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.

Pulmonary capillary recruitment during airway hypoxia in the dog

1975 ◽  
Vol 39 (6) ◽  
pp. 900-905 ◽  
Author(s):  
W. W. Wagner ◽  
L. P. Latham
Keyword(s):  
Cardiac Output ◽  
Pulmonary Artery ◽  
Left Atrial ◽  
Weak Correlation ◽  
Capillary Length ◽  
Capillary Recruitment ◽  
Pulmonary Capillaries ◽  
Pulmonary Capillary ◽  
Anesthetized Dogs ◽  
Measuring Tool

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.

Effects of left atrial pressure on the pulmonary vascular response to hypoxic ventilation

1991 ◽  
Vol 70 (5) ◽  
pp. 1991-1995 ◽  
Author(s):  
S. A. Gu ◽  
J. Ducas ◽  
U. Schick ◽  
R. M. Prewitt
Keyword(s):  
Arterial Pressure ◽  
Left Atrial ◽  
Pulmonary Arterial Pressure ◽  
Mean Value ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Vascular Response ◽  
Wide Range ◽  
Pulmonary Arterial ◽  
The Mean

We investigated the effects of hypoxic ventilation on the pulmonary arterial pressure- (P) flow (Q) relationship in an intact canine preparation. Mean pulmonary P-Q coordinates were obtained during hypoxic ventilation and during ventilation with 100% O2 at normal and at increased left atrial pressure. Specifically, we tested the hypothesis that, over a wide range, changes in left atrial pressure would alter the effects of hypoxic ventilation on pulmonary P-Q characteristics. Seven dogs were studied. When left atrial pressure was normal (5 mmHg), the mean value of the extrapolated intercept (PI) of the linear P-Q relationship was 10.9 mmHg and the slope (incremental vascular resistance, IR) of the P-Q relationship was 2.2 mmHg.l-1.min. Hypoxic ventilation increased PI to 18 mmHg (P less than 0.01) but did not affect IR. Subsequently, during ventilation with 100% O2, when left atrial pressure was increased to 14 mmHg by inflation of left atrial balloon, PI increased to 18 mmHg. IR was 1.6 mmHg.l-1.min. Again, hypoxic ventilation caused an isolated change in PI. Hypoxia increased PI from 18 to 28 mmHg (P less than 0.01). As in the condition of normal left atrial pressure, hypoxic ventilation did not affect IR. We conclude that, in an anesthetized intact canine preparation, hypoxic ventilation causes an isolated increase in the extrapolated pressure intercept of the pulmonary P-Q relationship. Furthermore the effects of hypoxic ventilation on pulmonary P-Q characteristics are not affected by the resting left atrial pressure.

A computed method for noninvasive MRI assessment of pulmonary arterial hypertension

2004 ◽  
Vol 96 (2) ◽  
pp. 463-468 ◽  
Author(s):  
Eric Laffon ◽  
Christophe Vallet ◽  
Virginie Bernard ◽  
Michel Montaudon ◽  
Dominique Ducassou ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Cross Sectional Area ◽  
Physical Parameters ◽  
Sectional Area ◽  
Biophysical Parameters ◽  
Cross Sectional ◽  
Mean Pulmonary Arterial Pressure ◽  
Pulmonary Arterial ◽  
The Mean

The present method enables the noninvasive assessment of mean pulmonary arterial pressure from magnetic resonance phase mapping by computing both physical and biophysical parameters. The physical parameters include the mean blood flow velocity over the cross-sectional area of the main pulmonary artery (MPA) at the systolic peak and the maximal systolic MPA cross-sectional area value, whereas the biophysical parameters are related to each patient, such as height, weight, and heart rate. These parameters have been measured in a series of 31 patients undergoing right-side heart catheterization, and the computed mean pulmonary arterial pressure value (PpaComp) has been compared with the mean pressure value obtained from catheterization (PpaCat) in each patient. A significant correlation was found that did not differ from the identity line PpaComp = PpaCat ( r = 0.92). The mean and maximal absolute differences between PpaComp and PpaCat were 5.4 and 11.9 mmHg, respectively. The method was also applied to compute the MPA systolic and diastolic pressures in the same patient series. We conclude that this computed method, which combines physical (whoever the patient) and biophysical parameters (related to each patient), improves the accuracy of MRI to noninvasively estimate pulmonary arterial pressures.

Flow-mediated release of nitric oxide in isolated, perfused rabbit lungs

2001 ◽  
Vol 91 (1) ◽  
pp. 363-370 ◽  
Author(s):  
Toshiyuki Ogasa ◽  
Hitoshi Nakano ◽  
Hiroshi Ide ◽  
Yasushi Yamamoto ◽  
Nobuhiko Sasaki ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Baseline Level ◽  
Pulmonary Arterial Pressure ◽  
Blood Perfusion ◽  
No Production ◽  
Perfusion Study ◽  
Capillary Recruitment ◽  
Physiological Conditions ◽  
Perfusate Flow ◽  
Pulmonary Arterial

The effects of changing perfusate flow on lung nitric oxide (NO) production and pulmonary arterial pressure (Ppa) were tested during normoxia and hypoxia and after N G-monomethyl-l-arginine (l-NMMA) treatment during normoxia in both blood- and buffer-perfused rabbit lungs. Exhaled NO (eNO) was unaltered by changing perfusate flow in blood-perfused lungs. In buffer-perfused lungs, bolus injections of ACh into the pulmonary artery evoked a transient increase in eNO from 67 ± 3 (SE) to 83 ± 7 parts/billion with decrease in Ppa, whereas perfusate NO metabolites (pNOx) remained unchanged. Stepwise increments in flow from 25 to 150 ml/min caused corresponding stepwise elevations in eNO production (46 ± 2 to 73 ± 3 nl/min) without changes in pNOx during normoxia. Despite a reduction in the baseline level of eNO, flow-dependent increases in eNO were still observed during hypoxia.l-NMMA caused declines in both eNO and pNOx with a rise in Ppa. Pulmonary vascular conductance progressively increased with increasing flow during normoxia and hypoxia. However,l-NMMA blocked the flow-dependent increase in conductance over the range of 50–150 ml/min of flow. In the more physiological conditions of blood perfusion, eNO does not reflect endothelial NO production. However, from the buffer perfusion study, we suggest that endothelial NO production secondary to increasing flow, may contribute to capillary recruitment and/or shear stress-induced vasodilation.

Pulsatile and nonpulsatile pressure-flow relationships in zone 3 excised rabbit lungs

1994 ◽  
Vol 76 (1) ◽  
pp. 370-379 ◽  
Author(s):  
O. Saito ◽  
W. J. Lamm ◽  
J. Hildebrandt ◽  
R. K. Albert
Keyword(s):  
Left Atrial ◽  
Pulmonary Arterial Pressure ◽  
Left Lung ◽  
Inertial Forces ◽  
Positive End Expiratory Pressure ◽  
Pump Frequency ◽  
Diaphragm Pump ◽  
Pulmonary Arterial ◽  
Lung Base ◽  
Nonpulsatile Flow

We compared the effects of pulsatile vs. nonpulsatile flow (Q) on pulmonary arterial pressure (Ppa)-Q relationships in zone 3 over wide ranges of pulse rate, stroke volume (SV), and Q. Excised left lungs of rabbits (n = 15) were perfused with tris(hydroxymethyl)aminomethane-buffered Tyrode solution containing 4% dextran, 1% albumin, and 10 mg/l of indomethacin and were ventilated with room air. Pulsatile Q was generated by a diaphragm pump delivering SV of 0.5, 1, or 2 ml (representing approximately 0.3, 0.6, and 1.2 times, respectively, the normal resting SV for rabbit left lung) and adjusting the pump frequency. Nonpulsatile Q was generated by raising an arterial reservoir to the required height. Mean pulmonary arterial (Ppa) and left atrial pressures were measured at end exhalation (positive end-expiratory pressure = 2.5 cmH2O) near the tips of the perfusion cannulas and were referenced to the lung base. Left atrial pressure was held constant at 7 cmH2O.Q was alternated between pulsatile and nonpulsatile, increasing Q stepwise from 100 to 600 ml/min (Q from approximately 0.3 to 2 times the normal resting Q for rabbit left lung), after which Q was reduced stepwise back to initial values. For the smallest SV there were no differences between Ppa-Q curves under pulsatile and nonpulsatile conditions. At the largest SV, Ppa was greater during pulsatile than nonpulsatile Q at Q > 100 ml/min. The slopes of the Ppa-Q curves were greater during pulsatile Q at the two larger SV values. These results can be explained by increasing Q turbulence and less ideal velocity profiles at higher peak Q resulting from the effects of rapidly changing inertial forces.

Perfusion through vessels open in zone 1 contributes to gas exchange in rabbit lungs in situ

1995 ◽  
Vol 79 (6) ◽  
pp. 1895-1899 ◽  
Author(s):  
W. J. Lamm ◽  
T. Obermiller ◽  
M. P. Hlastala ◽  
R. K. Albert
Keyword(s):  
High Frequency ◽  
Pulmonary Arterial Pressure ◽  
Venous Pressure ◽  
High Frequency Oscillation ◽  
Bias Flow ◽  
Flow Through ◽  
Pulmonary Arterial ◽  
Zero Reference ◽  
The Mean

We previously found that up to 15% of the normal cardiac output can flow through lungs that are entirely in zone 1 and that the zone 1 pathway utilizes alveolar corner vessels. Because of the proximity of these vessels to alveoli, we hypothesized that lungs perfused under zone 1 conditions would exchange gas. We used the multiple inert gas elimination technique to assess the ventilation-perfusion (VA/Q) distribution under zones 1 and 2 in six rabbit lungs perfused with tris(hydroxymethyl)aminomethane-buffered Tyrode solution containing 1% albumin, 4% dextran, and papaverine (25 mg/l). High-frequency oscillation (tidal volume = 2.8 ml at 20 Hz, bias flow = 1 l/min) kept alveolar pressure (PA) nearly constant at 10 or 20 cmH2O. Pulmonary arterial pressure was set 2.5 cmH2O below or 5 cmH2O above PA (zones 1 and 2, respectively). Pulmonary venous pressure was kept at 0 cmH2O, with zero reference being the bottom of the lung. At PA of 10 cmH2O, flow was 64 +/- 40 and 5 +/- 3 ml/min (P < 0.05) and the mean VA/Q for perfusion was 1.1 +/- 0.4 and > 5 (P < 0.05) in zones 2 and 1, respectively. At PA of 20 cmH2O, flow was 89 +/- 36 and 22 +/- 13 ml/min (P < 0.05) and the mean VA/Q for perfusion was 0.8 +/- 0.3 and 3.7 +/- 2.4 (P < 0.05) in zones 2 and 1, respectively. Shunt averaged < 5% of total flow in all conditions. Blood flowing through vessels remaining open under zone 1 conditions 1) exchanges gas, 2) does not occur through anatomic or physiological shunts, and 3) may explain the high VA/Q seen with positive end-expiratory pressure.

Hypoxic pulmonary hypertension of the calf with denervation of the lungs

1964 ◽  
Vol 19 (5) ◽  
pp. 976-980 ◽  
Author(s):  
John T. Reeves ◽  
James E. Leathers
Keyword(s):  
Spinal Cord ◽  
Central Nervous System ◽  
Nervous System ◽  
Arterial Pressure ◽  
Spinal Anesthesia ◽  
Pulmonary Arterial Pressure ◽  
Acute Hypoxia ◽  
Pressure Rise ◽  
The Central Nervous System ◽  
Pulmonary Arterial

Transection of the spinal cord at the level of C2, spinal anesthesia, and/or bilateral vagotomy were done in 11 healthy young male calves. These procedures did not block the pulmonary arterial pressure rise with 12 or 9% oxygen, but they did block the increase in heart rate and systemic arterial pressure which accompanied hypoxia when the central nervous system was intact. The central nervous system, therefore, appeared to mediate the response to acute hypoxia of the systemic circulation, but not the pulmonary arterial pressure rise. hypoxia; pulmonary circulation; spinal cord section; spinal anesthesia; vagotomy Submitted on February 19, 1964

Sign in / Sign up

Export Citation Format

Share Document