Predicting blood flow responses to rhythmic handgrip exercise from one second isometric contractions.

The aim of this work was to predict blood flow responses to rhythmic handgrip exercise from one second isometric contractions. Seven healthy men were studied. Each subject performed a single 1 s handgrip contraction at 10 %, 20 % and 40 % of the maximum handgrip strength. We then repeatedly summed hyperaemic responses from single contractions to predict hyperaemic response to a prolonged bout of rhythmic exercise. There was similarity between steady state brachial blood flow velocity (BBV) extrapolated from single handgrip contractions and during 2 min of rhythmic exercise for 20 % (10.0+/-3.8 cm/s vs. 10.2+/-2.6 cm/s, r=0.93, p=0.003) and 40 % of maximum contractions (14.2+/-5.5 cm/s vs. 15.6+/-3.4 cm/s, r=0.88, p=0.009), but not for 10 % (7.5+/-4.1 cm/s vs. 5.7+/-3.3 cm/s, r=0.94, p=0.018). BBV progressively rose substantially higher during rhythmic contractions than peak BBV observed during single contractions at matched intensity. Respective peak BBV during single contractions and steady state BBV rhythmic contractions were 4.4+/-2.1 and 5.7+/-3.3 cm.s(-1) at 10 % forearm strength (p=0.14), 5.6+/-2.4 and 10.2+/-2.8 cm.s(-1) at 20 % (p=0.002), and 7.0+/-2.5 and 15.6+/-3.6 cm.s(-1) at 40 % (p=0.003). In conclusion, there is similarity between the summated blood flow velocity calculated from a single 1 s muscle contraction and the steady state blood flow velocity response of rhythmic exercise.

Effect of upper airway negative pressure on proprioceptive afferents from the tongue.

We examined whether receptors in the tongue muscle respond to negative upper airway pressure (NUAP). In six cats, one hypoglossal nerve was cut and its distal end was prepared for single-fiber recording. Twelve afferent fibers were selected for study on the basis of their sensitivity to passive stretch (PS) of the tongue. Fiber discharge frequency was measured during PS of the tongue and after the rapid onset of constant NUAP. During PS of 1-3 cm, firing frequency increased from 17 +/- 7 to 40 +/- 11 (SE) Hz (P < 0.01). In addition, 8 of the 12 fibers responded to NUAP (-10 to -30 cmH2O), with firing frequency increasing from 23 +/- 9 to 41 +/- 9 Hz (P < 0.001). In two fibers tested, the increase in firing frequency in response to NUAP was not altered by topical anesthesia (10% lignocaine) applied liberally to the entire upper airway mucosa. Our results demonstrate that afferent discharges from the hypoglossal nerve are elicited by 1) stretching of the tongue and 2) NUAP before and after upper airway anesthesia. We speculate that activation of proprioceptive mechanoreceptors in the cat's tongue provides an additional pathway for the reflex activation of upper airway dilator muscles in response to NUAP, independent of superficially located mucosal mechanoreceptors.

Soft palate muscle responses to negative upper airway pressure.

The afferent pathways and upper airway receptor locations involved in negative upper airway pressure (NUAP) augmentation of soft palate muscle activity have not been defined. We studied the electromyographic (EMG) response to NUAP for the palatinus, tensor veli palatini, and levator veli palatini muscles in 11 adult, supine, tracheostomized, anesthetized dogs. NUAP was applied to the nasal or laryngeal end of the isolated upper airway in six dogs and to four to six serial upper airway sites from the nasal cavity to the subglottis in five dogs. When NUAP was applied at the larynx, peak inspiratory EMG activity for the palatinus and tensor increased significantly (P < 0.05) and plateaued at a NUAP of -10 cmH2O. Laryngeal NUAP failed to increase levator activity consistently. Nasal NUAP did not increase EMG activity for any muscle. Consistent NUAP reflex recruitment of soft palate muscle activity only occurred when the larynx was exposed to the stimulus and, furthermore, was abolished by bilateral section of the internal branches of the superior laryngeal nerves. We conclude that soft palate muscle activity may be selectively modulated by afferent activity originating in the laryngeal and hypopharyngeal airway.

Cardiorespiratory effects of manually compressing the rib cage during tidal expiration in mechanically ventilated patients recovering from acute severe asthma.

OBJECTIVES: To determine the cardiorespiratory effects of manual expiratory rib cage compression in mechanically ventilated patients recovering from acute severe asthma; and to extrapolate these findings to emergency asthma management where ventilation cannot be achieved by positive-pressure ventilation. DESIGN: A prospective, clinical study. SETTING: Intensive care unit. PATIENTS: Four intubated, mechanically ventilated (volume-controlled), adult patients recovering from acute severe asthma. INTERVENTIONS: Patients were studied before, during, and after a 2- to 3-min period of manual compressions applied bilaterally over the lower rib cage (ribs 8 to 10) during consecutive tidal expirations. MEASUREMENTS AND MAIN RESULTS: Air flow (pneumotachograph), airway pressure, radial or brachial arterial pressure, and the hand pressure applied to the patient's rib cage were monitored and recorded on magnetic tape. Playback of the recorded data enabled measurement of changes in lung volume (air flow integration). Changes during rib cage compression consisted chiefly of small decreases in lung volume and peak inspiratory airway pressure that were only observed in the least obstructed patient and were fully reversed after the cessation of compressions. Air flow-time and air flow-volume plots demonstrated expiratory air flow limitation during essentially the entire tidal expiration in each patient, except the least obstructed patient. CONCLUSION: The results suggest that manual compression of the rib cage during consecutive tidal expirations would be ineffective in reducing pulmonary hyperinflation during the emergency management of asthma when air flow obstruction is so severe that ventilation cannot be achieved by positive-pressure ventilation.

Effects of a synthetic lung surfactant on pharyngeal patency in awake human subjects.

We examined the effects of separate applications of saline and a synthetic lung surfactant preparation (Surf; Exosurf Neonatal) into the supraglottic airway (SA) on the anteroposterior pharyngeal diameter (Dap) and the airway pressures required to close (Pcl) and reopen (Pop) the SA in five awake normal supine subjects. Dap, Pcl, and P(op) were determined during lateral X-ray fluoroscopy and voluntary glottic closure when pressure applied to the SA lumen was decreased from 0 to -20 cmH2O and then increased to +20 cmH2O. After Surf application and relative to control, Dap was larger for most of the applied pressures, Pcl decreased (-12.3 +/- 1.9 to -18.7 +/- 0.9 cmH2O; P < 0.01), P(op) decreased (13.4 +/- 1.9 to -6.0 +/- 3.4 cmH2O; P < 0.01), and genioglossus electromyographic activity did not change (P > 0.05). Saline had no effect. These observations suggest that pharyngeal intraluminal surface properties are important in maintaining pharyngeal patency. We propose that surfactants enhance pharyngeal patency by reducing surface tension and adhesive forces acting on intraluminal SA surfaces.

Supraglottic airway pressure-flow relationships during oronasal airflow partitioning in dogs.

We studied pressure-flow relationships in the supraglottic airway of eight prone mouth-open anesthetized (intravenous chloralose or pentobarbital sodium) crossbred dogs (weight 15-26 kg) during increasing respiratory drive (CO2 administration; n = 4) and during graded-voltage electrical stimulation (SV; n = 4) of the soft palate muscles. During increased respiratory drive, inspiratory airflow occurred via both the nose (Vn) and mouth (Vm), with the ratio of Vn to Vm [%(Vn/Vm)] decreasing maximally from 16.0 +/- 7.0 (SD) to 2.4 +/- 1.6% (P < 0.05). Simultaneously, oral airway resistance at peak inspiratory flow decreased from 2.1 +/- 1.0 to 0.4 +/- 0.4 cmH2O (P < 0.05), whereas nasal airway resistance did not change (14.4 +/- 7.2 to 13.1 +/- 5.4 cmH2O; P = 0.29). Inspiratory pressure-flow plots of the oral airway were inversely curvilinear or more complex in nature. Nasal pathway plots, however, demonstrated a positive linear relationship in all animals (r = 0.87 +/- 0.11; all P < 0.001). During electrical stimulation of soft palate muscle contraction accompanied by graded constant-inspiratory airflows of 45-385 ml/s through an isolated upper airway, %(Vn/Vm) decreased from 69 +/- 50 to 10 +/- 13% at a SV of 84 +/- 3% of maximal SV (P < 0.001). At a SV of 85 +/- 1% of maximum, normalized oral airway resistance (expressed as percent baseline) fell to 5 +/- 3%, whereas normalized nasal resistance was 80 +/- 9% (both P < 0.03). Thus control of oronasal airflow partitioning in dogs appears mediated more by alterations in oral route geometry than by closure of the nasopharyngeal airway.

Control of epiglottic position in dogs: role of negative upper airway pressure.

We investigated the influence of negative upper airway pressure (NUAP) on hyoepiglotticus and genioglossus muscle electromyographic (EMG) activity in anaesthetised (sodium pentobarbitone/ chloralose) dogs breathing via a tracheostomy. Changes in pressure were not transmitted through the entire upper airway, thus confirming airway occlusion during NUAP. When NUAP was applied at the larynx, peak inspiratory and tonic EMG activity of the genioglossus and HE both increased significantly (p < 0.05) and reached a plateau at NUAP of -10 to -20 cmH2O. Nasal NUAP at any level failed to influence either genioglossus or HE EMG activity. Following bilateral section of the internal branches of the superior laryngeal nerves (SLNin), resting levels of HE and genioglossus EMG activity decreased to virtually zero. Moreover, NUAP applied at the larynx now failed to recruit EMG activity for either muscle. These findings suggest active control of epiglottic position in dogs during NUAP.

Influence of upper airway pressure oscillations on soft palate muscle electromyographic activity.

Snoring is characterized by high-frequency (30-50 Hz) pressure oscillations (HFPO) in the upper airway (UA). The soft palate is a major oscillating structure during snoring, and soft palate muscle (SPM) activity is an important determinant of velopharyngeal patency. Consequently, we examined the effect of artificial HFPO applied to the UA on the integrated electromyographic (EMG) activity of the SPMs in 11 supine mouth-closed anesthetized (pentobarbital sodium/chloralose) dogs breathing spontaneously via a tracheostomy. The EMGs of the palatinus (Pal; n = 11), levator veli palatini (LP; n = 9), and tensor veli palatini (TP; n = 8) were monitored with intramuscular fine-wire electrodes. Peak inspiratory and peak expiratory EMG activity was measured in arbitrary units (au) as the mean of five consecutive breaths. HFPO [+/- 4.5 +/- 0.4 (SE) cmH2O; 30 Hz] applied at the laryngeal end of the isolated UA increased peak inspiratory EMG from 3.3 +/- 2.0 to 8.4 +/- 1.7 au (P < 0.05) for Pal and from 2.0 +/- 1.1 to 7.3 +/- 2.7 au (P < 0.05) for LP. For the TP, increases were evident in four dogs, but mean values for the group did not change (5.8 +/- 2.4 to 11.0 +/- 4.1 au, P = 0.5). The peak expiratory EMG did not change for any SPM (all P > 0.3). Thus HFPO applied to the UA augments inspiratory SPM activity. Reflex augmentation of SPM activity by HFPO may serve to dilate the retropalatal airway and/or stiffen the soft palate during inspiration in an attempt to stabilize UA geometry during snoring.

Electromyographic activity of the hyoepiglotticus muscle in dogs.

We examined the respiratory-related electromyographic (EMG) activity of the hyoepiglotticus muscle using fine wire bipolar electrodes, inserted perorally in five anaesthetised (IV chloralose) tracheostomised dogs studied in the prone, mouth open position. The integrated HE EMG was measured in arbitrary units (a.u.) during resting breathing via the upper airway, and on a breath-by-breath basis during progressive increases in respiratory drive induced by infusion of CO2 into the inspired gas. The HE demonstrated inspiratory activity which increased linearly in relation to ventilation (r = 0.85 +/- 0.06, p < 0.001) due to an increase in both phasic (8.8 +/- 1.8 to 32.4 +/- 9.2 a.u.) and tonic (0.2 +/- 0.1 to 26.3 +/- 13.3 a.u.) activity (both p < 0.05). In addition, HE EMG developed substantial phasic expiratory activity (1.3 +/- 1.1 to 13.8 +/- 4.4 a.u., p < 0.05). We conclude that the canine HE exhibits inspiratory and expiratory related activity which is augmented during increased respiratory drive. These findings imply active control of epiglottic position during breathing in dogs.

Mechanisms of oronasal airflow partitioning in dogs.

We examined the integrated (MTA) electromyographic activity (EMG) of the hyoepiglotticus (HE) muscle and the soft palate muscles (SPM) during CO2 administration in 6 anaesthetised prone, mouth open dogs. As ventilation increased nasal flow (VN) as a percentage of total flow (VT), i.e. VN/VT%, decreased. Breath-by-breath peak inspiratory and peak expiratory HE EMG activity was strongly and inversely correlated with VN/VT% (both r > 0.8, p < 0.001), whereas the correlation between SPM MTA EMG activity and VN/VT% was highly variable. Severing of the HE muscles halved the rate at which VN/VT% was reduced with respect to increasing ventilation while electrical stimulation of HE muscle contraction resulted in a fall in VN/VT% to near zero levels. Active control of epiglottic position appears to be an important mechanism controlling the patency of the epiglottic-soft palate seal and thus the oronasal partitioning of airflow in dogs.

Soft palate muscle activity in response to hypoxic hypercapnia.

We studied the effects of increasing respiratory drive on electromyographic (EMG) soft palate muscle (SPM) activity in nine anesthetized tracheostomy-breathing dogs during hypoxic hypercapnia (HH) with a 14% O2-8% CO2-78% N2 inspired gas mixture. Moving time average EMG activity was recorded from palatinus (PAL), levator veli palatini (LP), and tensor veli palatini (TP) muscles (with bipolar fine-wire electrodes) and diaphragm (DIA; with bipolar hook electrodes). During HH, peak inspiratory DIA activity increased from 18.8 +/- 1.3 to 30.1 +/- 2.0 arbitrary units and minute ventilation increased from 6.2 +/- 0.3 to 18.3 +/- 1.8 l/min (both P < 0.001). Phasic inspiratory, expiratory, and/or tonic EMG activity was present in each SPM during room air breathing (control) and increased during HH (P < 0.05), except for phasic inspiratory PAL and phasic expiratory TP activities. Peak inspiratory LP and TP activities increased during HH to 250 and 179% of control, respectively, and peak expiratory activity increased to 187, 235, and 181% of control in PAL, LP, and TP, respectively. These findings demonstrate respiratory-related regulation of SPM activity independent of local reflex control from the upper airway. However, the combined inspiratory and expiratory phasic recruitment of these muscles differs from the inspiratory recruitment of known upper airway dilator muscles.

Respiratory-related activity of soft palate muscles: augmentation by negative upper airway pressure.

We studied respiratory-related activity of the soft palate muscles in 10 anesthetized tracheostomized supine dogs. Moving time average (MTA) electromyographic (EMG) activity was measured in the palatinus (PAL), levator veli palatini (LP), and tensor veli palatini (TP) with bipolar fine-wire electrodes and in the diaphragm with bipolar hook electrodes. Measurements were made during tracheostomy breathing and nasal breathing with the mouth sealed (NB). During tracheostomy breathing, all soft palate muscles displayed respiratory-related phasic inspiratory and expiratory as well as tonic EMG activity. During NB, peak inspiratory EMG activity increased in PAL, LP, and TP because of an increase in both phasic inspiratory and tonic MTA activity. In contrast, phasic expiratory activity did not change. A constant negative pressure equal to peak inspiratory tracheal pressure during NB was applied to the caudal end of the isolated upper airway with the nose occluded. This was associated with soft palate muscle responses qualitatively similar to the responses during NB but accounted for only 39, 25, and 32% of the magnitude of the peak inspiratory MTA EMG responses to NB in PAL, LP, and TP, respectively. Our results demonstrate that the soft palate muscles exhibit respiratory-related activity in common with other upper airway muscles. Furthermore, such activity is augmented in each soft palate muscle during NB, and negative upper airway pressure makes a substantial contribution to the recruitment of soft palate muscle activity.

Cardiorespiratory consequences of expiratory chest wall compression during mechanical ventilation and severe hyperinflation.

OBJECTIVES: To measure and compare the effects of manual expiratory compression of either the rib cage or abdomen on cardiac output, end-expiratory lung volume, and other cardiorespiratory variables in an animal model that mimics the severe pulmonary hyperinflation and hemodynamic impairment occurring in patients with severe acute asthma during mechanical ventilation. DESIGN: Prospective, randomized, crossover trial. SETTING: Research laboratory. SUBJECTS: Seven cross-bred, anesthetized, supine dogs. INTERVENTIONS: The following sequence was employed: a) spontaneous breathing without pulmonary hyperinflation; b) positive-pressure ventilation with severe pulmonary hyperinflation (produced by an external variable expiratory flow resistor); c) approximately 7 mins of manual expiratory compression of either the rib cage or abdomen during positive-pressure ventilation-hyperinflation. This sequence was then repeated, incorporating the alternative type of expiratory compression. MEASUREMENTS AND MAIN RESULTS: Cardiac output (measured by thermodilution), aortic pressure, pleural (esophageal) pressure, and changes in end-expiratory lung volume were measured. The decrease in cardiac output due to mechanical ventilation with pulmonary hyperinflation was exacerbated by rib cage compression (p < .001; spontaneous breathing 2.9 +/- 0.2 L/min, hyperinflation 1.5 +/- 0.1 L/min, and rib cage compression 1.0 +/- 0.1 [SEM] L/min). However, the positive-pressure ventilation-hyperinflation-induced decrease in cardiac output was attenuated by abdominal compression (p < .001; spontaneous breathing 3.3 +/- 0.2 L/min, hyperinflation 1.4 +/- 0.1 L/min, and abdominal compression 2.1 +/- 0.1 L/min). Mean aortic pressure returned to prehyperinflation levels during abdominal compression (p < .001; spontaneous breathing 126 +/- 2 mm Hg, hyperinflation 75 +/- 5 mm Hg, and abdominal compression 120 +/- 3 mm Hg). Both types of compression were similarly effective (p > .75) in increasing mean expiratory pleural pressure, so that end-expiratory lung volume was similarly (p > .25) reduced (0.45 +/- 0.05 and 0.40 +/- 0.05 L for rib cage and abdominal compressions, respectively) in this non-air flow, limiting animal model. CONCLUSIONS: The cardiorespiratory effects of manually compressing the rib cage or abdomen during expiration in this animal study suggest that these techniques should be carefully evaluated in mechanically ventilated patients with severe acute asthma.

Control of resting bronchial hemodynamics in the awake dog.

In the resting awake dog a continuous-wave Doppler flow transducer on the right bronchoesophageal artery inscribes a sharp early systolic spike and low flow in late systole and throughout diastole, indicating a highly resistive bed. An analysis of autonomic factors using intravenous, cumulative, and randomly applied cholinoceptor, beta 1- and beta 2-adrenoceptor, and alpha 1- and alpha 2-adrenoceptor antagonists indicates that the low vascular conductance is due to cholinoceptor and alpha 1- and alpha 2-adrenoceptor effects in a ratio 3.6:1. No beta-adrenoceptor tone is present. Sighing behavior invokes a transient (< 2 s) fall in intrapleural pressure (and thus rise in bronchovascular transmural pressure) of 10-30 mmHg, which is followed by a two- to threefold increase over 30 s in bronchial flow and conductance, an effect simulated in 50% of dogs when bronchovascular transmural pressure is acutely raised and maintained over 40-60 s by inflating an intra-aortic balloon distal to the origin of the bronchial artery. Autonomic blockade has no effect on bronchovascular dilatation evoked either by sighing or by balloon inflation. It is concluded that, in the resting bronchial circulation, there exists strong cholinoceptor and alpha-adrenoceptor-based vasoconstrictor activity which can be overpowered by strong nonadrenergic noncholinergic local vasodilator reflexes evoked by sudden changes in intrathoracic transmural pressure possibly acting on stretch-sensitive sensory nerve endings containing substance P, calcitonin gene-related peptide, and neurokinins. The tonic vasoconstrictor but not the sigh-evoked vasodilator effects are sensitive to pentobarbital sodium anesthesia.