Meibography and meibomian gland measurements in ocular graft-versus-host disease.

Meibomian gland loss in ocular GvHD was described as a mechanism contributing to dry eye and severe damage to the ocular surface. Infrared images of upper eyelid meibomian glands from 86 ocular GvHD patients, from 10 patients after allogeneic stem cell transplantation (aSCT) without ocular GvHD, from 32 patients prior to aSCT and from 30 healthy controls were analyzed retrospectively and evaluated using two grading schemes. The upper meibomian gland area (uMGA) was calculated and set in relation to the total tarsal area of the lid. Results demonstrate that meibomian gland loss is significantly increased in patients with ocular GvHD as well as in patients prior to aSCT in comparison with controls (P between 0.05 and <0.001). Patients after aSCT without ocular GvHD had no significant difference in uMGA in comparison with controls. This study suggests that meibomian gland loss in GvHD patients is likely to be a multifactorial process that also occurs prior to aSCT, possibly due to underlying diseases and/or secondary to chemotherapy or irradiation. In addition, the question has to be addressed whether meibomian gland loss could serve as a predictor for the development of ocular GvHD. Overall, infrared meibography should be included in routine examination of patients undergoing aSCT and during follow-up.

Pulmonary vascular dilatation and diffusion-dependent impairment of gas exchange in liver cirrhosis.

To test the hypothesis that diffusion-limitation for oxygen is due to abnormal vascular dilatation and significantly contributes to the arterial hypoxaemia of liver cirrhosis requires an experimental approach that detects both diffusion-limitation for oxygen and the presence of abnormal dilatation of pulmonary vessels exposed to alveolar gas. We therefore studied the gas exchange of a 64 year old man with alcoholic liver cirrhosis and severe resting arterial hypoxaemia (arterial oxygen tension (Pa,O2) 7.5 kPa) whilst breathing air and 100% O2 using conventional blood gas (CBG) analysis, the multiple inert gas elimination technique (MIGET) and whole body scintigraphy (WBS) following the i.v. administration of radiolabelled boli of macroaggregates with a minimum diameter of 15 microM. During air breathing, there was a consistently positive difference between the arterial oxygen tension predicted by MIGET and that actually measured (P-M Pa,O2, average 0.9 kPa). During O2 breathing, P-M Pa,O2 became negative, (average -12.2 kPa), and shunt estimated by the O2 method (% of Q') was consistently less than that measured by MIGET. Whereas both O2 method and MIGET estimates of shunt never exceeded 25%, the WBS shunt was 40%, indicating that a substantial fraction of cardiac output flowed through abnormally dilated pulmonary vessels, some of which were exposed to alveolar gas and, hence, participated in gas exchange. Although our observations pertain to one subject, we believe they provide the most convincing in vivo evidence to date that abnormal dilatation of interalveolar vessels may, per se, result in a significant diffusion impairment for O2. Furthermore, in view of the consistently negative P-M Pa,O2 observed during oxygen breathing, we speculate that such abnormal vascular dilatation may also have produced a significant diffusive impairment of one or more of the less soluble inert gases used in the MIGET analysis.

Effects of increased +Gz on chest wall mechanics in humans.

We studied the effects of head-to-foot acceleration (+Gz) on chest wall mechanics in five normal subjects seated in a human centrifuge. Results were compared with those previously obtained in the same subjects in microgravity during parabolic flights. In all subjects, end-expiratory abdominal pressure (Pga) and volume (Vab) increased with Gz. On average, end-expiratory Pga increased from 7.4 +/- 1.7 cmH2O at + 1 Gz to 14.9 +/- 2.8 cmH2O at + 3 Gz and end-expiratory Vab increased by 0.32 +/- 0.06 liter between + 1 and + 3 Gz. On the other hand, the abdominal contribution to tidal volume (Vab/VT) and abdominal compliance decreased from 34.7 +/- 5.9% and 52 +/- 6 ml/cmH2O at + 1 Gz to 29.3 +/- 5.1% and 26 +/- 4 ml/cmH2O at + 3 Gz, respectively. Changes in end-expiratory Pga were linear between 0 and + 3 Gz, but changes in end-expiratory Vab, Vab/VT, and abdominal compliance were greater in microgravity than in hypergravity. In contrast to weightlessness, which did not alter minute ventilation and tidal changes in Pga and transdiaphragmatic pressure, these variables increased with increasing Gz. These results indicate that, although changes in Gz have a linear effect on abdominal transmural pressure, hypergravity and weightlessness do not have symmetrical effects on chest wall mechanics.

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.

Blood flow distribution to upper airway muscles.

Radiolabeled (15-microns) microspheres were used to measure blood flow to upper airway muscles [alae nasi (AN), intrinsic laryngeal, tongue, cervical strap, and hyoid musculature], diaphragm (DI), and parasternals (PS) during spontaneous breathing in 24 anesthetized tracheotomized supine dogs. Six dogs were also studied while -28 +/- 3 (SE) cmH2O tracheal airway pressure was generated against an inspiratory resistance (IR) (upper airway bypassed). Blood flow to posterior cricoarytenoid muscle (PCA) [24.0 +/- 2.1 (SE) ml.min-1.100 g-1] was greater than that to DI (18.0 +/- 2.3 ml.min-1.100 g-1) and comparable to that to PS (21.4 +/- 2.9 ml.min-1.100 g-1). Blood flow per unit weight did not differ between AN, tongue muscles, laryngeal adductors, cervical strap muscles, and cricothyroid (CT). Average blood flow to these muscles was only 8.0 +/- 0.8 ml.min-1.100 g-1. With the exception of CT, blood flow to these upper airway muscles was less than that to DI and PCA. Relative to blood flow during spontaneous breathing, IR loading increased blood flow to AN by a factor of 7.5, to PCA by 3.4, to DI by 3.2 and to PS by 1.9. There was no change in blood flow in the other muscles during loading. Our results show that at rest blood flow to main glottic dilator (PCA) is similar to that to main inspiratory muscles. Furthermore, in response to an IR load, blood flow to PCA and AN increased by an equivalent or greater amount than that to DI.(ABSTRACT TRUNCATED AT 250 WORDS)

Abdominal compliance, parasternal activation, and chest wall motion.

We measured abdominal compliance (Cab) and rib cage displacement (delta Vrc) relative to abdominal displacement (delta Vab) during relaxation and tidal breathing in upright (U) and supine (S) postures in five normal subjects. In S, an abdominal binder was used to decrease Cab in two to five increments. We also measured the electrical activity of the parasternal muscle (EMGps) with the use of fine-wire intramuscular electrodes during CO2 rebreathing in U and in supine unbound (SU) and supine bound (SB) postures. During maximum binding (SB2), Cab decreased to 39 +/- 7% of the SU value (P = 0.01), matching Cab in U (P = 0.16). In the SB condition, the ratio of tidal delta Vrc/delta Vab to relaxation delta Vrc/delta Vab increased as Cab decreased, matching the data in U. For the group, this ratio decreased during SU to 47 +/- 10% (P = 0.02) but increased during SB2 to 86 +/- 7% (P = 0.18) of the value in U. During CO2 rebreathing, EMGps increased linearly with tidal volume (r > 0.727, P < 0.01). However, at any given tidal volume, the SU and SB2 EMGps were not significantly different (P = 0.12), and both were less than that in U (P < 0.02). The results suggest that the differences in chest wall motion between U and S may be due to the difference in Cab and not to different patterns of respiratory muscle recruitment. The mechanism may relate to changes in mechanical coupling between the diaphragm and the rib cage.

Lung volume and effectiveness of inspiratory muscles.

We related inspiratory muscle activity to inspiratory pressure generation (Pmus) at different lung volumes in five seated normal subjects. Integrated electromyograms were recorded from diaphragmatic crura (Edi), parasternals (PS), and lateral external intercostals (EI). At 20% increments in the vital capacity (VC) subjects relaxed and then made graded and maximal inspiratory efforts against an occluded airway. At any given level of pressure generation, Edi, PS, and EI increased with increasing lung volume. The Pmus generated at total lung capacity as a fraction of that at a low lung volume (between residual volume and 40% VC) was 0.39 +/- 0.15 (SD) for the diaphragm, 0.20 +/- 0.06 for PS, and 0.22 +/- 0.04 for the lateral EI muscles. Our results indicate a lesser volume dependence of the Pmus-EMG relationship for the diaphragm than for PS and EI muscles. This difference in muscle effectiveness with lung volume may reflect differences in length-tension and/or geometric mechanical advantage between the rib cage muscles and the diaphragm.

Chest wall and trunk muscle activity during inspiratory loading.

We measured the electromyographic (EMG) activity in four chest wall and trunk (CWT) muscles, the erector spinae, latissimus dorsi, pectoralis major, and trapezius, together with the parasternal, in four normal subjects during graded inspiratory efforts against an occlusion in both upright and seated postures. We also measured CWT EMGs in six seated subjects during inspiratory resistive loading at high and low tidal volumes [1,280 +/- 80 (SE) and 920 +/- 60 ml, respectively]. With one exception, CWT EMG increased as a function of inspiratory pressure generated (Pmus) at all lung volumes in both postures, with no systematic difference in recruitment between CWT and parasternal muscles as a function of Pmus. At any given lung volume there was no consistent difference in CWT EMG at a given Pmus between the two postures (P > 0.09). However, at a given Pmus during both graded inspiratory efforts and inspiratory resistive loading, EMGs of all muscles increased with lung volume, with greater volume dependence in the upright posture (P < 0.02). The results suggest that during inspiratory efforts, CWT muscles contribute to the generation of inspiratory pressure. The CWT muscles may act as fixators opposing deflationary forces transmitted to the vertebral column by rib cage articulations, a function that may be less effective at high lung volumes if the direction of the muscular insertions is altered disadvantageously.

Effects of inspiratory resistance, inhaled beta-agonists and histamine on canine tracheal blood flow.

Tracheobronchial blood flow is potentially important in asthma as it could either influence the clearance of mediators from the airways, thus affecting the duration and severity of bronchospasm, or enhance oedema formation with a resultant increase in airflow obstruction. In anaesthetized dogs, spontaneously breathing via a tracheostomy, we investigated the effects of three interventions which are relevant to acute asthma attacks and could potentially influence blood flow and its distribution to the mucosa and remaining tissues of the trachea: 1) increased negative intrathoracic pressure swings (-25 +/- 1 cmH2O) induced by an inspiratory resistance; 2) variable inhaled doses of a beta-adrenoceptor-agonist (terbutaline); and 3) aerosolized histamine sufficient to produce a threefold increase in pulmonary resistance. Microspheres labelled with different radioisotopes were used to measure blood flow. Resistive breathing did not influence tracheobronchial blood flow. Following a large dose of terbutaline, mucosal blood flow (Qmb) increased by 50%. After inhaled histamine, Qmb reached 265% of the baseline value. We conclude that, whereas increased negative pressure swings do not influence tracheobronchial blood flow or its distribution, inhalation of aerosolized terbutaline, corresponding to a conventionally nebulized dose, increases mucosal blood flow. Our results also confirm that inhaled histamine, in a dose sufficient to produce moderate bronchoconstriction, increases tracheal mucosal blood flow in the area of deposition.

O2 cost of breathing: ventilatory vs. pressure loads.

We compared the O2 cost of breathing (VO2resp) at high levels of ventilation (HV) with that against high inspiratory pressure loads (HP) using an external elastance when end-expiratory volume, work rate (W), and pressure-time product (P) were matched at two levels of ventilation and elastic loading. Each of five normal subjects performed three pairs of loaded runs (one HV and one HP) bracketed by two resting runs. Mean O2 consumption from the pairs of resting runs was subtracted from that of each of the loaded runs to give VO2resp during loaded breathing. Matching for W and P was within 15% in all 15 pairs of runs. During HV runs, ventilation was 398 +/- 24% of corresponding values during HP runs (P < 0.01). Although there was no difference in W (P > 0.05), the VO2resp during HV runs was 237 +/- 33% of that during HP (P < 0.01) and efficiency of HV was 51 +/- 5% of that during HP (P < 0.01). When W was normalized for the decrease in maximum inspiratory pressure with increased mean lung volume, efficiency during HV and HP runs did not differ (P > 0.05). In the second series of experiments, when both HV and HP runs were matched for W but P was allowed to vary, efficiency increased by 1.42 +/- 0.42% (P < 0.05) for each percent decrease in P during HV runs but was unchanged (P > 0.05) during HP runs despite a 193 +/- 10% increase in P.(ABSTRACT TRUNCATED AT 250 WORDS)

Pharyngeal dilation associated with cricothyroid muscle contraction in dogs.

The mechanical function of phasic respiratory-related activity of the cricothyroid muscle of the larynx is poorly understood. We studied five adult cross-bred dogs (weight 14-20 kg) deeply anesthetized with pentobarbitone sodium, mechanically ventilated via a tracheostomy, and placed prone with the mouth open. Bilateral cricothyroid muscle contraction was induced by supramaximal electrical stimulation of the external branches of the superior laryngeal nerve. Computerized axial tomography was used to assess effects of cricothyroid muscle contraction. During cricothyroid muscle contraction, oropharyngeal (tip of epiglottis) cross-sectional area increased by 18.0 +/- 3.0% (SE) (P = 0.008), whereas combined left and right piriform recess cross-sectional area increased by 85 +/- 25% (n = 4; P = 0.02) at the midepiglottic level and by 152 +/- 37% (P = 0.01) at the base of the epiglottis. Furthermore, at the base of the epiglottis the maximum horizontal distance between the alae of the thyroid cartilage increased by 21 +/- 8% (P = 0.05). In contrast, lateral glottic diameter decreased by 52 +/- 2% (n = 4; P = 0.01), whereas dorsoventral glottic diameter increased by 18 +/- 5% (n = 4; P less than 0.02). The cricothyroid muscle, therefore, has the capacity to act simultaneously as a pharyngeal dilator and a glottic constrictor and thus may play a role in the control of oropharyngeal as well as laryngeal patency.

Effects of cricothyroid muscle contraction on upper airway flow dynamics in dogs.

We studied the effects of cricothyroid muscle (CT) contraction on upper airway flow dynamics in eight prone open-mouth anesthetized dogs. Animals were mechanically ventilated via a tracheostomy while a constant airflow (Vuaw) passed through the isolated upper airway. Nasal airflow (Vn) was monitored using a nasal mask and pneumotachograph. Bilateral CT contraction was induced by electrical stimulation of the external branches of the superior laryngeal nerves. During CT contraction with Vuaw of 100-443 ml/s in the inspiratory direction, total upper airway resistance (Ruaw) fell by 49.1 +/- 5.4% (SE) while supraglottic resistance fell by 63.6 +/- 3.6%; simultaneously Vn fell by 55.3 +/- 3.8% and Vuaw increased by 7.2 +/- 1.7%. Similar results were obtained when Vuaw was in the expiratory direction. In three dogs in which the attachments of the CT to either the thyroid or cricoid cartilage were severed, superior laryngeal nerve stimulation had no systematic effect on Ruaw. Because visual assessment during CT contraction consistently revealed dilation of the piriform recesses, we suggest that CT contraction is associated with pharyngeal dilation, which in open-mouth dogs (with overlapping soft palate and epiglottis) redistributes flow to the oral route with a net reduction in Ruaw. Thus the CT may have a respiratory role as a pharyngeal dilator.

Influence of nasal airflow temperature and pressure on alae nasi electrical activity.

The influence of nasal airflow, temperature, and pressure on upper airway muscle electromyogram (EMG) was studied during steady-state exercise in five normal subjects. Alae nasi (AN) and genioglossus EMG activity was recorded together with nasal and oral airflows and pressures measured simultaneously by use of a partitioned face mask. At constant ventilations between 30 and 50 l/min, peak inspiratory AN activity during nasal breathing (7.2 +/- 1.4 arbitrary units) was greater than that during oral breathing (1.0 +/- 0.3 arbitrary units; P less than 0.005). In addition, the onset of AN EMG activity preceded inspiratory flow by 0.38 +/- 0.03 s during nasal breathing but by only 0.17 +/- 0.04 s during oral breathing (P less than 0.04). When the subject changed from nasal to oral breathing, both these differences were apparent on the first breath. However, peak AN activity during nasal breathing was uninfluenced by inspiration of hot saturated air (greater than 40 degrees C), by external inspiratory nasal resistance, or by changes in the expiratory route. The genioglossus activity did not differ between nasal and oral breathing (n = 2). Our findings do not support reflex control of AN activity sensitive to nasal flow, temperature, or surface pressure. We propose a centrally controlled feedforward modulation of phasic inspiratory AN activity linked with the tonic drive to the muscles determining upper airway breathing route.

Nasal and oral airway pressure-flow relationships.

We examined the inspiratory and expiratory pressure-flow relationships of both the oral and nasal airways before and after exercise in normal upright subjects. With the use of a partitioned facemask, nasal resistance was measured using posterior rhinomanometry, and oral resistance was measured by recording transoral pressure during oral breathing. Both the nasal and oral pressure-flow relationships for inspiration and expiration were curvilinear and were well described by a power function of the form delta P = aVb (where P is pressure, V is flow, a and b are constants) (r2 = 0.96 +/- 0.01). The exponent b describes the curvilinearity of the pressure-flow curve and can be used to infer the flow regimen. At rest, the inspiratory nasal and oral curves suggested a similar degree of turbulence (b = 1.77 +/- 0.06 and 1.83 +/- 0.04, respectively). However, inspiratory flow regimens were inferred to be more turbulent than those during expiration both before and after exercise. After exercise, decreases in inspiratory nasal resistance at low flows were associated with a change in flow regimen from fully turbulent to orifice flow over the entire flow range. Thus the application of a power function to nasal and oral pressure-flow data permits representation of the whole relationship and allows insight into the nature of the flow regimens.

Lung and chest wall mechanics in microgravity.

We studied the effect of 15-20 s of weightlessness on lung, chest wall, and abdominal mechanics in five normal subjects inside an aircraft flying repeated parabolic trajectories. We measured flow at the mouth, thoracoabdominal and compartmental volume changes, and gastric pressure (Pga). In two subjects, esophageal pressures were measured as well, allowing for estimates of transdiaphragmatic pressure (Pdi). In all subjects functional residual capacity at 0 Gz decreased by 244 +/- 31 ml as a result of the inward displacement of the abdomen. End-expiratory Pga decreased from 6.8 +/- 0.8 cmH2O at 1 Gz to 2.5 +/- 0.3 cmH2O at Gz (P less than 0.005). Abdominal contribution to tidal volume increased from 0.33 +/- 0.05 to 0.51 +/- 0.04 at 0 Gz (P less than 0.001) but delta Pga showed no consistent change. Hence abdominal compliance increased from 43 +/- 9 to 70 +/- 10 ml/cmH2O (P less than 0.05). There was no consistent effect of Gz on tidal swings of Pdi, on pulmonary resistance and dynamic compliance, or on any of the timing parameters determining the temporal pattern of breathing. The results indicate that at 0 G respiratory mechanics are intermediate between those in the upright and supine postures at 1 G. In addition, analysis of end-expiratory pressures suggests that during weightlessness intra-abdominal pressure is zero, the diaphragm is passively tensed, and a residual small pleural pressure gradient may be present.

Posterior cricoarytenoid activity and glottic size during hyperpnea in humans.

We measured the electromyographic activity of the posterior cricoarytenoid (PCA) muscle simultaneously with glottic width (dg) in five normal human subjects during hyperpnea induced by hypoxia (7% CO2 in N2) or hypercapnia (9% CO2 in 50% O2). The glottic aperture was measured during inspiration at the time corresponding to peak inspiratory PCA activity and during expiration at the time corresponding to the minimum tonic activity. During hyperpnea, peak and tonic PCA activity increased simultaneously with widening of the vocal cords in both phases of the respiratory cycle. The PCA activity during both inspiration and expiration showed a single curvilinear relationship with dg of the form dg = A - Be-k.PCA (where A, B, and k are constants) in three of the five subjects. At 50% of maximum PCA activity, dg already reached 95% of its maximum value, which was less than that recorded during a voluntary forced expiratory maneuver. The single curvilinear relationship between PCA activity and dg could be due to the length-tension relationship of the PCA muscle and/or changes in its mechanical coupling, as well as simultaneous agonist and antagonist laryngeal muscle activity during progressive chemical stimulation. Also, further widening of the glottis during forced expiration suggests recruitment of additional muscles, e.g., the arytenoideus.

Oronasal partitioning of ventilation during exercise in humans.

The partitioning of oronasal breathing was studied in five normal subjects during progressive exercise. Subjects performed three to five identical runs, each consisting of four 1-min work periods at increments of 50 W. Nasal and oral airflow were measured simultaneously using a partitioned face mask both during and for 4 min after exercise. Total mean flows were the sum of nasal and oral flows. At a total mean inspiratory flow of 2 l/s, the nasal fraction of total flow was 0.36 +/- 0.04 (SE) and decreased by 6 +/- 3% between total flows of 1.5 and 2.5 l/s. Throughout exercise, the nasal fraction of total mean inspiratory flow did not differ from that of total expiratory flow and was similar to that of total mean inspiratory flow during the postexercise period at a corresponding total mean flow (both P greater than 0.02). The results show that oronasal flow partitioning is not directly due to the exercise itself but is related to the level of ventilation and is uninfluenced by the direction of upper airway flow (i.e., inspiratory vs. expiratory). These findings suggest tightly controlled modulation of the relative resistances of the oral and/or nasal pathways.

Regional distribution of blood flow within the diaphragm.

We investigated the regional distribution of blood flow (Q) within the costal and crural portions of the diaphragm in a total of eight anesthetized supine mongrel dogs. Q was measured with 15-microns microspheres, radiolabeled with three different isotopes, injected into the left ventricle during spontaneous breathing (SB), inspiratory resistive loading (IR), and mechanical ventilation after paralysis (P). At necropsy, the costal and crural portions of each hemidiaphragm were arbitrarily subdivided along a sagittal plane into five to seven and three sections, respectively. During P, there was a dorsoventral Q gradient within the costal part of the diaphragm. During SB there was a fourfold increase in the gradient of Q. Furthermore, during IR, in which mouth pressures of -16 +/- 4 cmH2O were generated, there was a further increase in the gradient of Q. During both SB and IR, Q to the most ventral portion of the costal diaphragm was 26 +/- 6% less than the peak value. In two dogs, studied prone and supine, there was no difference in the Q gradients between the two postures. Over the dorsal 80% of the costal diaphragm there was also a dorsoventral gradient of muscle thickness, such that the most dorsal part was 54 +/- 2% (n = 5) that of the ventral portion. In contrast, there was no consistent gradient of Q or muscle thickness within the crural diaphragm. Our results demonstrate a topographical gravity-independent distribution of Q in the costal, but not the crural, diaphragm.(ABSTRACT TRUNCATED AT 250 WORDS)

Relationship between alae nasi activation and breathing route during exercise in humans.

We studied the relationship between alae nasi muscle (AN) activation and breathing route in normal subjects during exercise. Nasal and oral airflow were measured simultaneously using a partitioned face mask and were recorded with the AN electromyogram. Subjects breathed via 1) the nose and mouth (NM) 2) the nose only (N), or 3) the mouth only (M). As ventilation (VE) rose progressively, the peak phasic inspiratory AN activity (IAAN) increased for all breathing routes. IAAN during N [11.8 +/- 2.0 arbitrary units (AU)] was greater than during NM (3.3 +/- 1.3 AU) and M (2.4 +/- 1.0 AU; P less than 0.01) measured at the highest common VE (over a 10-l/min range). At the highest 20% of IAAN recorded during NM, the total VE during N (24 +/- 5 l/min). However, for the same IAAN, nasal VE during NM (27 +/- 3 l/min) was similar to that during N. Thus, as ventilation increases during exercise, AN activity and nasal ventilation are tightly correlated, independently of flow through the mouth. This suggests either reflex modulation of AN activity by nasal flow or coordination of AN activation with the flow-partitioning mechanism of the upper airway.