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Biomedical subjects

M H Stella

Publications and source records attributed to M H Stella.

6 recordsLinked to original sources

Respiratory response to mechanical stimulation of the gallbladder.

Since stimuli from abdominal or pelvic viscera can affect respiratory muscle function, we hypothesized that mechanical stimulation of the gallbladder would result in inhibition of motor activity to the diaphragm and to upper airway muscles. We studied 12 decerebrate, vagotomized, paralyzed, artificially ventilated cats and recorded hypoglossal (HG) and phrenic (PHR) nerve activities while applying 600-1000 g of traction on the gallbladder during four respiratory cycles. Traction resulted in an initial reduction of PHR activity to 87.6+/-15.0% (mean+/-S.D.% of its baseline value), a reduction of HG activity to 74.2+/-27.5% and a lengthening of expiratory time to 178.8+/-81.0%. Subsequently, PHR activity and expiratory time returned toward control values, while HG remained diminished, at 66.4+/-19.1%. Our results show that mechanical stimulation of the gallbladder results in a respiratory inhibition with a disproportionate reduction in HG activity relative to PHR discharge. We speculate that gallbladder stimulation by contractions or surgery may compromise breathing by inhibition of phrenic discharge and upper airway obstruction.

Animals↗

Modulation of breathing using imperceptible unloading.

We investigated the role of V(T) and V(T)/T(I) modulation of breathing in awake human subjects. We applied a PRBS of volume (incrementing ramp) or flow (decrementing wave) assist at levels below the perceptual threshold in order to stimulate respiratory feedback. We modeled the PRBS data with linear difference equations to obtain impulse-response profiles of V(T), V(T)/T(I), T(I) and factorial(P(MUS)). We limited cortical responses to our stimuli by applying sub-threshold levels of assist, and we limited humoral effects (O2 and CO2) by augmenting mechanical respiratory output intermittently and by small amounts. We found that flow or volume assist elicited similar significant increases in V(T) and V(T)/T(I). During flow assist there was a significant decrease in factorial(P(MUS)) and T(I) was reduced, albeit not significantly; however, volume assist did not modify T(I) or factorial(P(MUS)). The earlier onset of flow assist, relative to volume assist, may explain the difference between the responses. We conclude that vagally mediated inspiratory flow receptors in the chest wall or lungs may modulate breathing on a breath by breath basis when small, imperceptible increases in airflow occur early during inspiration. Furthermore, lung volume feedback during imperceptible unloading (occurring at the end of inspiration) was less effective. Finally, pseudorandom unloading with imperceptible stimuli provides a useful tool to study reflex regulation of ventilation in awake subjects without confounding cortical influences.

Adult↗

Respiratory response to baroreceptor stimulation and spontaneous contractions of the urinary bladder.

Spontaneous contractions of the urinary bladder (SBCs) and experimental elevations of carotid sinus pressure (CSP) have been shown to result in respiratory inhibition with preferential reduction in hypoglossal (HG) nerve activity as compared with that of phrenic nerve discharge. We assessed the interaction between these respiratory inhibitory stimuli in decerebrate, vagotomized, paralyzed and artificially ventilated cats. We denervated the right carotid sinus and pressurized the isolated left carotid sinus region within the linear range of the baroreflex, while maintaining systemic arterial pressure at approximately 100 mmHg. We monitored the HG and phrenic nerve responses to SBCs, to elevations in CSP between SBCs, and to elevations in CSP during SBCs. Our results show that superimposing these stimuli results in respiratory inhibition, especially of HG activity, that exceeds that resultant from either stimulus alone. We speculate that the combined presence of SBCs and episodic hypertension may contribute to the development of periodic breathing or obstructive apnea, particularly during sleep.

Animals↗

Modulation of laryngeal and respiratory pump muscle activities with upper airway pressure and flow.

The hypothesis that upper airway (UA) pressure and flow modulate respiratory muscle activity in a respiratory phase-specific fashion was assessed in anesthetized, tracheotomized, spontaneously breathing piglets. We generated negative pressure and inspiratory flow in phase with tracheal inspiration or positive pressure and expiratory flow in phase with tracheal expiration in the isolated UA. Stimulation of UA negative pressure receptors with body temperature air resulted in a 10--15% enhancement of phasic moving-time-averaged posterior cricoarytenoid electromyographic (EMG) activity above tonic levels obtained without pressure and flow in the UA (baseline). Stimulation of UA positive pressure receptors increased phasic moving-time-averaged thyroarytenoid EMG activity above tonic levels by 45% from baseline. The same enhancement of posterior cricoarytenoid or thyroarytenoid EMG activity was observed with the addition of flow receptor stimulation with room temperature air. Tidal volume and diaphragmatic and abdominal muscle activity were unaffected by UA flow and/or pressure, whereas respiratory timing was minimally affected. We conclude that laryngeal afferents, mainly from pressure receptors, are important in modulating the respiratory activity of laryngeal muscles.

Aging↗

Laryngeal muscle response to phasic and tonic upper airway pressure and flow.

The hypothesis that respiratory modulation due to upper airway (UA) pressure and flow is dependent on stimulus modality and respiratory phase-specific activation was assessed in anesthetized, tracheotomized, spontaneously breathing piglets. Negative pressure and flow applied to the isolated UA at room or body temperature during inspiration only enhanced posterior cricoarytenoid muscle activity from that present without UA pressure and flow (baseline) by 15--20%. Time shifting the onset of UA flow relative to tracheal flow decreased this enhancement. The same enhancement was observed with oscillatory or constant airflow. UA positive pressure and flow at room or body temperature applied during expiration only enhanced thyroarytenoid muscle activity from baseline by 50--160%. The same enhancement was observed with oscillatory or constant airflow at body temperature. Constant positive pressure and flow enhanced thyroarytenoid muscle activity more than oscillatory pressure and flow at room temperature. We conclude that the respiratory modulation of UA afferents is processed in a phase-specific fashion and is dependent on stimulus modality (tonic vs. phasic).

Animals↗

Respiratory response to spontaneous contractions of the urinary bladder in awake and decerebrate rats.

Spontaneous contractions of the urinary bladder (SBCs) have been shown to decrease the frequency and depth of respiration in anesthetized or unanesthetized, decerebrate cats. The respiratory responses to bladder voiding reflexes in the awake state have not been previously addressed. Because a chronic rat model for the study of bladder function has been established and breathing measurements can be made in the awake rat, we chose the rat as an experimental model to assess whether SBCs would alter breathing in the conscious, intact animal. Respiratory frequency increased during bladder contractions but tidal volume remained unaffected. To assess whether the respiratory response to bladder reflexes in rats differed from that previously observed in cats, we also studied decerebrate, vagotomized, paralyzed and artificially ventilated rats. Contrary to the respiratory inhibition observed in decerebrate cats, phrenic and hypoglossal nerve activities remained unaffected during SBCs in decerebrate rats. These results indicate a species difference in the coupling between respiration and bladder voiding reflexes.

Animals↗