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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↗
PubMed1984

Soft palate and oronasal breathing in humans.

In 20 naive patients without respiratory impairment, we investigated the ability of the soft palate to direct airflow during breathing. Patients were connected to a spirometer, without noseclip. No instructions were given on the breathing route. During quiet respiration, 15 patients breathed solely through the nose, despite an open mouth. During forced vital capacity (FVC) maneuvers, 19 patients expired exclusively through the mouth. When specifically asked to breathe quietly through the mouth, pure nasal breathing was no longer observed. Tidal volume (VT) or FVC were comparable when patients were asked to breathe through the mouth, with or without noseclip: 0.67 +/- 0.46 vs. 0.60 +/- 0.21 liter for VT (mean +/- SD); 4.05 +/- 0.65 vs. 4.18 +/- 0.70 liters for FVC. In eight separate healthy volunteers, the soft palate was shown by fluoroscopy to close the oropharyngeal isthmus during quiet breathing (resulting in pure nasal breathing) and to close the nasopharynx during FVC efforts (resulting in mouth breathing). During oronasal breathing, the soft palate lay in between the tongue and the posterior pharyngeal wall. These data suggest that when both mouth and nose are open, the soft palate is responsible for the partitioning of oronasal flow.

Fluoroscopy↗
PubMed1983

Smoking, lung function, and body weight.

In a cross-sectional study of steelworkers aged 45-55 years, smokers (n = 105; mean weight 76.1 kg) were found to weigh significantly less than non-smokers (n = 54; 81.6 kg) and ex-smokers (n = 51; 82.6 kg). The lower weight of smokers was attributable to a group with airflow obstruction (n = 37; forced expiratory volume in one second/vital capacity (FEV1/VC) less than 66%), who weighed less (4.8 kg; p less than 0.05) than smokers with normal FEV1/VC (n = 68). In smokers, but not in ex-smokers or non-smokers, body mass index and FEV1/VC ratio were closely related (r = 0.34; p less than 0.001). This association was apparently not due to an effect of body weight on lung function. Weight loss in smokers may be the consequence of impaired lung function or reflect the effect of cigarette smoking on both the respiratory tract and metabolism in susceptible subjects.

Body Weight↗
PubMed1983

Extrathoracic airways changes during plethysmographic measurements of lung volume.

In six healthy subjects cineradiographic studies during panting against a closed shutter showed widening and narrowing of the whole extrathoracic airways. At the epiglottic level, the mean lateral maximum diameter was 121% of the minimum diameter for an applied pressure of 11.4 cm H2O and 152% for 28.4 cm H2O, while posteroanterior diameter changes were 148% for 12.3 cm H2O and 182% for 28.2 cm H2O, respectively. There was a significant correlation between anteroposterior diameter changes and mouth pressure (Pm) swings (P less than 0.05). In 6 cadavers, the compliance of extrathoracic airways (isolated from the lower respiratory tract by an inflated balloon in the upper trachea) was 1.5 ml X cm H2O-1 after adding 30 ml of air, and 1 ml X cm H2O-1 after removing 30 ml of air. Flow rate in and out the extrathoracic airways averaged 0.089 and 0.163 L X sec-1 for swings in Pm of 9.5 and 18.5 cm H2O, respectively. There was a significant correlation (P less than 0.05) between flow rate and delta Pm. For a given delta Pm, flow was higher in those cadavers with more compliant extrathoracic airways. We conclude that extrathoracic airways change their volume during panting, and that these volume changes, as well as the internal flow rate thus created, depend on the Pm swings.

Adult↗
PubMed1983

Elastic properties of the lung in acute induced asthma.

In acute induced asthma, plethysmographic total lung capacity (TLCm) was reported to increase and lung elastic recoil [Pst(L)] to decrease. The increase in TLC is spurious (J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 52: 939-954, 1982), so that the rapid loss in Pst(L) could be due to errors in lung volume. We studied seven asthmatic patients before and during an induced bronchospasm. TLC was derived simultaneously from mouth and esophageal pressure vs. plethysmographic volume plots (TLCm and TLCes, respectively). Before bronchospasm, TLCm and TLCes were similar. During bronchospasm average TLCm increased, from 7.30 +/- 1.34 (SD) to 8.12 +/- 1.49 liters (P less than 0.001), whereas TLCes did not (P greater than 0.60). Static pressure-volume curves, derived from TLCes (P-Ves), were superimposed on prechallenge curves or only slightly shifted to the left, whereas those derived from TLCm (P-Vm) showed a clear-cut parallel shift to the left. At 70% of control TLC there was no significant change in Pst(L) measured from P-Ves curves (7.3 +/- 3.1 cmH2O before bronchospasm; 6.7 +/- 2.3 cmH2O during bronchospasm, P greater than 0.10), whereas Pst(L) measured from P-Vm curves decreased from 7.3 +/- 3.1 to 5.1 +/- 2.4 cmH2O (P less than 0.01). No significant change in Pst(L) at TLC was observed during bronchospasm. We conclude that in our patients acute decrease in Pst(L) during induced asthma was artifactual, secondary to lung volume overestimation by body plethysmography.

Acute Disease↗