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.

Pulmonary venous pressure increases during alveolar hypoxia in isolated lungs of newborn pigs

1992 ◽  
Vol 73 (2) ◽  
pp. 552-556 ◽  
Author(s):  
C. D. Fike ◽  
M. R. Kaplowitz
Keyword(s):  
Airway Pressure ◽  
Left Atrial ◽  
Pulmonary Arterial Pressure ◽  
Venous Pressure ◽  
Co2 Gas ◽  
Hypoxic Vasoconstriction ◽  
Alveolar Hypoxia ◽  
Pulmonary Arterial ◽  
Newborn Pigs ◽  
Isolated Lungs

The purpose of this study was to determine whether pulmonary venous pressure increases during alveolar hypoxia in lungs of newborn pigs. We isolated and perfused with blood the lungs from seven newborn pigs, 6–7 days old. We maintained blood flow constant at 50 ml.min-1.kg-1 and continuously monitored pulmonary arterial and left atrial pressures. Using the micropuncture technique, we measured pressures in 10 to 60-microns-diam venules during inflation with normoxic (21% O2–69–74% N2–5–10% CO2) and hypoxic (90–95% N2–5–10% CO2) gas mixtures. PO2 was 142 +/- 21 Torr during normoxia and 20 +/- 4 Torr during hypoxia. During micropuncture we inflated the lungs to a constant airway pressure of 5 cmH2O and kept left atrial pressure greater than airway pressure (zone 3). During hypoxia, pulmonary arterial pressure increased by 69 +/- 24% and pressure in small venules increased by 40 +/- 23%. These results are similar to those obtained with newborn lambs and ferrets but differ from results with newborn rabbits. The site of hypoxic vasoconstriction in newborn lungs is species dependent.

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.

Microvascular pressures during hypoxia in isolated lungs of newborn rabbits

1988 ◽  
Vol 65 (1) ◽  
pp. 283-287 ◽  
Author(s):  
C. D. Fike ◽  
S. J. Lai-Fook ◽  
R. D. Bland
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Airway Pressure ◽  
Left Atrial ◽  
Pulmonary Arterial Pressure ◽  
Hypoxic Conditions ◽  
Hypoxic Vasoconstriction ◽  
Pulmonary Arterial ◽  
Isolated Lungs ◽  
Ventilation Of The Lungs

The purpose of this study was to determine the sites of hypoxic vasoconstriction in lungs of newborn rabbits. We isolated and perfused with blood the lungs from 19 rabbit pups, 7-23 days old. We maintained blood flow constant, continuously monitored pulmonary arterial and left atrial pressures, and alternated ventilation of the lungs with 95% O2-5% CO2 (control), and 95% N2-5% CO2 (hypoxia). Using micropipettes and a servonulling device, we measured pressures in 20-60-micron-diam subpleural arterioles and venules during control and hypoxic conditions. We inflated the lungs to a constant airway pressure of 5-7 cmH2O and kept left atrial pressure greater than airway pressure (zone 3) during micropuncture. In eight lungs we measured microvascular pressures first during control and then during hypoxia. We reversed this order in four lungs. In seven lungs we measured microvascular pressures only during hypoxia. We found a significant increase in pulmonary arterial pressure with no change in microvascular pressures. These results indicate that the site of hypoxic vasoconstriction in lungs of newborn rabbits is arteries greater than 60 micron in diameter.

Effect of continuous postive-pressure ventilation (CPPV) on edema formation in dog lung

1975 ◽  
Vol 39 (4) ◽  
pp. 672-679 ◽  
Author(s):  
P. Caldini ◽  
J. D. Leith ◽  
M. J. Brennan
Keyword(s):  
Blood Flow ◽  
Pulmonary Arterial Pressure ◽  
Venous Pressure ◽  
Arterial Oxygen Tension ◽  
Lung Parenchyma ◽  
Arterial Oxygen ◽  
Morphometric Measurements ◽  
Edema Formation ◽  
Significant Difference ◽  
Pulmonary Arterial

The effect of CPPV on edema formation in lungs perfused at constant blood flow was studied in whole dogs and in isolated dog lungs. In intact animals, subjected to an increase in left atrial pressure relative to pleural pressure of 40 Torr, pulmonary shunts correlate inversely (r = -0.82) with the level of end-expiratory pressure (PEE). CPPV had no significant effect on total extravasation of liquid even though PEE higher than 20 Torr was effective in preventing liquid from accumulating in the airways. In isolated lobes, perfused at constant blood flow and at a venous pressure of zero, accumulation of liquid occurred when PEE was increased above 8–10 Torr. At comparable levels of pulmonary arterial pressure, an increase in PEE resulted in lesser accumulation of liquid than when pulmonary venous pressure was elevated. Morphometric measurements revealed no significant difference in the distribution of accumulated liquid within the lung parenchyma between lobes made edematous either by raising venous pressuure or by raising PEE. It would appear that CPPV, while beneficial in improving arterial oxygen tension in pulmonary edema, does not prevent extravasation of liquid in lungs perfused at constant blood flow. High levels of PEE appear to damage the lung by favoring accumulation of liquid in the extravascular spaces of the lung.

Developmental differences in vascular responses to hypoxia in lungs of rabbits

1994 ◽  
Vol 77 (2) ◽  
pp. 507-516 ◽  
Author(s):  
C. D. Fike ◽  
M. R. Kaplowitz
Keyword(s):  
Arterial Pressure ◽  
Left Atrial ◽  
Pulmonary Arterial Pressure ◽  
Developmental Differences ◽  
Age Group ◽  
Co2 Gas ◽  
Micropuncture Technique ◽  
Age Related ◽  
Hypoxic Vasoconstriction ◽  
Pulmonary Arterial

Our purpose was to determine whether postnatal age and prostaglandins influence the sites of hypoxic vasoconstriction in lungs of rabbits. To do this, we used the micropuncture technique to measure pressures in 20- to 80-microns-diam subpleural arterioles and venules during sequential inflation of lungs of newborn and adult rabbits with normoxic (21% O2–7–10% CO2–69–72% N2) and hypoxic (90–93% N2–7–10% CO2) gas mixtures. Indomethacin (40 micrograms/ml) was added to the perfusate of some lungs of each age group. During hypoxia in untreated lungs of newborn rabbits, both pulmonary arterial and 20- to 80-microns-diam arteriolar pressure increased by 5%, whereas 20- to 80-microns-diam venular pressure remained the same. In contrast, during hypoxia in untreated lungs of adult rabbits, pulmonary arterial pressure increased by 48%, whereas 20- to 80-microns-diam arteriolar pressure decreased slightly and 20- to 80-microns-diam venular pressure did not change. Regardless of the presence of indomethacin, location of vessels used for micropuncture, or level of left atrial pressure, pulmonary arterial pressure was the only measured vascular pressure that increased with hypoxia in adult lungs. Thus, in adult lungs, the site of hypoxia-induced vasoconstriction was limited to arteries > 80 microns diam, whereas in newborn lungs the site of hypoxia-induced vasoconstriction included vessels both larger and smaller than 20- to 80-microns-diam arteries. This age-related difference in the sites of hypoxia-induced vasoconstriction was not found in indomethacin-treated lungs.

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.

Blood flow vs. venous pressure effects on filtration coefficient in oleic acid-injured lung

1998 ◽  
Vol 84 (3) ◽  
pp. 1011-1023 ◽  
Author(s):  
Daniel Anglade ◽  
Michel Corboz ◽  
Ahmed Menaouar ◽  
James C. Parker ◽  
Sagazaga Sanou ◽  
...  
Keyword(s):  
Blood Flow ◽  
Oleic Acid ◽  
Surface Area ◽  
Venous Pressure ◽  
Pressure Profile ◽  
Pressure Effects ◽  
Filtration Coefficient ◽  
Vascular Compliance ◽  
Pulmonary Arterial ◽  
Filtration Surface

On the basis of changes in capillary filtration coefficient ( K fc) in 24 rabbit lungs, we determined whether elevations in pulmonary venous pressure (Ppv) or blood flow (BF) produced differences in filtration surface area in oleic acid-injured (OA) or control (Con) lungs. Lungs were cyclically ventilated and perfused under zone 3 conditions by using blood and 5% albumin with no pharmacological modulation of vascular tone. Pulmonary arterial, venous, and capillary pressures were measured by using arterial, venous, and double occlusion. Before and during each K fc-measurement maneuver, microvascular/total vascular compliance was measured by using venous occlusion. K fc was measured before and 30 min after injury, by using a Ppv elevation of 7 cmH2O or a BF elevation from 1 to 2 l ⋅ min−1 ⋅ 100 g−1 to obtain a similar double occlusion pressure. Pulmonary arterial pressure increased more with BF than with Ppv in both Con and OA lungs [29 ± 2 vs. 19 ± 0.7 (means ± SE) cmH2O; P < 0.001]. In OA lungs compared with Con lungs, values of K fc (200 ± 40 vs. 83 ± 14%, respectively; P < 0.01) and microvascular/total vascular compliance ratio (86 ± 4 vs. 68 ± 5%, respectively; P < 0.01) increased more with BF than with Ppv. In conclusion, for a given OA-induced increase in hydraulic conductivity, BF elevation increased filtration surface area more than did Ppv elevation. The steep pulmonary pressure profile induced by increased BF could result in the recruitment of injured capillaries and could also shift downstream the compression point of blind (zone 1) and open injured vessels (zone 2).

Role of nitric oxide in porcine liver circulation under normal and endotoxemic conditions

1995 ◽  
Vol 78 (4) ◽  
pp. 1319-1329 ◽  
Author(s):  
T. Ayuse ◽  
N. Brienza ◽  
J. P. Revelly ◽  
J. K. Boitnott ◽  
J. L. Robotham
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Arterial Pressure ◽  
Local Control ◽  
Pulmonary Arterial Pressure ◽  
Venous Pressure ◽  
Endotoxic Shock ◽  
Liver Blood Flow ◽  
Pulmonary Arterial

The role of nitric oxide (NO) in the liver vasculature during baseline and endotoxic shock states was evaluated in 17 anesthetized pigs. Mean systemic arterial pressure, pulmonary arterial pressure, and portal venous pressure and flow, hepatic arterial pressure and flow, and cardiac output were measured. Pressure-flow (P-Q) relationships defined resistances as a back pressure and a slope. Inhibition of nitric oxide synthase (NOS) with NG-nitro-L-arginine methyl ester (L-NAME) at baseline increased mean arterial pressure, pulmonary arterial pressure, hepatic arterial pressure, and the slopes of their P-Q relationships (P < 0.05) but had no effect on portal venous pressure or its P-Q relationship. After endotoxin (10 micrograms/kg iv), NO induced arterial dilation and attenuated increases in portal venous and pulmonary arterial resistances (P < 0.05) that were reversed by L-NAME. NOS inhibition was stereospecifically reversed by L-arginine. Local control of liver blood flow at baseline via the hepatic arterial buffer response and hepatic arterial autoregulation were increased in gain after L-NAME. Endotoxic shock ablated the hepatic arterial buffer response and autoregulation independent of either NO or an alpha-adrenergic-receptor agonist (P < 0.05). Under baseline conditions, NO modulates pulmonary, systemic, and hepatic arterial but not portal venous resistances. NO production during endotoxic shock induces arterial hypotension and hepatic arterial vasodilation and attenuates increases in both portal and pulmonary resistances. NOS inhibition in endotoxic shock could increase morbidity due to a loss of local control of liver blood flow and marked increases in resistance to venous return across both the liver and lungs.

Cardiovascular responses to vasoactive intestinal contractor, a novel endothelin-like peptide

1990 ◽  
Vol 259 (4) ◽  
pp. H1152-H1160
Author(s):  
R. K. Minkes ◽  
T. R. Higuera ◽  
G. F. Rogers ◽  
E. A. Sheldon ◽  
M. A. Langston ◽  
...  
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Vascular Resistance ◽  
Pulmonary Arterial Pressure ◽  
Venous Pressure ◽  
Cardiovascular Responses ◽  
Autonomic Reflexes ◽  
Pulmonary Arterial ◽  
Artery Flow ◽  
Higher Doses

Cardiovascular and pulmonary responses to vasoactive intestinal contractor (VIC), an endothelin (ET)-like peptide from the murine gastrointestinal tract, were investigated in the cat. VIC (0.1-1.0 nmol/kg iv) decreased or elicited biphasic changes in arterial pressure (AP) and increased central venous pressure, cardiac output, pulmonary arterial pressure, and left atrial pressure. VIC produced biphasic changes in systemic vascular resistance (SVR) and pulmonary vascular resistance (PVR). VIC increased heart rate (HR) and, at the 1 nmol/kg dose, a secondary decrease was observed. Hexamethonium blocked the changes in HR in response to VIC, whereas the ganglionic blocker, meclofenamate, or glybenclamide had no effect on changes in AP, SVR, and PVR elicited by the peptide. VIC caused small changes in right ventricular contractile force and increased distal aortic and carotid artery blood flow at all doses, with secondary decreases at the higher doses. VIC decreased superior mesenteric artery flow and decreased renal blood flow at the 1 nmol/kg dose. The changes in AP in response to VIC, ET-1, and ET-2 were similar, whereas those elicited by ET-3 and sarafotoxin 6b were similar. The present data show that VIC can produce both vasodilation and vasoconstriction in the systemic vascular bed and biphasic changes in PVR in the cat. These data show that VIC can produce complex cardiovascular responses similar to those elicited by the ET peptides and that these responses are largely independent of autonomic reflexes, release of cyclooxygenase products, and activation of ATP-regulated potassium channels. We conclude that VIC may act as an ET-like peptide.

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.

Sign in / Sign up

Export Citation Format

Share Document