Regional hypoxic pulmonary vasoconstriction in prone pigs

2005 ◽  
Vol 99 (1) ◽  
pp. 363-370 ◽  
Author(s):  
I. R. Starr ◽  
W. J. E. Lamm ◽  
B. Neradilek ◽  
N. Polissar ◽  
R. W. Glenny ◽  
...  

Hypoxic pulmonary vasoconstriction (HPV) is known to affect regional pulmonary blood flow distribution. It is unknown whether lungs with well-matched ventilation (V̇)/perfusion (Q̇) have regional differences in the HPV response. Five prone pigs were anesthetized and mechanically ventilated (positive end-expiratory pressure = 2 cmH2O). Two hypoxic preconditions [inspired oxygen fraction (FiO2) = 0.13] were completed to stabilize the animal's hypoxic response. Regional pulmonary blood Q̇ and V̇ distribution was determined at various FiO2 (0.21, 0.15, 0.13, 0.11, 0.09) using the fluorescent microsphere technique. Q̇ and V̇ in the lungs were quantified within 2-cm3 lung pieces. Pieces were grouped, or clustered, based on the changes in blood flow when subjected to increasing hypoxia. Unique patterns of Q̇ response to hypoxia were seen within and across animals. The three main patterns (clusters) showed little initial difference in V̇/Q̇ matching at room air where the mean V̇/Q̇ range was 0.92–1.06. The clusters were spatially located in cranial, central, and caudal portions of the lung. With decreasing FiO2, blood flow shifted from the cranial to caudal regions. We determined that pulmonary blood flow changes, caused by HPV, produced distinct response patterns that were seen in similar regions across our prone porcine model.

1980 ◽  
Vol 49 (5) ◽  
pp. 834-840 ◽  
Author(s):  
A. B. Malik ◽  
H. van der Zee ◽  
P. H. Neumann ◽  
N. B. Gertzberg

Regional pulmonary blood flow was determined in dogs during varying degrees of pulmonary edema induced by infusing 179.2-659.4 ml/kg normal saline over 2-3 h. Pulmonary hemodynamics and regional blood flows were measured during the base-line period and at 30 min postinfusion. The degree of pulmonary edema was determined by the final extravascular lung water-to-bloodless dry lung weight ratio (W/D). In dogs developing gross alveolar edema (W/D of 10.70 +/- 0.88 vs. 3.10 +/- 0.30 in controls), the blood flow was shifted to either upper or dependent lung regions. The shift to the upper regions was associated with an increased (P < 0.05) pulmonary arterial pressure (Ppa), whereas the shift to the dependent lung was not associated with a significant change in Ppa. Breathing 100% O2 did not prevent these shifts, suggesting that they were not due to localized hypoxic pulmonary vasoconstriction. The flow distribution patterns were also not related to regional differences in edema. In contrast to the changes during fulminant edema, blood flow distribution did not change after moderate levels of pulmonary edema (W/D of 6.03 0.69), suggesting that gross alveolar flooding is required for a redistribution of pulmonary blood flow. Flow redistribution to the upper lung during airway flooding may be due to increase in Ppa, whereas the increased flow in the dependent lung during the same degree of edema may be due to "bulging" of alveolar vessels into the air spaces, secondary to a decrease in surface activity.


Author(s):  
Kelly S. Burrowes ◽  
Annalisa J. Swan ◽  
Alys R. Clark ◽  
Quentin P.P. Croft ◽  
Keith L. Dorrington ◽  
...  

1957 ◽  
Vol 191 (3) ◽  
pp. 446-452 ◽  
Author(s):  
Hans G. Borst ◽  
James L. Whittenberger ◽  
Erik Berglund ◽  
Maurice McGregor

Effects of hypoxia and of hypercapnia on pulmonary blood flow distribution were examined in 19 dogs. The blood flow through each lung was continuously recorded; the test gas was administered to one lung, and the other lung was used as the control. Low oxygen gas mixtures were administered to one lung for periods of 2–47 minutes. When constriction occurred, it began within one-half minute after the gas administration was started and reached a plateau within 8–20 minutes. Vasodilation was never observed. In most animals no vasomotor effect of hypoxia was found early in the experiment (less than 6 hr. after induction of anesthesia), but seven of the early nonreactors became positive later in the experiment. After 6–8 hours from induction of anesthesia, all animals tested showed a vasoconstrictor response to hypoxia. The administration to one lung of 5 or 10% carbon dioxide for 2–10 minutes was always accompanied by vasoconstriction in that lung. In dogs that showed unilateral pulmonary vasoconstriction during hypoxia, further vasoconstriction was produced by adding 5% carbon dioxide. Some of the contradictory results of other investigators may be explained by the refractory period observed in these experiments.


1987 ◽  
Vol 62 (5) ◽  
pp. 1808-1813 ◽  
Author(s):  
D. P. Schuster ◽  
D. R. Dennis

We studied whether intravenously administered inhibitors of leukotriene synthesis (diethylcarbamazine, DEC) or end-organ effect (FPL-55712) would change the distribution of regional pulmonary blood flow (rPBF) caused by left lower lobe (LLL) alveolar hypoxia in dogs. Both drugs failed to alter rPBF. In addition, the pressor response to whole-lung hypoxia was not blocked by an FPL-55712 infusion. On the other hand, nitroprusside, as a nonspecific vasodilator also administered intravenously, was able to partially reverse the effects of LLL hypoxia on rPBF. Thus our data do not support a role for leukotriene mediation of hypoxic pulmonary vasoconstriction in dogs.


1989 ◽  
Vol 66 (2) ◽  
pp. 782-791 ◽  
Author(s):  
L. B. Wilson ◽  
M. G. Levitzky

We investigated the role of the autonomic nervous system in the arterial chemoreceptor attenuation of hypoxic pulmonary vasoconstriction (HPV) using anesthetized dogs. Total pulmonary blood flow (Qt) and left pulmonary blood flow (Ql) were determined using electromagnetic flow probes. Carotid body chemoreceptors were perfused using blood pumped from an extracorporeal circuit containing an oxygenator. Four groups were used: 1) prevagotomy (control), 2) bilateral vagotomy, 3) post-atropine, and 4) post-propranolol. Left lung hypoxia decreased Ql/Qt from 42.9 +/- 2.9 to 28.1 +/- 3.0%, from 41.1 +/- 5.3 to 26.7 +/- 4.2%, from 38.6 +/- 1.3 to 22.2 +/- 2.4%, and from 48.2 +/- 4.2 to 28.5 +/- 3.7% in the four groups, respectively. Chemoreceptor stimulation during unilateral hypoxia increased Ql/Qt from 28.1 +/- 3.0 to 39.1 +/- 4.9% and from 28.5 +/- 3.7 to 40.6 +/- 3.7% in the control and propranolol groups. However, chemoreceptor stimulation had no effect on Ql/Qt during left lung hypoxia after vagotomy or atropine, as Ql/Qt went from 26.7 +/- 4.2 to 29.3 +/- 5.2% and from 22.2 +/- 2.4 to 24.1 +/- 1.5% in groups 2 and 3, respectively. Because chemoreceptor stimulation did not affect HPV in groups 2 and 3, we conclude that the chemoreceptor attenuation of HPV is mediated by the parasympathetic nervous system.


1994 ◽  
Vol 86 (5) ◽  
pp. 639-644 ◽  
Author(s):  
N. W. Morrell ◽  
K. S. Nijran ◽  
T. Biggs ◽  
W. A. Seed

1. Acute hypoxic pulmonary vasoconstriction is important in the restoration of ventilation—perfusion balance in the presence of regional alveolar hypoventilation. However, the magnitude and time course of this response in man has not been adequately characterized in regions smaller than an entire lung. We have studied the effectiveness of hypoxic vasoconstriction in diverting blood from hypoxic lobes in normal supine subjects, and have documented the redistribution of pulmonary blood flow under these conditions. 2. Lobar hypoxia was induced for 80–300 s by placing occluding balloon-tipped catheters in lobar bronchi during fibreoptic bronchoscopy in 10 normal subjects. Respiratory gas partial pressures within occluded lobes were measured with a mass spectrometer. The percentage reduction in blood flow to the hypoxic lobes was assessed after injection of 99mTc-labelled albumin by γ-scintigraphy, and compared with a control scan performed 1 week later. A computer program was used to analyse changes in regional pulmonary perfusion. 3. During lobar bronchial occlusion respiratory gas partial pressures rapidly approached reported values for mixed venous partial pressures. After a mean time of occlusion of 3.5 min lobar blood flow was reduced by 47 ± 5%. During occlusions pulmonary blood flow was not evenly redistributed, but was preferentially redistributed to more cranial lung regions. 4. We conclude that acute hypoxic pulmonary vasoconstriction in occluded lobes is more effective at rapidly diverting pulmonary blood flow away from hypoxic lung regions than has previously been reported in man during unilateral hypoxia of an entire lung. Non-uniform redistribution of pulmonary blood flow in the supine subject is likely to be due to compression of the lung bases by the diaphragm in the supine position.


1992 ◽  
Vol 72 (3) ◽  
pp. 1173-1178 ◽  
Author(s):  
K. A. Jarvis ◽  
E. P. Steffey ◽  
W. S. Tyler ◽  
N. Willits ◽  
M. Woliner

Results of recent investigations in humans and dogs indicate that gravity-independent factors may be important in determining the distribution of pulmonary blood flow. To further evaluate the role of gravity-independent factors, pulmonary blood flow distribution was examined using 15-microns radionuclide-labeled microspheres in five prone ponies over 5 h of pentobarbital sodium anesthesia. The ponies were killed, and the lungs were excised and dried by air inflation (pressure 45 cmH2O). The dry lungs were cut into transverse slices 1–2 cm thick along the dorsal-ventral axis, parallel to gravity. Radioactivity of pieces cut from alternate slices was measured with a gamma well counter. The main finding was a preferential distribution of pulmonary blood flow to dorsal-caudal regions and higher flow in the center of each lung slice when compared with the slice periphery. Flow was lowest in cranial and ventral areas. Differences of +/- 2 SD were observed between core and peripheral blood flow. No medial-lateral differences were found. Pulmonary blood flow distribution did not change over 5 h of anesthesia, and the basic flow pattern was not different in the left vs. right lung. These results suggest that in the intact prone mechanically ventilated pony (inspired O2 fraction greater than or equal to 0.95) factors other than gravity are primary determinants of pulmonary blood flow.


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