Hypoxic vasoconstriction and fluid filtration in pig lungs

1981 ◽  
Vol 51 (5) ◽  
pp. 1065-1071 ◽  
Author(s):  
W. Mitzner ◽  
J. T. Sylvester
Keyword(s):  
Blood Flow ◽  
Pulmonary Blood Flow ◽  
Filtration Rate ◽  
Critical Pressure ◽  
Pulmonary Arterial Pressure ◽  
Parallel Channel ◽  
Fluid Filtration ◽  
Hypoxic Vasoconstriction ◽  
Pulmonary Arterial ◽  
The Mean

We have studied the effect of hypoxia [inspired partial pressure of O2 (Po2) 50 mmHg] on the relationships among pulmonary blood flow, pulmonary arterial pressure, and fluid filtration rates in isolated blood-perfused pig lungs. Our results indicate that hypoxia constricted the vasculature in a manner that caused a parallel shift of the pressure-flow curve to higher pressures. During normoxia, filtration rate was zero at flows less than 1.5 1/min but increased with increases in blood flow above this level. In both cases the shape of this relationship was similar, but during hypoxia it was shifted to higher filtration rates. These findings can be interpreted using a parallel-channel Starling resistor model of the lung with a distribution of critical pressures. All the effects of hypoxia found in this study could be explained simply by an increase in critical pressure. According to the model, this increase in critical pressure during hypoxia caused a greater filtration rate because of an increase in the mean intravascular filtration pressure and an increase in the mean filtration coefficient.

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.

Regional pulmonary blood flow during 96 hours of hypoxia in conscious sheep

1986 ◽  
Vol 61 (6) ◽  
pp. 2136-2143 ◽  
Author(s):  
D. C. Curran-Everett ◽  
K. McAndrews ◽  
J. A. Krasney
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Pulmonary Blood Flow ◽  
Pulmonary Arterial Pressure ◽  
Pressor Response ◽  
Superior Vena ◽  
Acute Hypoxia ◽  
Vena Cava ◽  
Normobaric Hypoxia ◽  
Pulmonary Arterial

The effects of acute hypoxia on regional pulmonary perfusion have been studied previously in anesthetized, artificially ventilated sheep (J. Appl. Physiol. 56: 338–342, 1984). That study indicated that a rise in pulmonary arterial pressure was associated with a shift of pulmonary blood flow toward dorsal (nondependent) areas of the lung. This study examined the relationship between the pulmonary arterial pressor response and regional pulmonary blood flow in five conscious, standing ewes during 96 h of normobaric hypoxia. The sheep were made hypoxic by N2 dilution in an environmental chamber [arterial O2 tension (PaO2) = 37–42 Torr, arterial CO2 tension (PaCO2) = 25–30 Torr]. Regional pulmonary blood flow was calculated by injecting 15-micron radiolabeled microspheres into the superior vena cava during normoxia and at 24-h intervals of hypoxia. Pulmonary arterial pressure increased from 12 Torr during normoxia to 19–22 Torr throughout hypoxia (alpha less than 0.049). Pulmonary blood flow, expressed as %QCO or ml X min-1 X g-1, did not shift among dorsal and ventral regions during hypoxia (alpha greater than 0.25); nor were there interlobar shifts of blood flow (alpha greater than 0.10). These data suggest that conscious, standing sheep do not demonstrate a shift in pulmonary blood flow during 96 h of normobaric hypoxia even though pulmonary arterial pressure rises 7–10 Torr. We question whether global hypoxic pulmonary vasoconstriction is, by itself, beneficial to the sheep.

Effects of blood flow on lung ACE kinetics: evidence for microvascular recruitment

1991 ◽  
Vol 71 (6) ◽  
pp. 2244-2254 ◽  
Author(s):  
H. J. Toivonen ◽  
J. D. Catravas
Keyword(s):  
Blood Flow ◽  
Pulmonary Blood Flow ◽  
Pulmonary Arterial Pressure ◽  
Left Lung ◽  
In Vivo Assays ◽  
Vascular Bed ◽  
Pulmonary Arterial ◽  
Microvascular Recruitment ◽  
The Relationship

The parameter Amax/Km (product of reactant enzyme mass in perfused microvessels and the constant kcat/Km), calculated from in vivo assays of pulmonary endothelial ectoenzymes (e.g., angiotensin-converting enzyme, ACE), can provide estimates of the perfused pulmonary microvascular surface area (PMSA) in the absence of enzyme dysfunction. We examined the relationship between PMSA and pulmonary blood flow (Qb) in anesthetized rabbits placed on total heart bypass, using [3H]benzoyl-Phe-Ala-Pro (BPAP) as the ACE substrate. When Qb was increased from 250 to 1,100 ml/min, at zone 3 conditions, pulmonary arterial pressure increased, pulmonary vascular resistance (PVR) decreased, and Amax/Km increased linearly, reflecting increasing PMSA. When only the left lung was perfused, increasing Qb from 250 to 636 +/- 17 ml/min (the last value representing fully recruited and/or distended vascular bed), PVR decreased, while Amax/Km increased. When Qb was further increased to 791 +/- 44 ml/min, both PVR and Amax/Km remained unchanged, confirming the lack of additional changes in PMSA. We conclude that Amax/Km provides a sensitive indication of PMSA, because it 1) increases with increasing Qb and decreasing PVR, 2) reaches a maximum at Qb values that correspond to the minimal values in PVR, and 3) like PVR, did not change with further increases in Qb. Compared with predicted changes in PMSA produced by either microvascular recruitment alone or distension alone, our data indicate that recruitment is a larger contributor to the observed increase in PMSA.

Acetylcholine increases pulmonary blood flow in intact fetuses via endothelium-dependent vasodilation

1992 ◽  
Vol 262 (2) ◽  
pp. H406-H410 ◽  
Author(s):  
M. H. Tiktinsky ◽  
J. J. Cummings ◽  
F. C. Morin
Keyword(s):  
Blood Flow ◽  
Pulmonary Blood Flow ◽  
Pulmonary Arterial Pressure ◽  
Control Protocol ◽  
Relaxing Factor ◽  
Fetal Lamb ◽  
Pulmonary Arterial ◽  
Endothelium Derived Relaxing Factor ◽  
Near Term

In vitro, acetylcholine causes vasodilation by releasing endothelium-derived relaxing factor (EDRF) from endothelial cells. EDRF may be nitric oxide, derived from the amino acid L-arginine (L-Arg), by a process that is inhibited by NG-monomethyl-L-arginine (L-NMMA) and restored by L-Arg. We studied the effect of L-NMMA and L-Arg on the increase in pulmonary blood flow caused by acetylcholine in unanesthetized intrauterine near-term fetal lambs. Three protocols were employed. In each protocol, acetylcholine (0.48 +/- 0.15 micrograms/kg) was injected at 15-min intervals for 120 min. In the control protocol, nothing else was given. In the second protocol, L-NMMA (14 +/- 5 mg/kg) was given at 35 min. In the third protocol, L-NMMA was given at 35 min followed by L-Arg (138 +/- 73 mg/kg) at 80 min. In the control protocol, acetylcholine increased pulmonary blood flow 179 +/- 17% while it decreased pulmonary arterial pressure 15 +/- 1% and did not affect left atrial pressure. The response to each injection lasted less than 1 min and did not change throughout the experiment. L-NMMA completely blocked, whereas L-Arg completely restored, the effect of acetylcholine on pulmonary blood flow. We conclude that acetylcholine increases pulmonary blood flow in the fetal lamb via the release of EDRF derived from L-Arg. We speculate that endothelium-dependent vasodilation may play a role in the increase in pulmonary blood flow at birth.

Pulmonary venular responses to anoxia, 5-hydroxytryptamine and histamine

1960 ◽  
Vol 198 (5) ◽  
pp. 1032-1036 ◽  
Author(s):  
Domingo M. Aviado
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Pulmonary Blood Flow ◽  
Pulmonary Arterial Pressure ◽  
Anesthetized Dogs ◽  
Pulmonary Arterial ◽  
Constrictor Response

In anesthetized dogs, the inhalation of 5% oxygen causes a rise in pulmonary arterial pressure but no rise in venular pressures measured by catheters with outside diameters of 0.4 mm and 1.0 mm. The venular pressure measured by the 0.4-mm catheter showed a consistent rise to 5-hydroxytryptamine. This venular constrictor response to 5-hydroxytryptamine is encountered even when pulmonary blood flow is kept constant by perfusion. The venular response to histamine is variable.

Pulmonary blood flow distribution measured by radionuclide-computed tomography

1983 ◽  
Vol 54 (1) ◽  
pp. 225-233 ◽  
Author(s):  
H. Maeda ◽  
H. Itoh ◽  
Y. Ishii ◽  
G. Todo ◽  
T. Mukai ◽  
...  
Keyword(s):  
Computed Tomography ◽  
Blood Flow ◽  
Arterial Pressure ◽  
Pulmonary Blood Flow ◽  
Pulmonary Arterial Pressure ◽  
Venous Pressure ◽  
Flow Distribution ◽  
Mitral Valve Stenosis ◽  
Blood Flow Distribution ◽  
Pulmonary Arterial

Distributions of pulmonary blood flow per unit lung volume were measured with subjects in the prone, supine, and sitting positions by means of radionuclide-computed tomography of intravenously administered 99mTc-labeled macroaggregates of human serum albumin. The blood flow was greater in the direction of gravity in all 31 subjects except one with severe mitral valve stenosis. With the subject in a sitting position, four different types of distribution were distinguished. One type had a three-zonal blood flow distribution as previously reported by West and co-workers (J. Appl. Physiol. 19: 713–724, 1964). Pulmonary arterial pressure and venous pressure estimated from this model showed reasonable agreement with pulmonary arterial pressure and capillary wedge pressure measured by Swan-Ganz catheter in 17 supine patients and in 2 sitting patients. The method makes possible noninvasive assessment of pulmonary vascular pressures.

Systemic and pulmonary vasomotor waves

1965 ◽  
Vol 209 (1) ◽  
pp. 37-50 ◽  
Author(s):  
Ricardo Ferretti ◽  
Neil S. Cherniack ◽  
Guy Longobardo ◽  
O. Robert Levine ◽  
Eugene Morkin ◽  
...  
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Pulmonary Blood Flow ◽  
Breathing Pattern ◽  
Pulmonary Arterial Pressure ◽  
Arterial Blood Flow ◽  
Mayer Waves ◽  
Arterial Blood ◽  
Vasomotor Activity ◽  
Pulmonary Arterial

Rhythmic oscillations in systemic arterial blood pressure (Mayer waves) were produced in the dog by metabolic acidosis; hypoxia generally augmented the amplitude of the Mayer waves. When the Mayer waves exceeded 20 mm Hg in amplitude, they were associated with rhythmic fluctuations in pulmonary arterial pressure. The pulmonary arterial waves resembled the Mayer waves with respect to frequency and independence of the breathing pattern but were generally smaller in amplitude Measurements of instantaneous pulmonary arterial blood flow indicate that the rhythmic fluctuations in pulmonary arterial pressure represent the passive effects of fluctuations in pulmonary blood flow rather than fluctuations in pulmonary vasomotor activity. In turn, the swings in pulmonary arterial blood flow appear to originate in rhythmic variations in systemic vasomotor activity.

Alterations in Endogenous Nitric Oxide Production After Cardiopulmonary Bypass in Lambs With Normal and Increased Pulmonary Blood Flow

Circulation ◽  
2000 ◽  
Vol 102 (suppl_3) ◽  
Author(s):  
D. Michael McMullan ◽  
Janine M. Bekker ◽  
Andrew J. Parry ◽  
Michael J. Johengen ◽  
Alexander Kon ◽  
...  
Keyword(s):  
Blood Flow ◽  
Pulmonary Hypertension ◽  
Cardiopulmonary Bypass ◽  
Pulmonary Blood Flow ◽  
Vascular Reactivity ◽  
Pulmonary Arterial Pressure ◽  
No Production ◽  
Protein Levels ◽  
Pulmonary Arterial ◽  
Nitrite Nitrate

Background —After cardiopulmonary bypass (CPB), altered vascular reactivity is a major source of complications, particularly for children with increased pulmonary blood flow. Although changes in agonist-induced NO activity are well described after CPB, potential changes in basal NO production and their role in post-CPB pulmonary hypertension remain unclear. By using aortopulmonary vascular graft placement in the fetal lamb (shunt lambs), we established a unique model of pulmonary hypertension that mimics congenital heart disease with increased pulmonary blood flow. The objective of the present study was to investigate potential alterations in endogenous NO production after CPB in lambs with normal and increased pulmonary blood flow. Methods and Results —Vascular pressures and blood flows were monitored in 1-month-old lambs (n=7) with increased pulmonary blood flow and 6 age-matched control lambs. After shunt closure, hypothermic CPB (25°C) was performed for 2 hours. The hemodynamic variables were monitored for 4 hours after CPB. Before, during, and after CPB, peripheral lung biopsies were performed to determine tissue NO, nitrite, nitrate, and cGMP concentrations; total NO synthase (NOS) activity; and endothelial NOS protein levels. Hypothermic CPB increased both mean pulmonary arterial pressure and left pulmonary vascular resistance ( P <0.05). The increase in pulmonary arterial pressure induced in shunt lambs was greater than that induced in control lambs ( P <0.05). Four hours after CPB, tissue concentrations of NO, nitrite, nitrate, and cGMP were decreased to ≈70% of pre-CPB levels in both control and shunt lambs ( P <0.05). Total NOS activity and endothelial NOS protein levels were unchanged. Conclusions —Modest decreases in basal NO production, the inability to increase NO production, or both may play a role in the altered pulmonary vascular reactivity after CPB. The decrease in NO is independent of gene expression. However, other mechanisms for this decrease, such as substrate or cofactor availability, warrant further study.

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