV was 60%. Significant increases in arterial PO2 (at -10- and -30-cmH2O NPV) and decreases in arterial PCO2 (at -30-cmH2O NPV) were found during NPV for the whole group of patients. One-to-one phase locking between the respirator and patients was the most common pattern of entrainment observed. However, 1:1 phase locking did not preclude the presence of dissociation between the two pacemakers. We conclude that short runs of NPV in naive patients do not result in changes in DEMG, as opposed to immediate and nearly complete cessation of inspiratory activity in trained patients.

Diaphragm↗
PubMed1988

[The role of the soft palate in respiration].

The soft palate is a muscular fold suspended from the posterior border of the bony palate and extending downwards and backwards into the oropharynx. Usually, the soft palate and tongue are in tight apposition, closing the oropharyngeal isthmus; the soft palate can however rise and touch the posterior pharyngeal wall, closing the nasopharynx: thus the soft palate regulates the flow of air through nose and/or mouth. During oronasal breathing (as during exercise, speech or smoking) the impedance of naso and oropharynx respectively is determined by the position of the soft palate. Hence partitioning of the airflow through nose and mouth will depend on the latter. This is true in both adults and babies. Babies are not obligatory nasal breathers (as was previously thought). This applies as well as to near miss for sudden infant death syndrome babies. The soft palate is also involved in the genesis of snoring and the sleep apnea syndrome.

Adult↗
PubMed1987

"Sensitive tests" are poor predictors of the decline in forced expiratory volume in one second in middle-aged smokers.

In 1978, we studied 3 groups of steelworkers 45 to 55 yr of age who were all smokers: "obstructive" smokers (OS) with a FEV1/VC less than 66.6% (59.8% in average) (n = 37), smokers with "small airways disease" (SAD) and an abnormal closing capacity and/or slope of phase III (delta N2) but normal FEV1/VC (n = 32), and "resistant" smokers (RS) with normal functional indices (n = 36). Smokers with SAD had a lower (p less than 0.05) FEV1/VC (71.7%) than did RS (74.9%). We studied again 6 yr later about 85% of survivors in each group. Analysis of variance showed that FEV1 decreased significantly (p less than 0.001) only in OS (from 2.67 to 2.46 L). In RS and smokers with SAD, FEV1 declined from 3.34 to 3.26 L and from 2.95 to 2.85 L, respectively (p greater than 0.05). In all 3 groups, delta N2 increased (p less than 0.001) from 0.77 to 1.30% N2/L in RS, 1.41 to 2.43% N2/L in smokers with SAD, and 2.22 to 4.20% N2/L in OS. A multivariate analysis showed that the initial N2 explained about 30% (p less than 0.001) of the decline in FEV1 in OS, but only 10% (p less than 0.001) in the 3 groups together. In fact, the link between delta N2 and fall in FEV1 was restricted to OS. Closing volume and maximal expiratory flow rates were not related to decline in FEV1. The link between uneveness of ventilation and subsequent loss of FEV1 is of physiopathologic interest.(ABSTRACT TRUNCATED AT 250 WORDS)

Forced Expiratory Volume↗
PubMed1985

Influence of the respiratory route on the resting breathing pattern in humans.

It has been shown that the pattern of breathing is modified when breathing through a mouthpiece (MP) with a noseclip (NC), although the reasons for this are not clear. We studied 14 healthy naïve subjects during unrestrained breathing, while connected to a spirometer without NC, and while connected to a spirometer with NC. Breathing pattern, studied with an inductive plethysmograph (Respitrace), was recorded during 4 min in each case, once a steady state was attained. During unrestrained breathing, all subjects breathed exclusively through the nose. During spirometric testing without NC, 9 of 14 subjects still breathed through the nose only (since the oropharynx is closed by the soft palate and the tongue, and flow proceeds through the nose). Tidal volume (VT), frequency (f), minute ventilation (VE), inspiratory time, mean inspiratory flow, and duty cycle (Tl/Ttot) were not different during the first 2 procedures (p greater than 0.1 by analysis of variance). By contrast, during spirometric testing with NC, mean VT increased from 530 (during unrestrained breathing) to 700 ml (p less than 0.02), whereas f decreased from 14.9 to 13.6 breaths X min-1 (p greater than 0.05), VE did not change, and Tl/Tot increased from 37 to 41% (p less than 0.05). These data suggest that the change in the pattern of breathing depends on the breathing route. To further confirm this, we asked 8 separate subjects to simply breathe through either the nose or the mouth (half of them starting with mouth breathing, half with nose breathing) while respiration was monitored with the Respitrace without any connection to the airways.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Infants are not obligatory nasal breathers.

It is widely believed that infants are obligatory nasal breathers. We studied 19 infants, 1 to 230 days of age, for respiratory response to acute nasal occlusion. Lips were kept apart. Oropharyngeal structures were monitored by fluoroscopy, whereas respiratory movements and oral flow were recorded. We systematically observed before and during nasal occlusion tight apposition of the soft palate and the tongue, closing the oropharyngeal isthmus. After a variable time (mean 7.8 s, range 0.6 to 32 s), the soft palate rose and oral breathing was initiated. Time required to mouth-breathe was related to age and/or conscious state, older and/or awake infants responding faster than younger and/or asleep infants. In 9 others, when nasal occlusion was performed with the mouth closed, results were comparable to those obtained in infants with mouths open. In 3 infants, electroencephalograph (EEG) records showed quiet non-REM sleep. Nasal occlusion resulted in an immediate arousal reaction, followed after a variable time by mouth breathing. We conclude that infants are not obligatory nasal breathers. They can breathe through the mouth by detaching the soft palate from the tongue, thus opening the oropharyngeal isthmus.

Female↗
PubMed1985

Pattern of inhalation of tobacco smoke in pipe, cigarette, and never smokers.

There is controversy on whether both primary and secondary pipe smokers do inhale tobacco smoke. We studied inhalation of tobacco smoke in 6 primary and 6 secondary pipe smokers and compared it with that in 20 cigarette smokers and 11 never smokers. Respiratory movements were assessed with inductive plethysmography, nasal flow through measurements of nasal pressure, oral flow with an oral thermistor, puffing through pressure measurements in the cigarette holder or the pipe, and upper airways by fluoroscopy. In all pipe smokers except 1, breathing and smoking appeared as independent activities. The former was exclusively nasal, whereas the latter was exclusively oral. Smoke was sucked and puffed by a to-and-fro movement of the tongue sliding along the soft palate. The oropharyngeal isthmus was closed (or only intermittently opened) by the apposition of the soft palate and the tongue, thus preventing overt inhalation of smoke. In most cigarette smokers, smoking interfered with the breathing route. Once smoke was sucked into the mouth, the oropharyngeal isthmus opened and inspiration proceeded through both mouth (with inhalation of smoke) and nose. Cigarette smoking interfered also with the evenness of ventilation. Never smokers avoided inhalation by oropharyngeal closure followed by oral expiration. We conclude that the oropharyngeal isthmus is the essential gate controlling smoke inhalation. Most secondary pipe smokers are able to change their smoking pattern and avoid overt inhalation when switching from cigarette to pipe smoking. The inhalation pattern appears to be acquired in the course of the smoking history.

Adult↗
PubMed1978

Even distribution of 133Xe bolus inhaled at residual volume in healthy subjects.

We selected from among 46 healthy students (22 to 31-yr-old) 7 subjects (group A) in whom the normalized height of phase IV (height of phase IV/phase IIIx100), after inhaling a bolus of He at RV, was very small (10%). We compared them with 6 subjects (group B) selected on the basis of a tall phase IV (78%, A vs. P P less than 0.005). Age and height were comparable, but weight was lower (P less than 0.05) and RV/TLC ratio (but not other spirographic indices) was larger (P less than 0.025) in group A. The average amplitude of cardiac oscillations was 4 times higher in group B (P less than 0.005). He closing volume, but not closing capacity was less in group A (P less than 0.05). A bolus of 133Xe inhaled at RV was nearly uniformly distributed in group A while producing a large vertical gradient in group B. The difference between groups A and B may reflect a difference in the mechanical properties of the chest wall leading to a less complete empting of the lung in the former group.

Adult↗
PubMed1975

Inflection point on transpulmonary pressure-volume curves and closing volume.

In 20 healthy subjects and 18 patients with bronchial obstruction, closing volume (CV) on single-breath nitrogen washout curves and inflection point (IP) on transpulmonary pressure-volume curves were recorded simultaneously during slow expiratory vital capacity maneuvers. IP and CV did not occur at identical lung volumes, IP being systematically larger than CV for small CV values. This discrepancy could not be attributed to an esophageal or mediastinal artifact. It is suggested that, though CV and IP both express "airway closure," their sensitivity to closure may differ: CV underestimates closure because of a dead space effect; the latter may vary individually. On the other hand, IP may not reflect the true beginning of closure, particularly when it occurs at higher lung volumes.

Adult↗
PubMed1975

A modified measurement of respiratory resistance by forced oscillation during normal breathing.

We have modified the measurements of the resistance of the respiratory system, Rrs, by the forced oscillation technique and we have developed equipment to automatically compute Rrs. Flow rate and mouth pressure are treated by selective averaging filters that remove the interference of the subject's respiratory flow on the imposed oscillations. The filtered mean Rrs represents a weighted ensemble average computer over both inspiration and expiration. This method avoids aberrant Rrs values, decreases the variability, and yields an unbiased mean Rrs. Rrs may be measured during slow or rapid spontaneous breathing, in normals and in obstructive patients, over a range of 3-9 Hz. A good reproducibility of Rrs at several days' interval was demonstrated. Frequency dependence of Rrs was found in patients with obstructive lung disease but not in healthy nonsmokers.

Airway Resistance↗
PubMed1975

Smoking and pulmonary diffusing capacity.

The pulmonary diffusing capacity (DLCO SB) and its two components, the capillary blood volume (Vc) and the diffusing capacity of the membrane (DMCO), expressed in absolute values and per litre of alveolar volume (VA'), were measured at rest and on exercise in healthy male smokers and nonsmokers of similar age and height, and with identical values for haemoglobin and spirographic data. DLCO, DLCO/VA', DMCO and DMCO/VA' are significantly lower in smokers, at rest and on exercise; the decrease in Vc and thetaVc/VA' in smokers at rest is due to a higher level of carboxyhaemoglobin. The decrease of DLCO, DLCO/VA', DMCO and DMCO/VA' is apparently not due to carboxyhaemoglobin or distributional factors but to anatomical lesions, probably of emphysematous nature, altering the pulmonary membrane. Formulas predicting DLCO, DMCO, Vc, DLCO/VA', DMCO/VA' and thetaVc/VA' in terms of age and height were established in smokers and in nonsmokers.

Adult↗