Effect of lung volume on the respiratory action of the canine pectoral muscles

1992 ◽  
Vol 73 (6) ◽  
pp. 2408-2412 ◽  
Author(s):  
S. R. Muza ◽  
G. J. Criner ◽  
S. G. Kelsen
Keyword(s):  
Electrical Stimulation ◽  
Lung Volume ◽  
Intrathoracic Pressure ◽  
Pectoral Muscle ◽  
Positive Pressure ◽  
Rib Cage ◽  
Mechanical Coupling ◽  
Negative Intrathoracic Pressure ◽  
Pressure Changes ◽  
Stimulation Of

Lung volume influences the mechanical action of the primary inspiratory and expiratory muscles by affecting their precontraction length, alignment with the rib cage, and mechanical coupling to agonistic and antagonistic muscles. We have previously shown that the canine pectoral muscles exert an expiratory action on the rib cage when the forelimbs are at the torso's side and an inspiratory action when the forelimbs are held elevated. To determine the effect of lung volume on intrathoracic pressure changes produced by the canine pectoral muscles, we performed isolated bilateral supramaximal electrical stimulation of the deep pectoral and superficial pectoralis (descending and transverse heads) muscles in 15 adult supine anesthetized dogs during hyperventilation-induced apnea. Lung volume was altered by application of a negative or positive pressure (+/- 30 cmH2O) to the airway. In all animals, selective electrical stimulation of the descending, transverse, and deep pectoral muscles with the forelimbs held elevated produced negative intrathoracic pressure changes (i.e., an inspiratory action). Moreover, with the forelimbs elevated, increasing lung volume decreased both pectoral muscle fiber precontraction length and the negative intrathoracic pressure changes generated by contraction of each of these muscles. Conversely, with the forelimbs along the torso, increasing lung volume lengthened pectoral muscle precontraction length and augmented the positive intrathoracic pressure changes produced by muscle contraction (i.e., an expiratory action). These results indicate that lung volume significantly affects the length of the canine pectoral muscles and their mechanical actions on the rib cage.

Mechanical coupling of the rib cage, abdomen, and diaphragm through their area of apposition

1991 ◽  
Vol 70 (3) ◽  
pp. 1235-1244 ◽  
Author(s):  
B. R. Boynton ◽  
G. M. Barnas ◽  
J. T. Dadmun ◽  
J. J. Fredberg
Keyword(s):  
Chest Wall ◽  
Lung Volume ◽  
Abdominal Pressure ◽  
Rib Cage ◽  
Mechanical Coupling ◽  
Reported Data ◽  
Pressure Changes ◽  
Limiting Case ◽  
Point Of Departure ◽  
Very High

Although volumetric displacements of the chest wall are often analyzed in terms of two independent parallel pathways (rib cage and abdomen), Loring and Mead have argued that these pathways are not mechanically independent (J. Appl. Physiol. 53: 756-760, 1982). Because of its apposition with the diaphragm, the rib cage is exposed to two distinct pressure differences, one of which depends on abdominal pressure. Using the analysis of Loring and Mead as a point of departure, we developed a complementary analysis in which mechanical coupling of the rib cage, abdomen, and diaphragm is modeled by a linear translational transformer. This model has the advantage that it possesses a precise electrical analogue. Pressure differences and compartmental displacements are related by the transformation ratio (n), which is the mechanical advantage of abdominal over pleural pressure changes in displacing the rib cage. In the limiting case of very high lung volume, n----0 and the pathways uncouple. In the limit of very small lung volume, n----infinity and the pathways remain coupled; both rib cage and abdomen are driven by abdominal pressure alone, in accord with the Goldman-Mead hypothesis. A good fit was obtained between the model and the previously reported data for the human chest wall from 0.5 to 4 Hz (J. Appl. Physiol. 66:350-359, 1989). The model was then used to estimate rib cage, diaphragm, and abdominal elastance, resistance, and inertance. The abdomen was a high-elastance high-inertance highly damped compartment, and the rib cage a low-elastance low-inertance more lightly damped compartment. Our estimate that n = 1.9 is consistent with the findings of Loring and Mead and suggests substantial pathway coupling.

Hemodynamic effects of electrical stimulation of forebrain angiotensin and osmosensitive sites

1978 ◽  
Vol 235 (4) ◽  
pp. H445-H451 ◽  
Keyword(s):  
Blood Flow ◽  
Electrical Stimulation ◽  
Arterial Pressure ◽  
Median Eminence ◽  
Regional Blood Flow ◽  
Renal Hypertension ◽  
Brain Structures ◽  
Ventromedial Hypothalamus ◽  
Pressure Changes ◽  
Stimulation Of

Previous studies from this laboratory have indicated an important role for angiotensin-sensitive anteroventral third ventricular (AV3V) brain structures in normal regulation of arterial pressure and development of renal hypertension. The present experiments examined the effects of electrical stimulation of these periventricular areas on arterial pressure and regional blood flow in the anesthetized rat. Electrodes were placed in the AV3V region 3–10 days prior to acute studies. Blood flow was measured in extracorporeal blood flow circuits. Electrical stimulation produced only small changes in arterial pressure. Despite the small pressure changes, stimulation caused marked frequency-dependent alterations in regional blood flow. Renal and splanchnic flows were reduced while hindlimb flow was increased. Resistance changes were abolished by surgical denervation or ganglionic blockade but were unaffected by adrenalectomy. Hemodynamic responses to AV3V stimulation were abolished by a lesion in the area of the median eminence. It may be concluded that AV3V stimulation, through activation of pathways descending through the ventromedial hypothalamus-median eminence region, produces profound regional blood flow shifts without greatly altering arterial pressure.

Synergism between the canine left and right hemidiaphragms

2003 ◽  
Vol 94 (5) ◽  
pp. 1757-1765 ◽  
Author(s):  
André De Troyer ◽  
Matteo Cappello ◽  
Nathalie Meurant ◽  
Pierre Scillia
Keyword(s):  
Intrathoracic Pressure ◽  
Respiratory Drive ◽  
Additive Interaction ◽  
Quiet Breathing ◽  
Rib Cage ◽  
Radiographic Measurements ◽  
Airway Opening ◽  
Left And Right ◽  
The Right ◽  
Stimulation Of

Expansion of the lung during inspiration results from the coordinated contraction of the diaphragm and several groups of rib cage muscles, and we have previously shown that the changes in intrathoracic pressure generated by the latter are essentially additive. In the present studies, we have assessed the interaction between the right and left hemidiaphragms in anesthetized dogs by comparing the changes in airway opening pressure (ΔPao) obtained during simultaneous stimulation of the two phrenic nerves (measured ΔPao) to the sum of the ΔPao values produced by their separate stimulation (predicted ΔPao). The measured ΔPao was invariably greater than the predicted ΔPao, and the ratio between these two values increased gradually as the stimulation frequency was increased; the ratio was 1.10 ± 0.01 ( P < 0.05) for a frequency of 10 Hz, whereas for a frequency of 50 Hz it amounted to 1.49 ± 0.05 ( P < 0.001). This interaction remained unchanged after the rib cage was stiffened and its compliance was made linear, thus indicating that the load against which the diaphragm works is not a major determinant. However, radiographic measurements showed that stimulation of one phrenic nerve extends the inactive hemidiaphragm toward the sagittal midplane and reduces the caudal displacement of the central portion of the diaphragmatic dome. As a result, the volume swept by the contracting hemidiaphragm is smaller than the volume it displaces when the contralateral hemidiaphragm also contracts. These observations indicate that 1) the left and right hemidiaphragms have a synergistic, rather than additive, interaction on the lung; 2) this synergism operates already during quiet breathing and increases in magnitude when respiratory drive is greater; and 3) this synergism is primarily related to the configuration of the muscle.

Comparison of magnetic and electrical phrenic nerve stimulation in assessment of diaphragmatic contractility

1996 ◽  
Vol 80 (5) ◽  
pp. 1731-1742 ◽  
Author(s):  
F. Laghi ◽  
M. J. Harrison ◽  
M. J. Tobin
Keyword(s):  
Electrical Stimulation ◽  
Lung Volume ◽  
Magnetic Stimulation ◽  
Respiratory Muscle Fatigue ◽  
Rib Cage ◽  
Lung Capacity ◽  
Constant Degree ◽  
Human Volunteers ◽  
Phrenic Nerves ◽  
The Difference

Unlike the standard electrical approach, cervical magnetic stimulation of the phrenic nerves is less painful and achieves a constant degree of diaphragmatic recruitment, features that should enhance its applicability in a clinical setting. An unexplained phenomenon is the greater transdiaphragmatic twitch pressure (Pditw) with magnetic vs. electrical stimulation. We hypothesized that this greater Pditw is due to coactivation of extradiaphragmatic muscles. Because impedance to rib cage expansion is increased at high lung volumes and efficiency of extradiaphragmatic muscles is less than that of the diaphragm, we reasoned that the difference between electrical Pditw and magnetic Pditw would be less evident at high volumes than at end-expiratory lung volume. In human volunteers, magnetic Pditw and electrical Pditw were 37.7 +/- 1.9 (SE) and 32.3 +/- 2.2 cmH2O, respectively, at end-expiratory lung volume (P < 0.005) and 24.0 +/- 2.9 and 27.2 +/- 2.8 cmH2O, respectively, at one-half inspiratory capacity (not significant); at total lung capacity, magnetic Pditw was less than electrical Pditw (10.6 +/- 0.8 and 16.2 +/- 2.9 cmH2O, respectively; P < 0.05). Magnetic stimulation caused significant extradiaphragmatic muscle depolarization and rib cage expansion, whereas electrical stimulation caused virtually no extradiaphragmatic muscle depolarization and rib cage deflation. Despite these differences, the induction of respiratory muscle fatigue produced reductions in both electrical and magnetic Pditw values (P < 0.01), which were of similar magnitude and closely correlated (r = 0.96). In conclusion, magnetic stimulation recruits both extradiaphragmatic and diaphragmatic muscles, and it is equally as effective as electrical stimulation in detecting diaphragmatic fatigue.

Action of intercostal muscles on the lung in dogs

1991 ◽  
Vol 70 (6) ◽  
pp. 2388-2394 ◽  
Author(s):  
V. Ninane ◽  
M. Gorini ◽  
M. Estenne
Keyword(s):  
Lung Volume ◽  
Internal Layer ◽  
Airflow Rate ◽  
Intercostal Muscle ◽  
Similar Action ◽  
Rib Cage ◽  
Intercostal Muscles ◽  
Maximal Stimulation ◽  
Residual Capacity ◽  
Stimulation Of

The action on the lung of interosseous intercostal muscles located in the third and the seventh interspaces was studied in 15 anesthetized-curarized supine dogs. Changes in pleural pressure, airflow rate, and lung volume produced by maximal stimulation of both intercostal muscle layers were measured at and above functional residual capacity (FRC). In five animals measurements were also obtained during isolated stimulation of the internal layer. At FRC, intercostal stimulation in the upper interspaces had invariably an inspiratory effect on the lung but no effect was detectable in the lower interspaces. Qualitatively similar results were obtained during isolated stimulation of the internal layer. Increasing lung volume reduced the inspiratory action of the upper intercostals and conferred an expiratory action to the lower intercostals. These results indicate the following: 1) when contracting in a single interspace, the external and internal intercostals have a qualitatively similar action on the lung; and 2) this action, however, depends critically on their location along the cephalocaudal axis of the rib cage: in the upper portion of the rib cage, both muscle layers have an inspiratory effect at and above FRC; in the lower portion of the rib cage, they have no respiratory action at FRC and act in the expiratory direction at higher lung volumes.

Interaction of pulmonary afferents and pneumotaxic center in control of respiratory pattern in cats

1976 ◽  
Vol 39 (1) ◽  
pp. 31-44 ◽  
Author(s):  
J. L. Feldman ◽  
H. Gautier
Keyword(s):  
Electrical Stimulation ◽  
Lung Volume ◽  
Phrenic Nerve ◽  
Respiratory Pattern ◽  
Lung Inflation ◽  
Linear Relationships ◽  
Before And After ◽  
Pneumotaxic Center ◽  
Stimulation Of ◽  
Nerve Discharge

The interaction between the pulmonary afferents (PA) and the pneumotaxic center (PC) in control of respiratory pattern was studied in lightly anesthetized paralyzed cats before and after bivagotomy or lesions of the PC using inflations controlled by the onset or cessation of phrenic nerve discharge, i.e., cycle-triggered inflations. This interaction was also studied using electrical stimulation of the central stumps of cut vagi. Introduction of a delay between inspiratory onset and the commencement of an inflation at constant flow and duration resulted in increases of the durations of inspiration (T1) and expiration (TE) and amplitude of the integrated phrenic nerve discharge (A). The lung volume at inspiratory cutoff, i.e., the volume threshold, increased markedly as T1 increased. There were linear relationships between T1 and TE and between T1 and A. At constant alveolar CO2 and tidal volume, the quantitative effects of delay were dependent on the rate of inflation; i.e., when the flow increased, the volume threshold for a given T1 decreased. Bilateral vagotomy abolished the effects of delay and flow. PC lesions, which resulted in apneusis when the cycle-triggered inflations were stopped, produced the following changes compared to the delay effects seen in intact cats: a) the volume threshold for zero delay doubled and its rate of decrease with increased T1 was significantly smaller, and b) the change in TE for a given change in T1 was reduced markedly. Introduction of a delay between inspiratory onset and the start of electrical stimulation of the afferent vagi resulted in effects similar to those seen for delays in cycle-triggered inflations. The T1-TE relationship remained linear when the stimulus trains ended with inspiratory cessation. These results suggest that: a) the inspiratory cutoff mechanism is responsive to the rate, as well as the level, of lung inflation; b) all of the lung volume information affecting inspiratory cutoff in paralyzed cats is carried via the vagi; c) an intact PC is necessary for the generation of a normal time dependence of the volume threshold for inspiratory cutoff; d) the PC plays an important role in matching TE to T1 when the latter changes. For inflations and vagal stimulations applied during expiration, with introduction of a delay between inspiratory cessation and the start of cycle-triggered inflation or vagal stimulation, the results indicated that the expiratory cutoff mechanism has an irrevocable phase of 300-450 ms.

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