Mechanics of the canine diaphragm in ascites: a CT study

2008 ◽  
Vol 104 (2) ◽  
pp. 423-428 ◽  
Author(s):  
Dimitri Leduc ◽  
Matteo Cappello ◽  
Pierre Alain Gevenois ◽  
André De Troyer
Keyword(s):  
Nerve Stimulation ◽  
Phrenic Nerve ◽  
Three Dimensional ◽  
Muscle Length ◽  
Phrenic Nerve Stimulation ◽  
Additional Increase ◽  
Transdiaphragmatic Pressure ◽  
Computed Tomographic ◽  
Muscle Shortening ◽  
Radiopaque Markers

Ascites causes an increase in the elastance of the abdomen and impairs the lung-expanding action of the diaphragm, but its overall effects on the pressure-generating ability of the muscle remain unclear. In the present study, radiopaque markers were attached to muscle bundles in the midcostal region of the diaphragm in five dogs, and the three-dimensional locations of the markers during relaxation and during phrenic nerve stimulation in the presence of increasing amounts of ascites were determined using a computed tomographic scanner. From these data, accurate measurements of muscle length and quantitative estimates of diaphragm curvature were obtained, and the changes in transdiaphragmatic pressure (Pdi) were analyzed as functions of muscle length and curvature. With increasing ascites, the resting length of the diaphragm increased progressively. In addition, the amount of muscle shortening during phrenic nerve stimulation decreased gradually. When ascites was 100 ml/kg body wt, therefore, the muscle during contraction was longer, leading to a 20–25% increase in Pdi. As ascites increased further to 200 ml/kg, however, muscle length during contraction continued to increase, but Pdi did not. This absence of additional increase in Pdi was well explained by the increase in the diameter of the ring of insertion of the diaphragm to the rib cage and the concomitant increase in the radius of diaphragm curvature. These observations indicate that the pressure-generating ability of the diaphragm is determined not only by muscle length as conventionally thought but also by muscle shape.

scholarly journals Diaphragm curvature modulates the relationship between muscle shortening and volume displacement

2011 ◽  
Vol 301 (1) ◽  
pp. R76-R82 ◽  
Author(s):  
Brad J. Greybeck ◽  
Matthew Wettergreen ◽  
Rolf D. Hubmayr ◽  
Aladin M. Boriek
Keyword(s):  
Nerve Stimulation ◽  
Phrenic Nerve ◽  
Spontaneous Breathing ◽  
Three Dimensional ◽  
Diaphragm Muscle ◽  
Phrenic Nerve Stimulation ◽  
Lung Volumes ◽  
Muscle Shortening ◽  
Residual Capacity ◽  
The Relationship

During physiological spontaneous breathing maneuvers, the diaphragm displaces volume while maintaining curvature. However, with maximal diaphragm activation, curvature decreases sharply. We tested the hypotheses that the relationship between diaphragm muscle shortening and volume displacement (VD) is nonlinear and that curvature is a determinant of such a relationship. Radiopaque markers were surgically placed on three neighboring muscle fibers in the midcostal region of the diaphragm in six dogs. The three-dimensional locations were determined using biplanar fluoroscopy and diaphragm VD, curvature, and muscle shortening were computed in the prone and supine postures during spontaneous breathing (SB), spontaneous inspiration efforts after airway occlusion at lung volumes ranging from functional residual capacity (FRC) to total lung capacity, and during bilateral maximal phrenic nerve stimulation at those same lung volumes. In supine dogs, diaphragm VD was approximately two- to three-fold greater during maximal phrenic nerve stimulation than during SB. The contribution of muscle shortening to VD nonlinearly increases with level of diaphragm activation independent of posture. During submaximal diaphragm activation, the contribution is essentially linear due to constancy of diaphragm curvature in both the prone and supine posture. However, the sudden loss of curvature during maximal bilateral phrenic nerve stimulation at muscle shortening values greater than 40% (ΔL/LFRC) causes a nonlinear increase in the contribution of muscle shortening to diaphragm VD, which is concomitant with a nonlinear change in diaphragm curvature. We conclude that the nonlinear relationship between diaphragm muscle shortening and its VD is, in part, due to a loss of its curvature at extreme muscle shortening.

scholarly journals Length and curvature of the dog diaphragm

2006 ◽  
Vol 101 (3) ◽  
pp. 794-798 ◽  
Author(s):  
Aladin M. Boriek ◽  
Ben Black ◽  
Rolf Hubmayr ◽  
Theodore A. Wilson
Keyword(s):  
Nerve Stimulation ◽  
Phrenic Nerve ◽  
Muscle Length ◽  
Lung Compliance ◽  
Chronic Obstructive ◽  
Phrenic Nerve Stimulation ◽  
Lung Volumes ◽  
Obstructive Pulmonary Disease ◽  
Transdiaphragmatic Pressure ◽  
Residual Capacity

Transdiaphragmatic pressure is a result of both tension in the muscles of the diaphragm and curvature of the muscles. As lung volume increases, the pressure-generating capability of the diaphragm decreases. Whether decrease in curvature contributes to the loss in transdiaphragmatic pressure and, if so, under what conditions it contributes are unknown. Here we report data on muscle length and curvature in the supine dog. Radiopaque markers were attached along muscle bundles in the midcostal region of the diaphragm in six beagle dogs of ∼8 kg, and marker locations were obtained from biplanar images at functional residual capacity (FRC), during spontaneous inspiratory efforts against a closed airway at lung volumes from FRC to total lung capacity, and during bilateral maximal phrenic nerve stimulation at the same lung volumes. Muscle length and curvature were obtained from these data. During spontaneous inspiratory efforts, muscle shortened by 15–40% of length at FRC, but curvature remained unchanged. During phrenic nerve stimulation, muscle shortened by 30 to nearly 50%, and, for shortening exceeding 52%, curvature appeared to decrease sharply. We conclude that diaphragm curvature is nearly constant during spontaneous breathing maneuvers in normal animals. However, we speculate that it is possible, if lung compliance were increased and the chest wall and the diameter of the diaphragm ring of insertion were enlarged, as in the case of chronic obstructive pulmonary disease, that decrease in diaphragm curvature could contribute to loss of diaphragm function.

Role of the mediastinum in the mechanics of the canine diaphragm

2010 ◽  
Vol 109 (1) ◽  
pp. 27-34 ◽  
Author(s):  
André De Troyer ◽  
Matteo Cappello ◽  
Dimitri Leduc ◽  
Pierre Alain Gevenois
Keyword(s):  
Nerve Stimulation ◽  
Phrenic Nerve ◽  
Three Dimensional ◽  
Vena Cava ◽  
Muscle Length ◽  
Phrenic Nerve Stimulation ◽  
Lung Volumes ◽  
Airway Opening ◽  
Generating Capacity

The objective of this study was to evaluate the role of the mediastinum in the mechanics of the canine diaphragm. Two sets of experiments were performed. In the first experiment on five animals, the mediastinum was severed from the sternum to the vena cava, and radiopaque markers were attached to muscle bundles in the midcostal region of the diaphragm. The three-dimensional location of the markers during relaxation at different lung volumes and during phrenic nerve stimulation at the same lung volumes was then measured using computed tomography. From these data, accurate measurements of muscle displacement and muscle length were obtained, and these measurements, together with the changes in airway opening pressure, were compared with those previously obtained in animals with an intact mediastinum. Severing the mediastinum per se appeared to have no influence on the pressure-generating capacity of the diaphragm or on the lung-volume dependence of this capacity. The great vessels and the esophagus in these animals, however, were left intact, so the possibility remained that these structures continued to impact on the diaphragm through their close attachments to the muscle. In the second experiment, therefore, loads were applied caudally to the central tendon to assess the force-displacement relationship of the entire mediastinum, and this relationship, combined with the known displacement of the diaphragm dome during phrenic nerve stimulation, was used to infer the force exerted by the mediastinum on the muscle during contraction. The results showed that this force is small compared with that developed by the diaphragm, except at very high lung volumes. It is concluded, therefore, that the mediastinum has only little influence on the mechanics of the canine diaphragm.

Effect of digitalis on the diaphragm in anesthetized dogs

1987 ◽  
Vol 63 (1) ◽  
pp. 277-284 ◽  
Author(s):  
Y. Kikuchi ◽  
W. Hida ◽  
C. Shindoh ◽  
T. Chonan ◽  
H. Miki ◽  
...  
Keyword(s):  
Nerve Stimulation ◽  
Phrenic Nerve ◽  
Stimulus Frequency ◽  
Dependent Manner ◽  
Phrenic Nerve Stimulation ◽  
Transdiaphragmatic Pressure ◽  
Mechanically Ventilated ◽  
Before And After ◽  
Residual Capacity ◽  
Anesthetized Dogs

We examined the effect of digitalis on diaphragmatic contractility and fatigability in 19 anesthetized mechanically ventilated dogs. The diaphragmatic force was assessed from transdiaphragmatic pressure (Pdi) developed at functional residual capacity against an occluded airway during cervical phrenic nerve stimulation. In a first group of five dogs, Pdi-stimulus frequency relationships were compared before and after administration of ouabain in doses of 0.01, 0.02, and 0.04 mg/kg. In a second group, diaphragmatic fatigue was produced by bilateral phrenic nerve stimulation at 30 Hz. Ten seconds of stimulation and 15 s of mechanical ventilation were repeated for 30 min. The rates of decrease in Pdi were compared between two groups, one of 0.05 mg/kg deslanoside-treated dogs (n = 7) and one of nontreated dogs (n = 7). After ouabain administration Pdi was significantly greater at each frequency in a dose-dependent manner. On the other hand, the rate of decrease in Pdi in the deslanoside group was significantly smaller than that in the nontreated group, whereas deslanoside did not greatly change the Pdi-frequency curves in fresh diaphragm. We conclude that ouabain improves contractility of the fresh diaphragm and that deslanoside has a protective effect against fatigability.

Arterial CO2 partial pressure affects diaphragmatic function

1985 ◽  
Vol 58 (3) ◽  
pp. 823-829 ◽  
Author(s):  
J. Y. Schnader ◽  
G. Juan ◽  
S. Howell ◽  
R. Fitzgerald ◽  
C. Roussos
Keyword(s):  
Partial Pressure ◽  
Nerve Stimulation ◽  
Phrenic Nerve ◽  
Phrenic Nerve Stimulation ◽  
Transdiaphragmatic Pressure ◽  
Arterial Pco2 ◽  
Co2 Partial Pressure ◽  
Diaphragmatic Function ◽  
Plaster Casts

The purpose of this study was to examine in an in vivo preparation acute variations of PCO2 on diaphragmatic contractility. Plaster casts were snugly fit around the abdomen of six open-chested dogs, moving the abdominal contents rostrally. Diaphragmatic contractions against this very fixed load in response to phrenic nerve stimulation (supramaximal voltage at 1, 20, 50, and 80 Hz) or during spontaneous inspiratory efforts were virtually isometric (quasi-isometric). Transdiaphragmatic pressure (Pdi) measured by an abdominal balloon was used as an index of diaphragmatic contractility. Arterial PCO2 (PaCO2) was reduced by hyperventilation and raised by increasing PICO2. Pdi values in response to stimulation at 1, 20, 50, and 80 Hz in ranges I (PaCO2 = 0–19 Torr) and II (PaCO2 = 20–34 Torr) did not differ statistically from the control Pdi values (range III; PaCO2 = 35–45 Torr). In range IV (PaCO2 = 46–70 Torr) Pdi values for stimulations of 20, 50, and 80 Hz were significantly lower than control. In range V (PaCO2 = 71–90 Torr), VI (PaCO2 = 91–101 Torr), and VII (PaCO2 greater than or equal to 102 Torr) Pdi values were significantly less than those in range IV at all frequencies of stimulation. In the four dogs measured during spontaneous inspiratory efforts the integrated diaphragmatic electromyogram (Edi) was correlated with the Pdi. As PaCO2 rose (range III to VII), the Pdi values observed at 25, 50, 75, 100% of the maximum Edi (of range III) were significantly lower than the Pdi value of range III.(

Effect of lung volume on in vivo contraction characteristics of human diaphragm

1987 ◽  
Vol 62 (5) ◽  
pp. 1893-1900 ◽  
Author(s):  
J. Smith ◽  
F. Bellemare
Keyword(s):  
Nerve Stimulation ◽  
Lung Volume ◽  
Phrenic Nerve ◽  
Pleural Pressure ◽  
Normal Male ◽  
Contraction Time ◽  
Phrenic Nerve Stimulation ◽  
Transdiaphragmatic Pressure ◽  
Gastric Pressure

We performed transcutaneous bilateral phrenic nerve stimulation at varying lung volumes between residual volume (RV) and total lung capacity (TLC) in six normal male volunteers. Peak twitch transdiaphragmatic pressure declined from 49.1 +/- 9.1 (SD) cmH2O at RV to 19.6 +/- 5.97 (SD) cmH2O at TLC. Twitch contraction time fell from 91.8 +/- 11.3 (SD) ms at RV to 57.7 +/- 7.4 (SD) ms at TLC. There was a good correlation between changes in contraction time and transdiaphragmatic pressure (r = 0.7). The fall in transdiaphragmatic pressure was almost all due to a fall in pleural pressure, with little change in gastric pressure between RV and TLC. At TLC the pleural pressure in response to phrenic nerve stimulation was -0.58 cmH2O. We conclude that, as lung volume increases and the diaphragm shortens, it becomes less effective as a pressure generator and that pressure it generates is less well converted into useful inspiratory pressure. At a lung volume close to TLC, the diaphragm ceases to act as an inspiratory muscle.

Diaphragmatic pressures: transvenous vs. direct phrenic nerve stimulation

1985 ◽  
Vol 59 (1) ◽  
pp. 269-273 ◽  
Author(s):  
R. F. Planas ◽  
R. H. McBrayer ◽  
P. A. Koen
Keyword(s):  
Analysis Of Variance ◽  
Respiratory System ◽  
Functional Residual Capacity ◽  
Nerve Stimulation ◽  
Phrenic Nerve ◽  
Phrenic Nerve Stimulation ◽  
Transdiaphragmatic Pressure ◽  
Residual Capacity ◽  
Anesthetized Dogs

Diaphragmatic force, determined by stimulating the phrenic nerve while simultaneously measuring the pressures in a closed respiratory system, was assessed in five anesthetized dogs over a 5-h period to evaluate the inherent variability of this technique. Transdiaphragmatic pressure (Pdi) was measured at functional residual capacity during stimulation (120 Hz, 0.2-ms duration) of one phrenic nerve by either direct phrenic nerve stimulation (DPNS) or transvenous phrenic nerve stimulation (TPNS). An analysis of variance showed no significant (P greater than 0.50) change during the 5-h period. There was a significant correlation (r = 0.94, P less than 0.001) between Pdi obtained by TPNS and that obtained by DPNS. It is concluded that either DPNS or TPNS can be used to evaluate diaphragmatic strength over a 5-h period and that TPNS can be used in lieu of DPNS.

Effect of separate hemidiaphragm contraction on left phrenic artery flow and O2 consumption

1990 ◽  
Vol 69 (1) ◽  
pp. 86-90 ◽  
Author(s):  
F. Hu ◽  
A. Comtois ◽  
E. Shadram ◽  
A. Grassino
Keyword(s):  
Blood Flow ◽  
Nerve Stimulation ◽  
Phrenic Nerve ◽  
Arterial Blood Flow ◽  
O2 Consumption ◽  
Phrenic Nerve Stimulation ◽  
Diaphragm Pacing ◽  
Transdiaphragmatic Pressure ◽  
Arterial Blood ◽  
Significant Difference

Phrenic arterial blood flow has been shown to increase during bilateral phrenic nerve stimulation (BPNS). However, the role of unilateral phrenic nerve stimulation [left (LPNS) or right (RPNS)] on the blood flow and O2 consumption of the contralateral hemidiaphragm is not known and is explored here. In six anesthetized, mechanically hyperventilated dogs, left phrenic arterial blood flow (Qlpha) was measured (Doppler technique). Supramaximal (10 V, 30 Hz, 0.25-ms duration) LPNS, RPNS, and BPNS at a pacing frequency 15/min and duty cycle of 0.50 were delivered in separate runs. Left hemidiaphragmatic blood samples for gas analyses were obtained by left phrenic venous cannulation. During RPNS, Qlpha and left hemidiaphragmatic O2 consumption (VO2ldi) did not change significantly compared with control. During LPNS and BPNS, there was a significant increase in Qlpha and VO2ldi (P less than 0.01). There was no significant difference in Qlpha and VO2ldi between LPNS and BPNS (P greater than 0.05). We conclude 1) that there is a complete independence of left-right hemidiaphragmatic circulation both at rest and during diaphragm pacing and 2) that during unilateral stimulation transdiaphragmatic pressure is not related to diaphragmatic blood flow.

Mechanism of the lung-deflating action of the canine diaphragm at extreme lung inflation

2012 ◽  
Vol 112 (8) ◽  
pp. 1311-1316 ◽  
Author(s):  
Dimitri Leduc ◽  
Matteo Cappello ◽  
Pierre Alain Gevenois ◽  
André De Troyer
Keyword(s):  
Nerve Stimulation ◽  
Phrenic Nerve ◽  
Pleural Pressure ◽  
Phrenic Nerve Stimulation ◽  
Lung Volumes ◽  
Lung Inflation ◽  
Lower Lung ◽  
Airway Opening ◽  
Radiopaque Markers ◽  
Phrenic Nerves

When lung volume in animals is passively increased beyond total lung capacity (TLC; transrespiratory pressure = +30 cmH2O), stimulation of the phrenic nerves causes a rise, rather than a fall, in pleural pressure. It has been suggested that this was the result of inward displacement of the lower ribs, but the mechanism is uncertain. In the present study, radiopaque markers were attached to muscle bundles in the midcostal region of the diaphragm and to the tenth rib pair in five dogs, and computed tomography was used to measure the displacement, length, and configuration of the muscle and the displacement of the lower ribs during relaxation at seven different lung volumes up to +60 cmH2O transrespiratory pressure and during phrenic nerve stimulation at the same lung volumes. The data showed that 1) during phrenic nerve stimulation at 60 cmH2O, airway opening pressure increased by 1.5 ± 0.7 cmH2O; 2) the dome of the diaphragm and the lower ribs were essentially stationary during such stimulation, but the muscle fibers still shortened significantly; 3) with passive inflation beyond TLC, an area with a cranial concavity appeared at the periphery of the costal portion of the diaphragm, forming a groove along the ventral third of the rib cage; and 4) this area decreased markedly in size or disappeared during phrenic stimulation. It is concluded that the lung-deflating action of the isolated diaphragm beyond TLC is primarily related to the invaginations in the muscle caused by the acute margins of the lower lung lobes. These findings also suggest that the inspiratory inward displacement of the lower ribs commonly observed in patients with emphysema (Hoover's sign) requires not only a marked hyperinflation but also a large fall in pleural pressure.

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