Pulmonary capillary recruitment during airway hypoxia in the dog

Wagner, Wiltz W.; Latham, L. P.

doi:10.1152/jappl.1975.39.6.900

Cited by 62 publications

(38 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This finding supports the observations of Glazier et al (6) studying rapidly frozen lungs and studies from our own laboratory using in vivo microscopy (3,(24)(25)(26). This pattern of gradual recruitment reflected the average pattern for all of the alveoli (Fig.…”

supporting

confidence: 90%

See 1 more Smart Citation

Heterogeneous capillary recruitment among adjoining alveoli

Baumgartner

Jaryszak

Peterson

et al. 2003

Journal of Applied Physiology

View full text Add to dashboard Cite

. Heterogeneous capillary recruitment among adjoining alveoli. J Appl Physiol 95: 469-476, 2003; 10.1152/ japplphysiol.01115.2002.-Pulmonary capillaries recruit when microvascular pressure is raised. The details of the relationship between recruitment and pressure, however, are controversial. There are data supporting 1) gradual homogeneous recruitment, 2) sudden and complete recruitment, and 3) heterogeneous recruitment. The present study was designed to determine whether alveolar capillary networks recruit in a variety of ways or whether one model predominates. In isolated, pump-perfused canine lung lobes, fields of six neighboring alveoli were recorded with video microscopy as pulmonary venous pressure was raised from 0 to 40 mmHg in 5-mmHg increments. The largest group of alveoli (42%) recruited gradually. Another group (33%) recruited suddenly (sheet flow). Half of the neighborhoods had at least one alveolus that paradoxically derecruited when pressure was increased, even though neighboring alveoli continued to recruit capillaries. At pulmonary venous pressures of 40 mmHg, 86% of the alveolar-capillary networks were not fully recruited. We conclude that the pattern of recruitment among neighboring alveoli is complex, is not homogeneous, and may not reach full recruitment, even under extreme pressures. pulmonary microcirculation; isolated perfused lung lobes; video microscopy; dogs PULMONARY CAPILLARIES ARE recruited with increasing microvascular pressure. Different investigators, however, have found different patterns of recruitment. With the introduction of the zone model, West et al. (31) showed that pulmonary blood flow increased down a vertical gradient as pulmonary arterial and venous pressures increased relative to alveolar pressure. Glazier and colleagues (6) studied red blood cell distributions in rapidly frozen lungs and showed that there was gradual, homogeneous recruitment as capillary pressure increased, especially in zone 2. Fung and Sobin (5) developed the sheet flow theory, which suggested that the entire capillary bed opened suddenly and completely as capillary transmural pressure exceeded alveolar pressure. This hypothesis was supported experimentally by Sobin et al. (19), who studied latex casts of the capillary bed. Godbey et al. (9) showed in excised lungs that sheet flow tended to occur at low airway pressure when alveoli were not highly distended, whereas gradual recruitment tended to occur in more distended alveoli. Although the zone and sheet flow models predict homogeneous recruitment, Warrell et al. (28), studying rapidly frozen lungs under zone 2 conditions, found an uneven distribution of capillary red blood cells within areas likely to have been supplied by a common arteriole. The scatter in the data of Godbey et al. as capillaries recruited suggests confirmation of the Warrell data, i.e., that capillary recruitment could be heterogeneous. West et al. (32), using an elegant computer model, deduced that recruitment in a network of resistors could be heterogeneous. Nevertheless...

show abstract

supporting

confidence: 90%

“…In accordance with institutional guidelines, healthy adult male mongrel dogs (20)(21)(22)(23)(24) kg, n ϭ 6) were anesthetized by intravenous injection of pentobarbital sodium dissolved in 0.9% saline (30-40 mg/kg). The animals were intubated and ventilated with room air (Harvard Apparatus 607D).…”

Section: Methodsmentioning

confidence: 99%

Heterogeneous capillary recruitment among adjoining alveoli

Baumgartner

Jaryszak

Peterson

et al. 2003

Journal of Applied Physiology

View full text Add to dashboard Cite

show abstract

“…Likewise, ventilated areas with abnormal surfactant may be underperfused with resultant arterial hypoxemia. Severe hypoxia induces pulmonary vasoconstriction mediated by pulmonary arterial vascular small muscle contraction (35)(36)(37). Hypoxia induced vasoconstriction when oxygen saturation is under 50% in all species so far examined (36,38,39).…”

Section: Discussionmentioning

confidence: 99%

Pulmonary Surfactant Surface Tension Influences Alveolar Capillary Shape and Oxygenation

Ikegami

Weaver

Grant

et al. 2009

Am J Respir Cell Mol Biol

View full text Add to dashboard Cite

Alveolar capillaries are located in close proximity to the alveolar epithelium and beneath the surfactant film. We hypothesized that the shape of alveolar capillaries and accompanying oxygenation are influenced by surfactant surface tension in the alveolus. To prove our hypothesis, surfactant surface tension was regulated by conditional expression of surfactant protein (SP)-B in Sftpb 2/2 mice, thereby inhibiting surface tension-lowering properties of surfactant in vivo within 24 hours after depletion of Sftpb. Minimum surface tension of isolated surfactant was increased and oxygen saturation was significantly reduced after 2 days of SP-B deficiency in association with deformation of alveolar capillaries. Intravascularly injected 3.2-mmdiameter microbeads through jugular vein were retained within narrowed pulmonary capillaries after reduction of SP-B. Ultrastructure studies demonstrated that the capillary protrusion typical of the normal alveolar-capillary unit was reduced in size, consistent with altered pulmonary blood flow. Pulmonary hypertension and intrapulmonary shunting are commonly associated with surfactant deficiency and dysfunction in neonates and adults with respiratory distress syndromes. Increased surfactant surface tension caused by reduction in SP-B induced narrowing of alveolar capillaries and oxygen desaturation, demonstrating an important role of surface tension-lowering properties of surfactant in the regulation of pulmonary vascular perfusion.Keywords: surfactant protein-B; transgenic mice; pulmonary blood flow; acute respiratory distress syndrome; pulmonary vascular perfusion Pulmonary surfactant is a complex mixture of lipids and associated proteins that are required for formation and stability of surfactant film in the alveolus. After secretion from type II epithelial cells, surfactant forms a lipid rich film that covers the entire alveolar surface, reducing surface tension at the air/liquid interface from 70 mN/m to near 0 mN/m (1). The reduction of alveolar surface tension is required for the maintenance of alveolar surface area, upon which respiration depends. Surfactant function requires the presence of surfactant protein (SP)-B, a small hydrophobic protein that is tightly associated with surfactant phospholipids in the alveolus (1, 2). In humans and mice, SP-B deficiency or mutations in SFTPB cause respiratory failure and death in adults and neonates (3-5). Conditional reduction of SP-B for 4 days in adult mice causes respiratory failure associated with abnormal high surface tension of the surfactant present in bronchoalveolar lavage fluid (BALF) (6-8). This conditional SP-B mouse provides a useful model for study of the influence of surface tension on lung structure, function, and inflammation in adult lung in vivo. The loss of surfactant surface activity influences the shape and function of cells beneath the surfactant film. For example, reduction in SP-B increases the surface tension of surfactant, influencing both cell shape and phagocytic activity of alveolar macrophages in vivo...

show abstract

“…Studies using other techniques, performed in both experimental animals and humans, have suggested that under conditions of generalised hypoxia there is a redistribution of blood from dependent to nondependent lung regions [32][33][34]. Studies in experimental animals have shown that this redistribution of blood flow is secondary to recruitment of previously unperfused capillaries in these regions, with minimal evidence of capillary dilatation [35]. This recruitment phenomenon has been found to correlate strongly with the increased pulmonary artery pressure [36], secondary to arterial vasoconstriction seen under conditions of generalised hypoxia, with other possible variables (changes in left atrial pressure and cardiac output) having a minimal role.…”

Section: Discussionmentioning

confidence: 99%

Pulmonary perfusion quantified by electron-beam computed tomography: effects of hypoxia and inhaled NO

Jones¹,

Hansell²,

Evans³

2003

Eur Respir J

View full text Add to dashboard Cite

Patients with acute lung injury may benefit from the manipulation of pulmonary blood flow using inhaled nitric oxide (iNO) to optimise ventilation/perfusion matching. Current techniques for studying changes in regional pulmonary perfusion are difficult to apply clinically. This study therefore investigated the potential of electronbeam computed tomography (EBCT) to quantify the effects of hypoxia and iNO on regional pulmonary perfusion in five healthy subjects.Contrast-enhanced sections were obtained sequentially under conditions of normoxia, hypoxia (fractional concentration of oxygen in inspired gas (FI,O 2 ) 0.12) and hypoxia, with iNO (14.8 parts per million (ppm)) administered during inspiration in the supine position. Regions of interest were placed along the nondependent to dependent axis and values for relative perfusion derived.Under normoxic conditions a vertical gradient of perfusion existed, which became less apparent due to increased perfusion in nondependent regions after the induction of hypoxia (FI,O 2 0.12). Under physiological circumstances, the distribution of pulmonary blood flow is regulated by a local action of alveolar oxygen tension on precapillary pulmonary vessels. Thus, the reflex of hypoxic pulmonary vasoconstriction (HPV) ensures that blood flow is diverted away from areas of damaged lung, thereby preserving the matching of ventilation (V9) and perfusion (Q9) [1,2]. In contrast, patients with acute lung injury (ALI) demonstrate diminished HPV leading to adverse changes in V9/Q9 matching, manifesting clinically as refractory hypoxaemia [3]. The favourable manipulation of V9/Q9 therefore assumes considerable therapeutic significance. In this context, nitric oxide (NO), an endothelially derived vasodilator that modulates vascular tone in health and disease [4], has been demonstrated to be a selective pulmonary vasodilator when administered by inhalation both in experimental animals [5,6] and humans [7], improving physiological variables (specifically pulmonary artery pressure (Ppa) and arterial oxygen tension) in patients with ALI [4]. The effects of NO on HPV in terms of the modulation of changes in regional pulmonary blood flow induced by hypoxaemia are, however, unknown.Although techniques for studying regional pulmonary perfusion have been difficult to apply clinically, a gravitational distribution of pulmonary perfusion has been described in normal subjects, determined by the interrelationship between hydrostatic, alveolar and interstitial pressures [8,9]. Moreover, animal studies employing high spatial-resolution techniques suggest that the influence of gravity is less important than the structure of the pulmonary vascular tree in determining regional blood flow in the lung [10,11]. The authors have recently employed electron-beam computed tomography (EBCT) to quantify regional pulmonary perfusion in normal subjects placed in the supine and prone positions, demonstrating that a gravitational gradient of pulmonary perfusion existed in both supine and prone positions [12]....

show abstract

Pulmonary capillary recruitment during airway hypoxia in the dog

Cited by 62 publications

References 0 publications

Heterogeneous capillary recruitment among adjoining alveoli

Heterogeneous capillary recruitment among adjoining alveoli

Pulmonary Surfactant Surface Tension Influences Alveolar Capillary Shape and Oxygenation

Pulmonary perfusion quantified by electron-beam computed tomography: effects of hypoxia and inhaled NO

Contact Info

Product

Resources

About