Asymmetrical action of the canine diaphragm after single-lung inflation

2011 ◽  
Vol 110 (6) ◽  
pp. 1519-1525 ◽  
Author(s):  
André De Troyer ◽  
Dimitri Leduc ◽  
Pierre Alain Gevenois ◽  
Matteo Cappello

Single-lung transplantation (SLT) in patients with emphysema leads to a cranial displacement of the diaphragm on the transplanted side and a shift of the mediastinum toward the transplanted lung. The objective of the present study was to assess the effect of unilateral lung inflation on the mechanics of the diaphragm. Two endotracheal tubes were inserted in the two main stem bronchi of six anesthetized dogs, and radiopaque markers were attached along muscle fibers in the midcostal region of the two halves of the diaphragm. The animals were then placed in a computed tomographic scanner, the left or the right lung was passively inflated, and the phrenic nerves were stimulated while the two endobronchial tubes were occluded. As lung volume increased, the fall in airway opening pressure (ΔPao) in the inflated lung during stimulation decreased markedly, whereas ΔPao in the noninflated lung decreased only moderately ( P < 0.001). Also, the two hemidiaphragms shortened both during relaxation and during phrenic stimulation, but the ipsilateral hemidiaphragm was consistently shorter than the contralateral hemidiaphragm. In addition, the radius of curvature of the ipsilateral hemidiaphragm during stimulation increased, whereas the radius of the contralateral hemidiaphragm remained unchanged. These observations indicate that 1) in the presence of unilateral lung inflation, the respiratory action of the diaphragm is asymmetric; and 2) this asymmetry is primarily determined by the differential effect of inflation on the length and curvature of the two halves of the muscle. These observations also imply that in patients with emphysema, SLT improves the action of the diaphragm on the transplanted side.

2012 ◽  
Vol 112 (8) ◽  
pp. 1311-1316 ◽  
Author(s):  
Dimitri Leduc ◽  
Matteo Cappello ◽  
Pierre Alain Gevenois ◽  
André De Troyer

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.


1993 ◽  
Vol 264 (6) ◽  
pp. H1836-H1846 ◽  
Author(s):  
D. R. Kostreva ◽  
S. P. Pontus

Pericardial mechanoreceptors with afferents in the phrenic nerves were studied in anesthetized dogs. The specific aims determined 1) if pericardial receptors with phrenic afferents exist in the dog; 2) the stimuli needed to activate these receptors; 3) the anatomic distribution of these pericardial receptors; and 4) which pericardial layer contains the receptors. Afferent activity was recorded from the phrenic nerves while the pericardium was probed. In 15 of 18 animals, pericardial receptors were found on the right side. In 12 of 18 animals pericardial receptors were located on the left side. Most of the mechanoreceptors were found in a band that paralleled the pericardiophrenic attachment, in the fibrous layer of the pericardium, overlying the atria and atrioventricular grooves. Some receptors had a cardiac rhythm, whereas others were stimulated by the inflating lung. None of the receptors were chemosensitive to capsaicin, bradykinin, or saline. This study is the first to demonstrate that the pericardium of the dog contains mechanosensitive receptors which are innervated by the phrenic nerve.


2006 ◽  
Vol 100 (3) ◽  
pp. 858-863 ◽  
Author(s):  
Dimitri Leduc ◽  
André De Troyer

Inflation induces a marked decrease in the lung-expanding ability of the diaphragm, but its effect on the parasternal intercostal muscles is uncertain. To assess this effect, the phrenic nerves and the external intercostals were severed in anesthetized, vagotomized dogs, such that the parasternal intercostals were the only muscles active during inspiration, and the endotracheal tube was occluded at different lung volumes. Although the inspiratory electromyographic activity recorded from the muscles was constant, the change in airway opening pressure decreased with inflation from −7.2 ± 0.6 cmH2O at functional residual capacity to −2.2 ± 0.2 cmH2O at 20-cmH2O transrespiratory pressure ( P < 0.001). The inspiratory cranial displacement of the ribs remained virtually unchanged, and the inspiratory caudal displacement of the sternum decreased moderately. However, the inspiratory outward rib displacement decreased markedly and continuously; at 20 cmH2O, this displacement was only 23 ± 2% of the value at functional residual capacity. Calculations based on this alteration yielded substantial decreases in the change in airway opening pressure. It is concluded that, in the dog, 1) inflation affects adversely the lung-expanding actions of both the parasternal intercostals and the diaphragm; and 2) the adverse effect of inflation on the parasternal intercostals is primarily related to the alteration in the kinematics of the ribs. As a corollary, it is likely that hyperinflation also has a negative impact on the parasternal intercostals in patients with chronic obstructive pulmonary disease.


2008 ◽  
Vol 105 (3) ◽  
pp. 887-893 ◽  
Author(s):  
André De Troyer

To assess the coupling between a particular hemidiaphragm and the individual lungs, the left and right phrenic nerves were separately stimulated in anesthetized dogs, and the mean changes in pleural pressure over the two lungs were evaluated by measuring the changes in airway opening pressure (ΔPao) in the two bronchial trees. Stimulation induced a fall in Pao in both lungs. However, ΔPao in the contralateral lung was only 65% of that in the ipsilateral lung. Thus, although the canine ventral mediastinum is a delicate structure, it sustained a significant pressure gradient. The hypothesis was then considered that this gradient was allowed to develop through the stretching and stiffening of the mediastinum caused by the descent of the diaphragm, and it was tested by measuring ΔPao in the two lungs during isolated, unilateral contraction of the inspiratory intercostal muscles. In this condition, ΔPao in the contralateral lung was 92% of that in the ipsilateral lung. A model analysis of the respiratory system led to the estimate that mediastinal elastance was ∼25 times greater during hemidiaphragmatic contraction than during unilateral intercostal contraction. These observations indicate that 1) a particular hemidiaphragm has an expanding action on both lungs and 2) during contraction, however, it makes the mediastinum stiffer so that the pressure transmission from the ipsilateral to the contralateral pleural cavity is reduced. These observations imply that the mediastinum may play a significant role in determining the pressure-generating ability of the diaphragm.


1963 ◽  
Vol 18 (4) ◽  
pp. 681-686 ◽  
Author(s):  
J. G. Widdicombe ◽  
J. A. Nadel

Transient lung inflation increased the volume of a bypassed tracheal segment in anesthetized dogs, whether spontaneously breathing or paralyzed and artificially ventilated. The degree of dilation during inflation varied with the state of “tone” of the tracheal muscle and with the inflation volume. Pulmonary denervation caused maintained constriction of the trachea and blocked the dilation during lung inflation. Cooling the cervical vagus nerves to between 7 and 12 C had the same effect. Both of these procedures blocked the Hering-Breuer inflation reflex, but the trachea still constricted following carotid body chemoreceptor stimulation by KCN. In paralyzed dogs, injection of veratrine into the right heart caused tracheal dilation, presumably by stimulating pulmonary stretch receptors. Left heart injection dilated the trachea much less. The former effect was abolished by pulmonary denervation. In anesthetized spontaneously breathing dogs carotid body chemoreceptor stimulation by KCN constricted the trachea; this was followed by increased ventilation and secondary tracheal dilation. Pulmonary denervation or muscular paralysis and artificial ventilation prevented the secondary dilation. These results establish the reflex nature of tracheal dilation during transient lung inflation and suggest that Hering-Breuer stretch receptors are the responsible end organs. Submitted on January 15, 1963


1990 ◽  
Vol 69 (6) ◽  
pp. 2175-2182 ◽  
Author(s):  
W. M. Petroll ◽  
H. Knight ◽  
D. F. Rochester

Diaphragmatic volume displacement (Vdi) is calculated from two models using measurements obtained from anteroposterior fluoroscopic images of supine anesthetized dogs. In model 1, diaphragmatic descent was treated as if it were a "piston in a cylinder." In contrast, model 2 incorporated thoracic configuration as well as inspiratory changes in rib cage diameter and diaphragm shape. In one dog, a computerized tomography reconstruction of Vdi was compared with Vdi calculated using the models. Vdi calculated from model 2 lay within 11% of the computerized tomographic value, whereas Vdi based on model 1 was 30% larger. In seven animals, radiopaque markers were sewn to the right costal diaphragm. Digitized fluoroscopic images were used to measure intermarker distance, an index of muscle shortening. For four tidal breaths per dog, in model 2 Vdi averaged 49 +/- 18% of tidal volume and was weakly correlated with costal diaphragm muscle shortening (R = 0.74). It is concluded that Vdi can be estimated from linear dimensions in the coronal plane, provided that inspiratory changes in rib cage diameter and diaphragmatic shape change are taken into account.


1988 ◽  
Vol 64 (4) ◽  
pp. 1433-1438 ◽  
Author(s):  
G. S. Mitchell ◽  
B. D. Selby

Hypercapnia attenuates the effects of static airway pressure (Paw) on phrenic burst frequency (f) and the expiratory duration (TE) in chloralose-urethan-anesthetized dogs. Surgical removal of the carotid bodies abolishes this interaction. Since halothane anesthesia in hyperoxia greatly impairs peripheral chemoreflexes, experiments were conducted to determine whether hypercapnia would attenuate the effects of Paw on f and TE in halothane-anesthetized dogs (approximately 1.5 minimum alveolar concentration). Integrated activity of the phrenic nerve was monitored as a function of Paw (2-12 cmH2O) in a vascularly isolated left lung at varied levels of arterial PCO2 (PaCO2; 38-80 Torr) controlled by inspired gas concentrations ventilating the denervated but perfused right lung. Halothane was administered only to the right lung. The results were as follows: 1) integrated phrenic amplitude increased with PaCO2 but was unaffected by Paw; 2) f decreased as Paw increased but was not affected by PaCO2; 3) the inspiratory duration (TI) increased as PaCO2 increased but was unaffected by Paw; 4) TE increased as Paw increased but was unaffected by PaCO2; and 5) there was no phrenic response to intravenous sodium cyanide (50-100 micrograms/kg). Thus, unlike chloralose-urethan-anesthetized dogs, hypercapnia does not attenuate the effect of lung inflation on f or TE in halothane-anesthetized dogs. Furthermore, hypercapnia increases TI during halothane anesthesia, an effect found after carotid denervation but not found in intact chloralose-urethan-anesthetized dogs. It is suggested that these differences between chloralose-urethan- and halothane-anesthetized dogs may be due to functional carotid chemoreceptor denervation by halothane.


2009 ◽  
Vol 107 (6) ◽  
pp. 1736-1742 ◽  
Author(s):  
André De Troyer ◽  
Dimitri Leduc ◽  
Matteo Cappello ◽  
Benjamin Mine ◽  
Pierre Alain Gevenois ◽  
...  

The lung-expanding action of the diaphragm is primarily related to the descent of the dome produced by the shortening of the muscle fibers. However, when the phrenic nerves in dogs are selectively stimulated at functional residual capacity, the muscle insertions into the lower ribs also move caudally. This rib motion should enhance the descent of the dome and increase the fall in pleural pressure (ΔPpl). To quantify the role of this mechanism in determining ΔPpl during isolated diaphragm contraction and to evaluate the volume dependence of this role, radiopaque markers were attached to muscle bundles in the midcostal region of the muscle in six animals, and the three-dimensional location of the markers during relaxation at different lung volumes and during phrenic nerve stimulation at the same lung volumes was measured using computed tomography. From these data, accurate measurements of muscle length, dome displacement, and lower rib displacement were obtained. The values of dome displacement were then corrected for lower rib displacement, and the values of ΔPpl corresponding to the corrected dome displacements were obtained using the measured relationship between ΔPpl and dome displacement. The measurements showed that phrenic stimulation at all lung volumes causes a caudal displacement of the lower ribs and that this displacement, taken alone, contributes ∼25% of the ΔPpl produced by the diaphragm. To the extent that this lower rib displacement is itself caused by ΔPpl, the lung-expanding action of the diaphragm during isolated contraction may therefore be viewed as a self-facilitating phenomenon.


2021 ◽  
pp. 154431672110023
Author(s):  
Winnie Nguyen ◽  
Tammy Albanese ◽  
Vanessa Tran ◽  
Anne Moore ◽  
Laligam Sekhar

This is a case report of a 35-year-old female pedestrian struck by a semi-truck. computed tomographic angiography (CTA) revealed a pseudoaneurysm at the proximal brachiocephalic artery measuring 1.8 cm in cranio-caudal length and 1.2 × 0.6 cm transverse. Just distal to the pseudoaneurysm, there was severe luminal narrowing caused by either a dissection flap or mural thrombus. Due to profound left-sided weakness, transcranial Doppler ultrasound was performed which demonstrated “hesitant” waveforms in the right middle cerebral and right vertebral arteries secondary to proximal obstruction. Hesitant waveforms display mid-systolic velocity deceleration and may also be referred to as the “bunny” waveform. Emboli monitoring of the right middle cerebral and basilar arteries were positive for active embolization


1986 ◽  
Vol 61 (6) ◽  
pp. 2095-2101 ◽  
Author(s):  
T. C. Lloyd

Anesthetized open-chest dogs on cardiopulmonary bypass were used to test the hypothesis that breathing reflexly responds to distension of the left-heart chambers. Bypass perfusion withdrew systemic flow from the right atrium and returned it to the aorta after gas exchange. Ventricles were fibrillated. The left heart was isolated by tying all pulmonary veins, and it was perfused separately at low flow admitted through one pulmonary vein and withdrawn from the ventricle. Left-heart pressure was intermittently raised abruptly from a nominal base line of 0 by partial occlusion of outflow. Pressures from approximately 10 to 50 cmH2O caused proportional increases in breathing frequency and decreases in expiratory and inspiratory times. Changes occurred immediately, reached a plateau within approximately 20 s, and were sustained for periods of observation as long as 3 min. Recovery to base line followed stimulus removal. Vagal cooling to 8 degrees C prevented responses, but autonomic ganglion blockade with hexamethonium had no effect. I conclude that breathing may be stimulated by left-heart distension and that this is mediated by large myelinated vagal afferents.


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