Cardiopulmonary adaptations to pneumonectomy in dogs. III. Ventilatory power requirements and muscle structure

Hsia, Connie C. W.; Herazo, Luis F; Ramanathan, Murugappan; Claassen, Horst; Fryder-Doffey, F.; Hoppeler, Hans; Johnson, Robert L.

doi:10.1152/jappl.1994.76.5.2191

Cited by 21 publications

(22 citation statements)

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“…These two latter dogs had left ventricular catheters inserted at the time of pneumonectomy instead of bilateral carotid artery loops. Physiologic measurements of cardiopulmonary function at work loads up to maximal exercise are reported elsewhere (7)(8)(9)(10). Animals were killed at about 5 mo (n = 2) or 16 mo (n = 3) after surgery in the pneumonectomy group, and at 16 mo (n = 5) after surgery in the SHAM group.…”

Section: Methodsmentioning

confidence: 99%

Compensatory lung growth occurs in adult dogs after right pneumonectomy.

Hsia¹,

Herazo²,

et al. 1994

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We investigated the structural changes in the left lung of five adult male foxhounds 5 mo (n = 2) or 16 mo (n = 3) after right pneumonectomy (-54% of lung resected) and five sex-and age-matched foxhounds 15-16 mo after right thoracotomy without pneumonectomy. Lungs were fixed by intratracheal instillation of glutaraldehyde and analyzed by standard morphometric techniques. After right pneumonectomy, volume of the left lung increased by 72%. Volumes of all septal structures increased significantly and were more pronounced at 5 than at 16 mo after pneumonectomy. At 16 mo, the relative increases in volume with respect to the control left lung were as follows: epithelium 73%, interstitium 100%, endothelium 55%, and capillary blood volume 43%. Surface areas of alveoli and capillary increased significantly by 52% and 34%, respectively. At 5 mo after pneumonectomy, harmonic mean thickness of the tissueplasma barrier was significantly greater but at 16 mo it was not different from controls. There was a significant increase in diffusing capacity for oxygen (33% above controls) at 16 mo after pneumonectomy. These data suggest that, in contrast to previous findings after left pneumonectomy, compensatory lung growth does occur in adult dogs after resection of > 50% of lung. (J. Clin. Invest. 1994. 94:405-412.)

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Section: Methodsmentioning

confidence: 99%

Compensatory lung growth occurs in adult dogs after right pneumonectomy.

Hsia¹,

Herazo²,

et al. 1994

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“…Airway-parenchyma dissociation also occurs during postpneumonectomy lung growth, evidenced by a disproportionally low maximal expiratory flow rate, increased airways resistance, and elevated work of breathing in both animal models (184,(447)(448)(449)(450) as well as in patients after lung resection (451)(452)(453)(454). Abnormal airway function persists in spite of a doubling of lung volume and normalization of the static recoil of the remaining lung parenchyma.…”

Section: Limits Imposed By Dysanaptic Lung Growthmentioning

confidence: 99%

Mechanisms and Limits of Induced Postnatal Lung Growth

2004

Am J Respir Crit Care Med

145

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Abnormal DevelopmentClinical syndromes. Syndromes that alter expression of growth factors, cytokines, transcription factors, or extracellular matrix (ECM) proteins provide models to explore mechanisms that control alveolar development. Signals that regulate the saccularto-alveolar morphologic transition are poorly understood, but disrupting lung septation during this transition impairs alveolar formation, resulting in a loss of alveolar surface area (20, 21). There are several syndromes of abnormal lung alveolarization in humans. Trisomy 21 (Down syndrome) is associated with reduced lung volumes, alveolar surface area, fewer alveoli, defective elastin deposition, and vascular abnormalities (22, 23). Leprechaunism, caused by a defect of the insulin/insulin-like growth factor-I receptor, is associated with reduced lung surface areas as well as fewer and larger alveoli (24). Oligohydramnios (25), congenital diaphragmatic hernia (CDH) (26), and intrathoracic mass lesions are all associated with pulmonary hypoplasia caused by the lack of interplay between thoracic expansion and stretch imposed on the lung. Lung hypoplasia in CDH is not just a consequence of mechanical lung compression caused by a hole in the diaphragm but also involves primary developmental defects (27). Prenatal tracheal occlusion markedly increases lung size in some fetuses with severe CDH; however, survival remains poor because of respiratory insufficiency and prematurity (28). After CDH repair, significant postnatal alveolar growth and vascular remodeling are seen (26); long-term survivors show lower lung volumes but normal airway function and exercise tolerance (29), suggesting the occurrence of "catch-up" lung growth once the underlying abnormalities are corrected.By far the most common cause of abnormal postnatal human lung development is bronchopulmonary dysplasia (BPD). Classically, BPD occurs in the preterm infant lung exposed to hyperoxia and mechanical ventilation (30-32), resulting in extensive alveolar fibroproliferation, bronchovascular smooth muscle hyperplasia, and inhibition of distal lung formation leading to longterm pulmonary dysfunction persisting into adolescence and adulthood. The advent of antenatal steroids, postnatal surfactant replacement, and improved intensive care has ushered in the "new BPD," which lacks the severe bronchovascular lesions and interstitial fibrosis but is characterized by abnormal lung development with simplified acinar structure, poorly formed secondary crests, dysmorphic alveolar capillaries, and blunted expression of angiogenic growth factors and their receptors (33-36). There is little information on the pathology of "new BPD" in infants who survive; it remains to be seen whether long-term "catch-up" lung growth occurs in these survivors.

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“…The cardiac lobe is retained and continues to separate the heart from the diaphragm; thus distortion of the diaphragm is minimal. apparatus was calculated from the end-tidal difference in esophageal pressure (⌬Pes), the tidal volume, and the area of the ⌬Pes-tidal volume loop not recovered from the stored lung elastic recoil, as described previously (13,16). Transpulmonary pressure was defined as the difference between Pes and mouth pressure.…”

Section: Measurement Of ẇmentioning

confidence: 99%

“…Three foxhounds are included in which RM weights and muscle Q were measured in a previous study; Q was measured by the radioactive microsphere technique more than a year after adult L-PNX had been performed (16). RM weights have been included from five foxhounds after adult R-PNX and five Sham dogs; in these two groups, Ẇ was measured at rest and exercise, and muscle morphometry was studied (13). Seven additional adult R-PNX dogs that were part of an unpublished study have also been included.…”

Section: Statistical Comparisonmentioning

confidence: 99%

“…1). Ventilatory power requirements or work (Ẇ ) increased more significantly after R-PNX than after L-PNX, due to the greater loss of lung units and airway cross-sectional area (13); the increase is greater when R-PNX is performed as an adult than as an immature animal (32). Thoracic distortion in adult dogs after R-PNX and the increase in Ẇ are associated with an increase of muscle mass and total mitochondrial volume of the right hemidiaphragm compared with the left (13).…”

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confidence: 99%

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Adaptation of respiratory muscle perfusion during exercise to chronically elevated ventilatory work

Hsia

Takeda

et al. 2000

Journal of Applied Physiology

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Pneumonectomy (PNX) leads to chronic asymmetric ventilatory loading of respiratory muscles (RM). We measured RM energy requirements during exercise from RM blood flow (Q) using a fluorescent microsphere technique in dogs that had undergone right PNX as adults (adult R-PNX) or as puppies (puppy R-PNX), compared with dogs subjected to right thoracotomy without PNX as puppies (Sham) and to left PNX as adults (adult L-PNX). Ventilatory work (W) was measured during exercise. RM weight was determined post mortem. After adult and puppy R-PNX, the right hemidiaphragm becomes grossly distorted, but W and right costal muscle mass increased only after adult R-PNX. After adult L-PNX, the diaphragm was undistorted; W and left hemidiaphragm RM Q were elevated, but muscle mass did not increase. Mass of parasternal muscle did not increase after adult R-PNX, despite increased Q. Thus muscle mass increased only in response to the combination of chronic stretch and dynamic loading. There was a dorsal-to-ventral gradient of increasing Q within the diaphragm, but the distribution was unaffected by anatomic distortion, hypertrophy, or workload, suggesting a fixed pattern of neural activation. The diaphragm and parasternals were the primary muscles compensating for the asymmetric loading from PNX.

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Cardiopulmonary adaptations to pneumonectomy in dogs. III. Ventilatory power requirements and muscle structure

Cited by 21 publications

References 0 publications

Compensatory lung growth occurs in adult dogs after right pneumonectomy.

Compensatory lung growth occurs in adult dogs after right pneumonectomy.

Mechanisms and Limits of Induced Postnatal Lung Growth

Adaptation of respiratory muscle perfusion during exercise to chronically elevated ventilatory work

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