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

1988 ◽  
Vol 64 (6) ◽  
pp. 2272-2278 ◽  
Author(s):  
D. O. Rodenstein ◽  
G. Cuttitta ◽  
D. C. Stanescu

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.

1981 ◽  
Vol 50 (1) ◽  
pp. 149-161 ◽  
Author(s):  
A. I. Pack ◽  
R. G. DeLaney ◽  
A. P. Fishman

Studies were conducted in anesthetized paralyzed dogs using a cycle-triggered constant-flow ventilator, which ventilated the animal in phase with the recorded phrenic neural activity. Intermittently tests were performed in which the animal was ventilated with a different airflow for a single breath. Increased airflows, within the range generated during spontaneous breathing, caused an increased rate of rise of the moving average phrenic neurogram and a shortening of the duration of the nerve burst. The magnitude of the increase in the rate of rise of the neurogram was related to the level of inspiratory airflow. Tests with brief pulses of airflow showed that an increase in the rate of rise of the phrenic neurogram could be produced without inflating the lung above the resting tidal volume of the animal. Similar results were obtained with negative-pressure ventilation and the effects were abolished by vagotomy. This vagally mediated augmentation of phrenic neural output may accelerate the inspiratory volume change in the lung during spontaneous breathing at hyperpneic levels.


1993 ◽  
Vol 75 (2) ◽  
pp. 546-552 ◽  
Author(s):  
A. Sanna ◽  
C. Veriter ◽  
D. Stanescu

Negative-pressure ventilation (NPV) induces sleep-related upper airway obstruction. However, the precise mechanism and site of upper airway obstruction during NPV have not been worked out. We studied seven awake healthy volunteers (23–30 yr old) in an Emerson tank respirator. Subjects had the head outside the iron lung and breathed through a pneumotachograph, which yielded the airflow (V) signal. Supraglottic pressure (Psg) was measured with a catheter with the tip at the retroepiglottic level. Diaphragmatic electromyograms (EMGdi) were obtained from an esophageal bipolar electrode. Tidal volume was measured with an inductance plethysmograph. Measurements were done at -10, -20, and -30 cmH2O. At each pressure run subjects were asked to repeatedly relax or to actively breathe in phase with the respirator. Subjects had been previously trained to relax during NPV. During the relax runs there was no EMGdi activity. Stridor or wheezing occurred in all seven subjects during the relax runs but not during the active runs. Two patterns were associated with NPV during relax runs. One pattern was decreases in both V and Psg followed by zero values of these indexes, which corresponded to an inspiratory narrowing and closure of the glottis. These changes were visualized by fiber-optic bronchoscopy in one subject. The second pattern was a decrease in V and increase in Psg, which corresponded to an inspiratory supraglottic obstruction. In five subjects a supraglottic pattern was observed, whereas in two subjects glottic closure was seen. We conclude that muscular relaxation during NPV produces a decrease in the caliber of the upper airways at the glottic or supraglottic level. An uncoupling of upper airway muscle activity and the diaphragm might be the mechanism responsible for these changes.


1994 ◽  
Vol 112 (2) ◽  
pp. 551-554 ◽  
Author(s):  
Ricardo Marques Dias ◽  
Carlos Stabile ◽  
Pedro Dotto ◽  
José Roberto Jardim

In order to analyze the effect of intermittent negative pressure ventilation (NPV) on renal function, we studied 20 healthy male volunteers (mean age 29±4.1 years). NPV was performed with an "Emerson Chest Respirator Pump", adjusted to a breathing frequency of 10 respirations per minute, with inspiratory time/total respiratory time ratio of 0.4 and negative pressure of 25 cmH2O. The experimental protocol was carried out in two phases of two hours each - spontaneous breathing and NPV breathing. At the end of each phase, urine volume of the whole period was collected as well as venous blood sample for biochemical determinations. During NPV there was significant increase (P<0.05) in urine flow rate (1.43±0.81 to 2.76±1.95 ml/min) as well as in natriuresis (258±201 to 389±175 mcEq/min), kaliuresis (61±45 to 98±49 mcEq/min), fractional sodium excretion (1.38±0.88 to 1.96±0.98%), osmolar clearance (3.13±1.82 to 4.32±1.24 ml/min) and pH (7.37± 0.04 to 7.41±0.07) with unchanged creatinine and free water clearances. We concluded that NPV increases urine flow rate, kaliuresis and natriuresis but the data we have do not allow us to explain the mechanisms underlying such a phenomenon.


CHEST Journal ◽  
1991 ◽  
Vol 99 (5) ◽  
pp. 1186-1192 ◽  
Author(s):  
Francesco Gigliotti ◽  
Roberto Duranti ◽  
Andrea Fabiani ◽  
Mario Schiavina ◽  
Giorgio Scano

1987 ◽  
Vol 57 (02) ◽  
pp. 222-225 ◽  
Author(s):  
A H Soberay ◽  
M C Herzberg ◽  
J D Rudney ◽  
H K Nieuwenhuis ◽  
J J Sixma ◽  
...  

SummaryThe ability of endocarditis and dental strains of Streptococcus sanguis to induce platelet aggregation in plasma (PRP) from normal subjects were examined and compared to responses of PRP with known platelet membrane glycoprotein (GP) and response defects. S. sanguis strains differed in their ability to induce normal PRPs to aggregate. Strains that induced PRP aggregation in more than 60% of donors were significantly faster agonists (mean lag times to onset of aggregation less than 6 min) than those strains inducing response in PRPs of fewer than 60% of donors.Platelets from patients with Bernard-Soulier syndrome aggregated in response to strains of S. sanguis. In contrast, platelets from patients with Glanzmann’s thrombasthenia and from a patient with a specific defect in response to collagen were unresponsive to S. sanguis. These observations show that GPIb and V are not essential, but GPIIb-IIIa and GPIa are important in the platelet response mechanism to S. sanguis. Indeed, the data suggests that the platelet interaction mechanisms of S. sanguis and collagen may be similar.


Author(s):  
Akanksha Singh ◽  
Shival Srivastav ◽  
Kavita Yadav ◽  
Dinu S. Chandran ◽  
Ashok Kumar Jaryal ◽  
...  

1991 ◽  
Vol 144 (2) ◽  
pp. 390-394 ◽  
Author(s):  
Enrique Fernandez ◽  
Paltiel Weiner ◽  
Ephraim Meltzer ◽  
Mary M. Lutz ◽  
David B. Badish ◽  
...  

2018 ◽  
Vol 37 (4) ◽  
pp. 520-530 ◽  
Author(s):  
Nader S. Aboelnazar ◽  
Sayed Himmat ◽  
Sanaz Hatami ◽  
Christopher W. White ◽  
Mohamad S. Burhani ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document