scholarly journals Pulmonary capillary recruitment in exercise and pulmonary hypertension

2018 ◽  
Vol 51 (3) ◽  
pp. 1702559
Author(s):  
David Langleben ◽  
Stylianos E. Orfanos
2018 ◽  
Vol 51 (3) ◽  
pp. 1800260
Author(s):  
Horst Olschewski ◽  
Gabor Kovacs ◽  
Philippe Herve

1993 ◽  
Vol 34 (5) ◽  
pp. 596-599 ◽  
Author(s):  
Lynda J Means ◽  
Wendy L Hanson ◽  
Kyle O Mounts ◽  
Wiltz W Wagner

2015 ◽  
Vol 24 (138) ◽  
pp. 665-673 ◽  
Author(s):  
Harrison W. Farber ◽  
Simon Gibbs

Pulmonary hypertension (PH) associated with left heart disease (PH-LHD) is the most common type of PH, but its natural history is not well understood. PH-LHD is diagnosed by right heart catheterisation with a mean pulmonary arterial pressure ≥25 mmHg and a pulmonary capillary wedge pressure >15 mmHg. The primary causes of PH-LHD are left ventricular dysfunction of systolic and diastolic origin, and valvular disease. Prognosis is poor and survival rates are low. Limited progress has been made towards specific therapies for PH-LHD, and management focuses on addressing the underlying cause of the disease with supportive therapies, surgery and pharmacological treatments. Clinical trials of therapies for pulmonary arterial hypertension in patients with PH-LHD have thus far been limited and have provided disappointing or conflicting results. Robust, long-term clinical studies in appropriate target populations have the potential to improve the outlook for patients with PH-LHD. Herein, we discuss the knowledge gaps in our understanding of PH-LHD, and describe the current unmet needs and challenges that are faced by clinicians when identifying and managing patients with this disease.


Medicine ◽  
2002 ◽  
Vol 81 (6) ◽  
pp. 417-424 ◽  
Author(s):  
PEDRO ALMAGRO ◽  
JOAQUIM JULIÀ ◽  
MARIA SANJAUME ◽  
GUADALUPE GONZÁLEZ ◽  
JAUME CASALOTS ◽  
...  

2002 ◽  
Vol 92 (3) ◽  
pp. 1183-1190 ◽  
Author(s):  
Robert G. Presson ◽  
William A. Baumgartner ◽  
Amanda J. Peterson ◽  
Robb W. Glenny ◽  
Wiltz W. Wagner

Capillaries recruit when pulmonary arterial pressure rises. The duration of increased pressure imposed in such experiments is usually on the order of minutes, although recent work shows that the recruitment response can occur in <4 s. In the present study, we investigate whether the brief pressure rise during cardiac systole can also cause recruitment and whether the recruitment is maintained during diastole. To study these basic aspects of pulmonary capillary hemodynamics, isolated dog lungs were pump perfused alternately by steady flow and pulsatile flow with the mean arterial and left atrial pressures held constant. Several direct measurements of capillary recruitment were made with videomicroscopy. The total number and total length of perfused capillaries increased significantly during pulsatile flow by 94 and 105%, respectively. Of the newly recruited capillaries, 92% were perfused by red blood cells throughout the pulsatile cycle. These data provide the first direct account of how the pulmonary capillaries respond to pulsatile flow by showing that capillaries are recruited during the systolic pulse and that, once open, the capillaries remain open throughout the pulsatile cycle.


CHEST Journal ◽  
2015 ◽  
Vol 148 (4) ◽  
pp. 989A
Author(s):  
Glenda Euceda ◽  
Michael Denson ◽  
Steven Sieber ◽  
David Oelberg

ESC CardioMed ◽  
2018 ◽  
pp. 2558-2560
Author(s):  
Barbara Girerd ◽  
David Montani ◽  
Marc Humbert

Pre-capillary pulmonary hypertension can be heritable in the context of pulmonary arterial hypertension (an autosomal dominant disease mainly due to mutations in BMPR2), and pulmonary veno-occlusive disease or pulmonary capillary haemangiomatosis (an autosomal recessive disease due to biallelic mutations in the EIF2AK4 gene). Genetic counselling can be implemented in referral centres for pulmonary hypertension as outlined in this chapter.


1975 ◽  
Vol 39 (6) ◽  
pp. 900-905 ◽  
Author(s):  
W. W. Wagner ◽  
L. P. Latham

To study the effect of hypoxia on the pulmonary capillaries, windows were inserted in the chest wall of 9 pentobarbital-anesthetized dogs. A microscope with an image-superimposing device was used to make drawings of the perfused capillaries. Summed lengths of individual perfused capillaries in the drawing were determined with a map-measuring tool. Total capillary length was constant between PaO2 of 160 and 70 Torr. As PaO2 fell below 70 Torr, recruitment of previously unperfused capillaries occurred in every case; at PaO2 of 40 Torr, the total length of perfused capillaries was about 4 times greater than during normoxia. There was no correlation between the recruitment of capillaries and alterations in left atrial pressure, only a weak correlation with cardiac output changes, but a very strong correlation with increased pulmonary artery pressure. This implies that recruitment was probably caused by vasoconstriction within the lung.


Sign in / Sign up

Export Citation Format

Share Document