Effect of capillary pressure and lung distension on capillary recruitment

Godbey, P. S.; Graham, J. A.; Presson, Robert G.; Wagner, Wiltz W.; Lloyd, Thomas

doi:10.1152/jappl.1995.79.4.1142

Cited by 39 publications

(31 citation statements)

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“…D (or H ) was then updated based on the pressure values and the solution was iterated until convergence was reached. where the constants F rec = 0.65 and s rec = 22.7 cm H2O (2.23 kPa) were fitted to the raw data of Godbey et al [90]. Capillary surface area (A in equation (A 4)) was scaled by p cap in the flow and pressure calculations.…”

Section: (D) the Blood Flow Equationsmentioning

confidence: 99%

Pulmonary embolism: predicting disease severity

Burrowes

Clark

Marcinkowski

et al. 2011

Phil. Trans. R. Soc. A.

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Pulmonary embolism (PE) is the most common cause of acute pulmonary hypertension, yet it is commonly undiagnosed, with risk of death if not recognized promptly and managed accordingly. Patients typically present with hypoxemia and hypocapnia, although the presentation varies greatly, being confounded by co-mordidities such as preexisting cardio-respiratory disease. Previous studies have demonstrated variable patient outcomes in spite of similar extent and distribution of pulmonary vascular occlusion, but the pathophysiological determinants of outcome remain unclear. Computational models enable exact control over many of the compounding factors leading to functional outcomes and therefore provide a useful tool to understand and assess these mechanisms. We review the current state of pulmonary blood flow models. We present a pilot study within 10 patients presenting with acute PE, where patient-derived vascular occlusions are imposed onto an existing model of the pulmonary circulation enabling predictions of resultant haemodynamics after embolus occlusion. Results show that mechanical obstruction alone is not sufficient to cause pulmonary arterial hypertension, even when up to 65 per cent of lung tissue is occluded. Blood flow is found to preferentially redistribute to the gravitationally non-dependent regions. The presence of an additional downstream occlusion is found to significantly increase pressures.

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Section: (D) the Blood Flow Equationsmentioning

confidence: 99%

Pulmonary embolism: predicting disease severity

Burrowes

Clark

Marcinkowski

et al. 2011

Phil. Trans. R. Soc. A.

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“…4). These data show that the transmural pressures within the capillary network in each alveolus were similar, because the level of capillary recruitment is controlled by the capillary transmural pressure (9).…”

Section: Discussionmentioning

confidence: 57%

Blood flow switching among pulmonary capillaries is decreased during high hematocrit

Baumgartner

Peterson

Presson³

et al. 2004

Journal of Applied Physiology

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. Blood flow switching among pulmonary capillaries is decreased during high hematocrit. J Appl Physiol 97: 522-526, 2004; 10.1152/japplphysiol.00068.2003.-Pulmonary capillary perfusion within a single alveolar wall continually switches among segments, even when large-vessel hemodynamics are constant. The mechanism is unknown. We hypothesize that the continually varying size of plasma gaps between individual red blood cells affects the likelihood of capillary segment closure and the probability of cells changing directions at the next capillary junction. We assumed that an increase in hematocrit would decrease the average distance between red blood cells, thereby decreasing the switching at each capillary junction. To test this idea, we observed 26 individual alveolar capillary networks by using videomicroscopy of excised canine lung lobes that were perfused first at normal hematocrit (31-43%) and then at increased hematocrit (51-62%). The number of switches decreased by 38% during increased hematocrit (P Ͻ 0.01). These results support the idea that a substantial part of flow switching among pulmonary capillaries is caused by the particulate nature of blood passing through a complex network of tubes with continuously varying hematocrit. pulmonary microcirculation; pulmonary capillary recruitment; isolated canine lung lobes; dogs IN THE CLASSIC STUDY of Wearn et al. (34), the switching of blood flow among the pulmonary capillaries was described as the "normal behavior of these vessels." These investigators speculated that variations in pulmonary arterial pressure were responsible for the switching, although they were unable to measure that pressure in their preparation with the technology available in 1933. These observations remained unconfirmed for 60 years until Okada et al. (17) repeated their study. The Okada et al. study also demonstrated considerable switching of blood flow among capillaries. The variations, however, did not correlate with the small temporal variations in pulmonary arterial pressure or cardiac output in their preparation. This suggested that factors more subtle than large-vessel hemodynamics were affecting capillary perfusion consistency. Recently, Wagner et al. (33) showed that the capillary switching pattern was not random. Because there was virtually no correlation between the perfusion patterns among neighboring alveoli (33), the cause of the switching appeared to lie within the capillary networks of the individual alveolar walls. The mechanism of the switching, however, remains unknown.

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“…With exercise, significant elevation of PA pressure is prevented by recruitment of unopened capillaries and, to a smaller extent, distension of the elastic vessels [41]. Thus, at rest, a substantial portion of the capillary bed is unrecruited; some or all of these capillaries open when cardiac output increases in order to increase the total cross-sectional area of capillary bed, and decrease the PVR [42]. Because of this, when a healthy person exercises and the cardiac output is enhanced sixfold, the PA pressure increases only moderately [43].…”

Section: Structure and Function Of The Pulmonary Circulationmentioning

confidence: 99%

The Pulmonary Circulation

Tapson

2015

Diagnosis and Management of Pulmonary Hypertension

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The pulmonary circulation carries oxygen-depleted blood from the right heart to the lungs and returns oxygenated blood to the left heart for delivery to the systemic circulation while serving as a source of humoral mediator production and a barrier to the exchange of fluid and solutes. This chapter discusses several aspects of this unique circulation, including a brief history of its discovery and the tools used to explore it; an overview of pulmonary hemodynamics and how they affect right ventricular function; structure and mechanical properties of the pulmonary circulation; and neural/humoral regulation of the pulmonary vascular tone and barrier properties that prevent leakage of fluid and solutes into the alveolar space. The chapter is written to highlight those unique properties of the pulmonary circulation that are involved with the pathogenesis of pulmonary hypertension and the response of the right ventricle and pulmonary blood vessels to disease development. The overall aim is to prepare the reader for an in-depth discussion of pulmonary hypertensive diseases that follows in the subsequent chapters.

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Effect of capillary pressure and lung distension on capillary recruitment

Cited by 39 publications

References 0 publications

Pulmonary embolism: predicting disease severity

Pulmonary embolism: predicting disease severity

Blood flow switching among pulmonary capillaries is decreased during high hematocrit

The Pulmonary Circulation

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