Search PubMed⌕ Search

Biomedical subjects

J R Rodarte

Publications and source records attributed to J R Rodarte.

At least 19 recordsLinked to original sources
PubMed1996

Lung mechanics during induced bronchoconstriction.

To elucidate differences in lung mechanics, we investigated the relative changes of partial forced expiratory flows at 50 and 30% of vital capacity, pulmonary resistance (RL), dynamic elastance (Edyn), and the effects of a deep inhalation (DI) on maximal flows, Edyn, and RL in eight asthmatic and eight normal individuals during bronchial challenges with methacholine, histamine, and ATP. RL was partitioned into inspiratory and expiratory resistance. Different constrictor agents did not induce specific patterns of response. For a given decrement of flow at 50 and 30% vital capacity, RL increased significantly more in normal than in asthmatic individuals. The ratio of inspiratory to expiratory RL was always < 1 at baseline but became > 1 in the majority of asthmatic and normal individuals when RL exceeded 12.2 +/- 0.9 cmH2O.1-1.s, suggesting that tidal inspiration may have induced transient bronchodilation in more constricted subjects. In asthmatic individuals, DI had a significantly smaller effect on flow but not on RL compared with normal individuals. The recovery of RL and Edyn after DI was faster than Edyn for both normal and asthmatic individuals. These findings are consistent with the idea that asthmatic individuals have a stronger peripheral response to agonists than normal individuals.

Adenosine Triphosphate↗
PubMed1996

Zone of apposition in the passive diaphragm of the dog.

We determined the regional area of the diaphragmatic zone of apposition (ZAP) as well as the regional craniocaudal extent of the ZAP (ZAPht) of the passive diaphragm in six paralyzed anesthetized beagle dogs (8-12 kg) at residual lung volume (RV), functional residual capacity (FRC), FRC + 0.25 and FRC + 0.5 inspiratory capacity, and total lung capacity (TLC) in prone and supine postures. To identify the caudal boundary of the ZAP, 17 lead markers (1 mm) were sutured to the abdominal side of the costal and crural diaphragms around the diaphragm insertion on the chest wall. Two weeks later, the dogs' caudal thoraces were scanned by the use of the dynamic spatial reconstructor (DSR), a prototype fast volumetric X-ray computer tomographic scanner, developed at the Mayo Clinic. The three-dimensional spatial coordinates of the markers were identified (+/- 1.4 mm), and the cranial boundary of the ZAP was determined from 30-40 1.4-mm-thick sagittal and coronal slices in each DSR image. We interpolated the DSR data to find the position of the cranial and caudal boundaries of the ZAP every 5 degrees around the thorax and computed the distribution of regional variation of area of the ZAP and ZAPht as well as the total area of ZAP. The ZAPht and area of ZAP increased as lung volume decreased and were largest near the lateral extremes of the rib cage. We measured the surface area of the rib cage cephaled to the ZAP (AL) in both postures in another six beagle dogs (12-16 kg) of similar stature, scanned previously in the DSR. We estimated the entire rib cage surface area (Arc = AZAP + AL). The AZAP as a percentage of Arc increased more than threefold as lung volume decreased from TLC to RV, from approximately 9 to 29% of Arc.

Anesthesia, General↗
PubMed1994

Displacements and strains in the costal diaphragm of the dog.

Radiopaque markers were attached at 1- to 2-cm intervals along three nearby muscle bundles to cover rectangular regions of the mid-costal diaphragms of seven dogs. The markers were tracked by biplane video fluoroscopy during spontaneous breathing (SB), mechanical ventilation with the same tidal volume (MV), and at inflation to total lung capacity (TLC) in the prone and supine positions. The three-dimensional positions of the markers at functional residual capacity (FRC), at end inspiration during SB and MV, and at TLC were determined, and the strains in the plane of the diaphragm relative to FRC were calculated. The principal strains were found to lie nearly along the muscle bundle direction and perpendicular to it. The principal strains along the muscle bundles, which describe muscle shortening, were uniform among the three bundles and uniform along the bundle for MV. For SB, in the prone and supine positions, shortening was approximately 30% greater in the middle of the bundle than near the central tendon and chest wall. Although the tidal volumes were the same for SB and MV, the shortening was larger for SB. The strains perpendicular to the bundle direction were not significantly different from zero. It appears that, for the loads that occur during tidal breathing, the diaphragm is inextensible in the direction perpendicular to the muscle direction. There is a very small displacement of the costal diaphragm at its insertion on the chest wall. The displacement at the central tendon is primarily a result of muscle shortening and rotation of the arc of the muscle around its insertion on the chest wall.

Animals↗
PubMed1994

Finite-element analysis of stress in the canine diaphragm.

Stress in the diaphragm, transdiaphragmatic pressure, and diaphragm shape are interrelated by a balance of forces. Using precise in vivo measurements of diaphragm shape and transdiaphragmatic pressure distribution in combination with finite-element analysis (ANSYS), we determined the direction and magnitude of stress in the passive diaphragm at relaxation volume. Lead spheres sutured along muscle bundles identified muscle bundle location and orientation in vivo. The x, y, and z coordinates of the lead spheres and entire surface of the diaphragm, excluding the zone of apposition, were determined to within 1.4 mm. Thin shell elements were used to construct a finite-element model of the diaphragm with a 2.1- to 4.2-mm internodal spacing. The diaphragm was assumed to have a uniform thickness of 2.5 mm, and magnitude and direction of the principal stresses were computed. The results show that 1) diaphragm stress is nonuniform and anisotropic (i.e., varies both with location on diaphragm surface and direction examined), 2) largest stress (sigma 1) is aligned with muscle bundles and is two to four times larger than sigma 2 (perpendicular to sigma 1 in diaphragm plane), and 3) stress along the muscle bundles is larger in vivo under conditions of biaxial stress than at same length in vitro under uniaxial stress. Although diaphragm stress and tension have often been assumed to be uniform, our finding that stress is oriented primarily along the muscle fibers should be considered in future models of the diaphragm.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Inferences on passive diaphragm mechanics from gross anatomy.

The diaphragm is a relatively thin curved structure that is categorized in mechanics as a membrane. Tension in the membrane is given by the product of muscle thickness and stress parallel to the fiber bundles. If all muscle fibers were cylindrical and extended from origin to insertion, the ratio of thickness near the chest wall (CW) to thickness near the central tendon (CT) would vary inversely with the ratio of CW to CT perimeters. In freshly excised diaphragms of 36 mongrel dogs, the ratios of the perimeters (CT/CW) in the right and left costal diaphragm were 0.63 +/- 0.04 and 0.62 +/- 0.04, respectively. The means of the ratio of thickness near CW to that near CT in the right and left costal regions were 0.96 +/- 0.07 and 0.95 +/- 0.05, respectively, consistent with a nearly constant relationship between costal diaphragm membrane tension and muscle stress in the direction of the fibers. In the crural diaphragm, the average ratio of the perimeters of the insertions on CT to CW was 1.16 +/- 0.10. The average ratio of thickness of crural CW to CT was 1.25 +/- 0.11. The discrepancy between the perimeter ratio and thickness ratio in the costal diaphragm is incompatible with the muscle consisting of uniform fibers extending from CW to CT. Our data suggest that muscle fibers are either in series with a smaller number along the smaller perimeter or that they terminate by tapering within the muscle bundle. Both arrangements are consistent with previous anatomic studies (Gordon et al. J. Morphol. 201: 131-143, 1989). Having a nonuniform number of fibers mechanically in series is compatible with uniform stress in the fibers if the membrane is sufficiently curved as in a domed structure.

Animals↗
PubMed1993

Estimation of ventilatory capacity during submaximal exercise.

There is presently no precise way to determine ventilatory capacity for a given individual during exercise; however, this information would be helpful in evaluating ventilatory reserve during exercise. Using schematic representations of maximal expiratory flow-volume curves and individual maximal expiratory flow-volume curves from four subjects, we describe a technique for estimating ventilatory capacity. In these subjects, we measured maximal expiratory flow-volume loops at rest and tidal flow-volume loops and inspiratory capacity (IC) during submaximal cycle ergometry. We also compared minute ventilation (VE) during submaximal exercise with calculated ventilatory maxima (VEmaxCal) and with maximal voluntary ventilation (MVV) to estimate ventilatory reserve. Using the schematic flow-volume curves, we demonstrated the theoretical effect of maximal expiratory flow and lung volume on ventilatory capacity and breathing pattern. In the subjects, we observed that the estimation of ventilatory reserve with use of VE/VEmaxCal was most helpful in indicating when subjects were approaching maximal expiratory flow over a large portion of tidal volume, especially at submaximal exercise levels where VE/VEmaxCal and VE/MVV differed the most. These data suggest that this technique may be useful in estimating ventilatory capacity, which could then be used to evaluate ventilatory reserve during exercise.

Adult↗
PubMed1993

Expiratory flow limitation and regulation of end-expiratory lung volume during exercise.

To investigate the impact of expiratory flow limitation (FL) on breathing pattern and end-expiratory lung volume (EELV), we imposed a small expiratory threshold load for a few breaths during exercise in nine volunteers (29-62 yr): six were healthy and three had mild-to-moderate airflow obstruction (67-71% predicted forced expiratory volume in 1 s). Six subjects showed evidence of FL, i.e., tidal expiratory flow impinging on maximal forced expiratory flow, at one or more exercise levels. Whenever an expiratory threshold load was imposed, mean expiratory flow decreased (P < 0.02) in association with an increased expiratory time (TE; P < 0.05). When the load was imposed during non-FL conditions, TE increased less than expiratory flow decreased and EELV tended to increase. In contrast, during FL, with the load, TE increased more than expiratory flow decreased, subjects did not achieve maximal expiratory flow until a lower volume, and EELV decreased (P < 0.001). Under both FL and no-FL conditions, unloading reversed the changes associated with loading. These data indicate that the increase in EELV during exercise is linked to the occurrence of FL. We suggest that compression of airways downstream from the flow-limiting segment may elicit a reflex mechanism that influences breathing pattern by terminating expiration prematurely, thus increasing EELV.

Adult↗
PubMed1993

Costal diaphragm curvature in the dog.

The curvature of the midcostal region of the diaphragm in seven dogs was determined at functional residual capacity (FRC) and end inspiration during spontaneous breathing and mechanical ventilation and at total lung capacity in the prone and supine positions. Metallic markers were attached to muscle fibers on the abdominal surface of the diaphragm, and the dog was allowed to recover from surgery. The three-dimensional positions of the markers were determined by biplane videofluoroscopy. A quadratic surface was fit to the bead positions. The principal axes of the quadratic surface lie nearly along and perpendicular to the muscle fibers. In both the supine and prone positions, the values of the principal curvatures were similar at FRC and end inspiration during spontaneous breathing, when muscle tension and transdiaphragmatic pressure both increase with increasing lung volume, and during mechanical ventilation and passive inflation to total lung capacity, when both decrease relative to their magnitude at FRC. No abrupt change of curvature, which might be expected at the edge of the zone of apposition, was apparent. The curvature along the muscle fiber was 0.35 +/- 0.07 cm-1; the curvature perpendicular to the muscle fiber was much smaller, 0.06 +/- 0.01 cm-1. The costal region of the diaphragm displaces and shortens as lung volume increases, but its shape, as described by its curvatures, does not change substantially.

Animals↗
PubMed1993

Expiratory airflow limitation and hyperinflation during methacholine-induced bronchoconstriction.

To investigate the role of airflow limitation on the increase of end-expiratory lung volume (EELV) during bronchoconstriction, nine stable asthmatic subjects and seven healthy subjects were challenged with inhaled methacholine (MCh). Changes in airway caliber were assessed by using forced expiratory volume in 1 s, partial forced expiratory flow at 50% of control forced vital capacity, and specific airway conductance. To detect airflow limitation, tidal flow-volume curves were superimposed on partial forced flow-volume curves at absolute lung volume. The electromyogram of the diaphragm was recorded by surface electrodes in four asthmatic and four healthy subjects, and the electrical diaphragmatic activity (DIA) during expiration was expressed as a percentage of the duration of expiratory time. In 10 subjects (9 asthmatic and 1 healthy) the partial forced expiratory flow recorded after some MCh dose impinged on tidal expiratory flow recorded before MCh. When this occurred it was associated with an increase in EELV by 0.54 +/- 0.07 (SE) liter (P < 0.001), which was larger than that occurring when lower MCh doses (0.11 +/- 0.04 liter, P < 0.05) were used, and with a moderate increase in DIA of 15 +/- 2.5% (P < 0.01). Six healthy subjects did not increase EELV after MCh despite a significant degree of bronchoconstriction; in these subjects tidal expiratory flow never impinged on forced expiratory flow, and DIA never increased. These results suggest that hyperinflation during MCh-induced bronchoconstriction is triggered by dynamic compression of the airways and is associated with moderate increase of DIA during expiration.

Adolescent↗
PubMed1992

Changes in functional residual capacity and regional diaphragm lengths after upper abdominal surgery in anesthetized dogs.

The respiratory performance of the diaphragm may be altered by changes in mechanical or neural factors, or both, induced by upper abdominal surgery. We conducted this study to examine the effects of upper abdominal surgery on postoperative respiratory function. We studied resting lengths of four diaphragm regions, three in the costal and one in the crural diaphragm, with biplane video-roentgenography in six dogs immediately after upper abdominal surgery and up to 30 days postoperatively. Functional residual capacity was 16.7% smaller immediately after surgery compared with values obtained in the same animals after 30 days. Simultaneously measured resting lengths of each of the diaphragm regions immediately after surgery were longer, on average by 8.3%, than 30 days postoperatively. During the postoperative course, resting diaphragm lengths gradually and uniformly decreased as functional residual capacity increased. Phrenic nerve stimulation in four other dogs immediately after identical surgery resulted in large diaphragm shortening (from 42% to 55%), indicating that neither the diaphragm nor phrenic nerves were injured by the surgical manipulation. We hypothesize that respiratory dysfunction after upper abdominal surgery may be, at least in part, attributed to a decreased central drive for breathing caused by activation of the afferent limb of an inhibitory reflex owing to stretching of the diaphragm.

Abdomen↗
PubMed1992

Exercise capacity and breathing mechanics in patients with airflow limitation.

To investigate the impact of expiratory airflow limitation on ventilation during exercise, we studied six control subjects with normal lung function (FEV1/FVC = 79 +/- 6%) and eight patients with borderline-to-mild airflow limitation (FEV1/FVC = 68 +/- 4%) during cycle ergometry. VO2, HR, and VE/MVV were not different between the control subjects or patients during maximal or submaximal exercise. In contrast, five of the eight patients achieved maximal expiratory flow over a large portion (37%) of their tidal volume (VT) during submaximal exercise, whereas none of the control subjects achieved maximal expiratory flow. To estimate the fraction of expiratory capacity used by the control subjects and the patients, we calculated a mechanical ventilatory maximum (VEmaxCal) for each level of exercise using the individual's VT, end-expiratory lung volume (EELV), and maximal expiratory flow-volume curve. The patients used a greater fraction of their VEmaxCal at each level of submaximal exercise (P less than 0.03). Despite the flow limitation during submaximal exercise, EELV was similar between the control subjects and patients. In conclusion, even patients with borderline-to-mild airflow limitation achieve maximal expiratory flow during submaximal exercise and these restrictions are not reflected by VE/MVV nor by EELV.

Exercise↗
PubMed1991

Effect of mild-to-moderate airflow limitation on exercise capacity.

To determine the effect of mild-to-moderate airflow limitation on exercise tolerance and end-expiratory lung volume (EELV), we studied 9 control subjects with normal pulmonary function [forced expired volume in 1 s (FEV1) 105% pred; % of forced vital capacity expired in 1 s (FEV1/FVC%) 81] and 12 patients with mild-to-moderate airflow limitation (FEV1 72% pred; FEV1/FVC % 58) during progressive cycle ergometry. Maximal exercise capacity was reduced in patients [69% of pred maximal O2 uptake (VO2max)] compared with controls (104% pred VO2max, P less than 0.01); however, maximal expired minute ventilation-to-maximum voluntary ventilation ratio and maximal heart rate were not significantly different between controls and patients. Overall, there was a close relationship between VO2max and FEV1 (r2 = 0.62). Resting EELV was similar between controls and patients [53% of total lung capacity (TLC)], but at maximal exercise the controls decreased EELV to 45% of TLC (P less than 0.01), whereas the patients increased EELV to 58% of TLC (P less than 0.05). Overall, EELV was significantly correlated to both VO2max (r = -0.71, P less than 0.001) and FEV1 (r = -0.68, P less than 0.001). This relationship suggests a ventilatory influence on exercise capacity; however, the increased EELV and associated pleural pressures could influence cardiovascular function during exercise. We suggest that the increase in EELV should be considered a response reflective of the effect of airflow limitation on the ventilatory response to exercise.

Exercise↗
PubMed1991

Lung volumes during low-intensity steady-state cycling.

The use of inspiratory capacity (IC) to estimate end-expiratory lung volume (EELV) during exercise has been questioned because of the assumption of constant total lung capacity (TLC). To investigate lung volumes during low-intensity steady-state cycling, we measured EELV by the open-circuit N2 washout method (MR-1, currently Sensormedics 2100) in eight healthy men while at rest and during unloaded and 60-W cycling. TLC was calculated by adding EELV and IC. Measurement variation of TLC was 142 ml at rest, 121 ml during unloaded cycling, and 158 ml during 60-W cycling. TLC did not differ significantly among the three conditions studied. EELV decreased during unloaded (P less than 0.002) and 60-W cycling (P less than 0.001) compared with rest. End-inspiratory lung volume increased only during 60-W cycling (P = 0.03). The decrease in EELV accounted for 100% of the increase in tidal volume during unloaded cycling. Although minute ventilation was similar in the subjects during unloaded cycling, we noted that breathing patterns varied among the subjects. The increase in respiratory frequency was negatively correlated to the change in tidal volume (R2 = 0.54, P = 0.038) and to the change in end-inspiratory lung volume (R2 = 0.68, P = 0.012). We conclude that TLC does not differ significantly during low-intensity steady-state cycling and that use of IC to estimate changes in EELV is appropriate.

Adult↗
PubMed1991

Pleural pressure distribution and its relationship to lung volume and interstitial pressure.

The mechanics of the pleural space has long been controversial. We summarize recent research pertaining to pleural mechanics within the following conceptual framework, which is still not universally accepted. Pleural pressure, the force acting to inflate the lung within the thorax, is generated by the opposing elastic recoils of the lung and chest wall and the forces generated by respiratory muscles. The spatial variation of pleural pressure is a result of complex force interactions among the lung and other structures that make up the thorax. Gravity contributes one of the forces that act on these structures, and regional lung expansion and pleural pressure distribution change with changes in body orientation. Forces are transmitted directly between the chest wall and the lung through a very thin but continuous pleural liquid space. The pressure in pleural liquid equals the pressure acting to expand the lung. Pleural liquid is not in hydrostatic equilibrium, and viscous flow of pleural liquid is driven by the combined effect of the gravitational force acting on the liquid and the pressure distribution imposed by the surrounding structures. The dynamics of pleural liquid are considered an integral part of a continual microvascular filtration into the pleural space. Similar concepts apply to the pulmonary interstitium. Regional differences in lung volume expansion also result in regional differences in interstitial pressure within the lung parenchyma and thus affect regional lung fluid filtration.

Body Fluids↗