Microvascular pressure profile in intact in situ lung

1992 ◽  
Vol 72 (1) ◽  
pp. 332-339 ◽  
Author(s):  
D. Negrini ◽  
C. Gonano ◽  
G. Miserocchi
Keyword(s):  
Left Atrial ◽  
Pressure Profile ◽  
Parietal Pleura ◽  
Pulmonary Capillary ◽  
Null System ◽  
Pulmonary Capillary Pressure ◽  
Residual Capacity ◽  
Pulmonary Arterial ◽  
Venous Segment

We measured the microvascular pressure profile in lungs physiologically expanded in the pleural space at functional residual capacity. In 29 anesthetized rabbits a caudal intercostal space was cleared of its external and internal muscles. A small area of endothoracic fascia was surgically thinned, exposing the parietal pleura through which pulmonary vessels were clearly detectable under stereomicroscopic view. Pulmonary microvascular pressure was measured with glass micropipettes connected to a servo-null system. During the pressure measurements the animal was kept apneic and 50% humidified oxygen was delivered in the trachea. Pulmonary arterial and left atrial pressures were 22.3 +/- 1.5 and 1.6 +/- 1.5 (SD) cmH2O, respectively. The segmental pulmonary vascular pressure drop expressed as a percentage of the pulmonary arterial to left atrial pressure was approximately 33% from pulmonary artery to approximately 130-microns-diam arterioles, 4.5% from approximately 130- to approximately 60-microns-diam arterioles, approximately 46% from approximately 60-microns-diam arterioles to approximately 30-microns-diam venules, approximately 9.5% from 30- to 150-microns-diam venules, and approximately 7% for the remaining venous segment. Pulmonary capillary pressure was estimated at approximately 9 cmH2O.

Pulmonary capillaries are recruited during pulsatile flow

2002 ◽  
Vol 92 (3) ◽  
pp. 1183-1190 ◽  
Author(s):  
Robert G. Presson ◽  
William A. Baumgartner ◽  
Amanda J. Peterson ◽  
Robb W. Glenny ◽  
Wiltz W. Wagner
Keyword(s):  
Pulsatile Flow ◽  
Left Atrial ◽  
Pulmonary Arterial Pressure ◽  
Pressure Rise ◽  
Capillary Recruitment ◽  
Pulmonary Capillaries ◽  
Pulmonary Capillary ◽  
Direct Measurements ◽  
Pulmonary Arterial ◽  
The Mean

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.

Protein kinase inhibitor prevents pulmonary edema in response to H2O2

1989 ◽  
Vol 256 (4) ◽  
pp. H1012-H1022 ◽  
Author(s):  
A. Johnson ◽  
P. Phillips ◽  
D. Hocking ◽  
M. F. Tsan ◽  
T. Ferro
Keyword(s):  
Protein Kinase ◽  
Pulmonary Edema ◽  
Kinase Inhibitor ◽  
Ringer Solution ◽  
Lung Weight ◽  
Kinase C ◽  
Pulmonary Capillary ◽  
Thromboxane Synthetase ◽  
Pulmonary Capillary Pressure ◽  
Pulmonary Arterial

We investigated the effect of H2O2 (92 microM) in isolated guinea pig lungs perfused with a buffered Ringer solution. Pulmonary arterial pressure (Ppa), pulmonary capillary pressure (Ppc), and change in lung weight (delta W) were recorded at 0 min and at 15, 30, and 60 min after the H2O2. The capillary filtration coefficient (Kfc) was measured at 0 and 30 min. The perfusion of H2O2 increased the Ppa, Ppc, delta W, and Kfc. The thromboxane synthetase inhibitor Dazoxiben, or the vasodilator papaverine, prevented the increases in Ppa and Ppc. The protein kinase C (PKC) inhibitor H7 [1-(5-isoquinolinesulfonyl)-2-methylpiperazine dihydrochloride] prevented the increases in Ppa, Ppc, delta W, and Kfc, whereas the inactive isoquinoline HA1004 [N-(2-guanidinoethyl)-5-isoquinolinesulfonamide hydrochloride] had little effect on the H2O2 response. H2O2 increased the number of stress fibers and disrupted the peripheral band of cultured confluent endothelial cells, changes that were prevented with pretreatment with H7. PKC may mediate the increases in vascular permeability and pulmonary edema that occur in response to H2O2.

Pulmonary vascular response to leukotriene D4 in unanesthetized sheep: role of thromboxane

1986 ◽  
Vol 60 (3) ◽  
pp. 765-769 ◽  
Author(s):  
T. C. Noonan ◽  
A. B. Malik
Keyword(s):  
Capillary Pressure ◽  
Pulmonary Veins ◽  
Thromboxane B2 ◽  
Base Line ◽  
Vascular Response ◽  
Leukotriene D4 ◽  
Pulmonary Hemodynamic ◽  
Pulmonary Capillary ◽  
Pulmonary Capillary Pressure ◽  
Pulmonary Arterial

We examined the pulmonary vascular response to an intravenous leukotriene D4 (LTD4) injection of (1 microgram X kg-1 X min-1 for 2 min) immediately followed by infusion of 0.133 microgram X kg-1 X min-1 for 15 min in awake sheep prepared with lung lymph fistulas. LTD4 resulted in rapid generation of thromboxane A2 as measured by an increase in plasma thromboxane B2 concentration. The thromboxane B2 generation was associated with increases in pulmonary arterial and pulmonary arterial wedge pressures while left atrial pressure did not change significantly. Pulmonary lymph flow (Qlym) increased (P less than 0.05) transiently from base line 6.87 +/- 1.88 (SE) ml/h to maximum value of 9.77 +/- 1.27 at 15 min following the LTD4 infusion. The maximum increase in Qlym was associated with an increase in the estimated pulmonary capillary pressure. The increase in Qlym was not associated with a change in the lymph-to-plasma protein concentration (L/P) ratio. Thromboxane synthetase inhibition with dazoxiben (an imidazole derivative) prevented thromboxane B2 generation after LTD4 and also prevented the increases in pulmonary vascular pressures and Qlym. We conclude that LTD4 in awake sheep increases resistance of large pulmonary veins. The small transient increase in Qlym can be explained by the increase in pulmonary capillary pressure. Thromboxane appears to mediate both the pulmonary hemodynamic and lymph responses to LTD4 in sheep.

Phasic capillary pressure determined by arterial occlusion in intact dog lung lobes

1989 ◽  
Vol 67 (6) ◽  
pp. 2205-2211 ◽  
Author(s):  
Y. Yamada ◽  
M. Suzukawa ◽  
M. Chinzei ◽  
T. Chinzei ◽  
N. Kawahara ◽  
...  
Keyword(s):  
Capillary Pressure ◽  
Vascular Resistance ◽  
Control Period ◽  
Arterial Occlusion ◽  
Lung Lobe ◽  
Pulmonary Capillary ◽  
Pulmonary Capillary Pressure ◽  
Lower Lung ◽  
Pulmonary Arterial ◽  
Electrocardiogram Ecg

In six open-chest dogs, electrocardiogram- (ECG) controlled pulmonary arterial occlusion was performed during the control period and during the infusions of serotonin and histamine. A temporal series of instantaneous pulmonary capillary pressure and the longitudinal distributions of vascular resistance and compliance were evaluated in the intact left lower lung lobe. In the control period, we found a significant phasic variation of pulmonary capillary pressure (Pc) with the cardiac cycle. The ratio of arterial to venous resistances (Ra/Rv) was 6:4, and the ratio of arterial to capillary compliances (Ca/Cc) was 1:11. During the infusions of serotonin and histamine, Pc showed similar phasic variations, despite significant hemodynamic changes induced by these agents. Serotonin predominantly increased Ra, whereas histamine predominantly increased Rv. The ratio of Rv to the total resistance decreased significantly from 0.42 to 0.32 during the infusion of serotonin and increased significantly to 0.62 during the infusion of histamine. The data suggest that phasic Pc determined by ECG-controlled arterial occlusion reflects the pulsatility in the pulmonary microvascular bed under control conditions and after alterations of the pulmonary vascular resistance by serotonin and histamine.

PMA-induced pulmonary edema: mechanisms of the vasoactive response

1988 ◽  
Vol 65 (5) ◽  
pp. 2302-2312 ◽  
Author(s):  
A. Johnson
Keyword(s):  
Superoxide Dismutase ◽  
Pulmonary Arterial Pressure ◽  
Ringer Solution ◽  
Myristate Acetate ◽  
Lung Weight ◽  
Kinase C ◽  
Pulmonary Capillary ◽  
Capillary Filtration Coefficient ◽  
Pulmonary Capillary Pressure ◽  
Pulmonary Arterial

We investigated the effect of phorbol myristate acetate (PMA) in isolated guinea pig lungs perfused with phosphate-buffered Ringer solution. Pulmonary arterial pressure (Ppa), pulmonary capillary pressure (Ppc), and change in lung weight were recorded at 0, 10, 25, 40, and 70 min. The capillary filtration coefficient (Kf), an index of vascular permeability, was measured at 10 and 70 min. The perfusion of PMA (0.5 x 10(-7) M) increased Ppa, Ppc, and lung weight at 70 min. The ratio of arterial-to-venous vascular resistance (Ra/Rv) decreased and the Kf did not change with PMA. The perfusion of the lung with 4 alpha-phorbol didecanoate (inactive toward the protein kinase C analogue of PMA) did not affect the lung. The inhibition of TxA2 synthase with dazoxiben inhibited the response to PMA. The inhibition of the 5-lipoxygenase with U-60257 and the SRS-A receptor antagonist FPL 55712 also prevented the response to PMA. The addition of superoxide dismutase (SOD), catalase, or SOD plus catalase (the enzymes that remove O.2 H2O2, and OH., respectively) did not prevent the PMA effect or the release of TxA2; however, dimethylthiourea (DMTU), a scavenger of OH., did prevent the response to PMA. The data indicate that PMA causes a neutrophil-independent increase in lung weight due to increases in Ppc mediated by TxA2 and SRS-A. The protective effect of DMTU may be due to the inhibition of TxA2 generation.

Pulmonary arterial and venous constriction during hypoxia in 3- to 5-wk-old and adult ferrets

1990 ◽  
Vol 69 (6) ◽  
pp. 2183-2189 ◽  
Author(s):  
J. U. Raj ◽  
R. Hillyard ◽  
P. Kaapa ◽  
M. Gropper ◽  
J. Anderson
Keyword(s):  
Blood Flow ◽  
Pressure Drop ◽  
Left Atrial ◽  
Pulmonary Arterial Pressure ◽  
Venous Pressure ◽  
Pressure Profile ◽  
Fluid Filtration ◽  
Pressure Drops ◽  
Hypoxic Vasoconstriction ◽  
Pulmonary Arterial

We have determined the sites of hypoxic vasoconstriction in ferret lungs. Lungs of five 3- to 5-wk-old and five adult ferrets were isolated and perfused with blood. Blood flow was adjusted initially to keep pulmonary arterial pressure at 20 cmH2O and left atrial and airway pressures at 6 and 8 cmH2O, respectively (zone 3). Once adjusted, flow was kept constant throughout the experiment. In each lung, pressures were measured in subpleural 20- to 50-microns-diam arterioles and venules with the micropipette servo-nulling method during normoxia (PO2 approximately 100 Torr) and hypoxia (PO2 less than 50 Torr). In normoxic adult ferret lungs, approximately 40% of total vascular resistance was in arteries, approximately 40% was in microvessels, and approximately 20% was in veins. With hypoxia, the total arteriovenous pressure drop increased by 68%. Arterial and venous pressure drops increased by 92 and 132%, respectively, with no change in microvascular pressure drop. In 3- to 5-wk-old ferret lungs, the vascular pressure profile during normoxia and the response to hypoxia were similar to those in adult lungs. We conclude that, in ferret lungs, arterial and venous resistances increase equally during hypoxia, resulting in increased microvascular pressures for fluid filtration.

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