Effect of lung inflation on pulmonary vascular resistance by arterial and venous occlusion

1982 ◽  
Vol 53 (5) ◽  
pp. 1110-1115 ◽  
Author(s):  
T. S. Hakim ◽  
R. P. Michel ◽  
H. K. Chang
Keyword(s):  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Venous Pressure ◽  
Venous Occlusion ◽  
Lung Inflation ◽  
Pressure Drops ◽  
Constant Flow Rate ◽  
Initial Decrease ◽  
Occlusion Technique ◽  
First Time

To explain the changes in pulmonary vascular resistance (PVR) with positive- and negative-pressure inflation (PPI and NPI, respectively), we studied their effects in isolated canine left lower lobes perfused at constant flow rate. The venous pressure was kept constant relative to atmospheric pressure during lung inflation. The total arteriovenous pressure drop (delta Pt) was partitioned with the arterial and venous occlusion technique into pressure drops across arterial and venous segments (large indistensible extra-alveolar vessels) and a middle segment (small distensible extra-alveolar and alveolar vessels). PPI caused a curvilinear increase in delta Pt due to a large Starling resistance effect in the alveolar vessels associated with a small volume-dependent increase in the resistance of alveolar and extra-alveolar vessels. NPI caused an initial decrease in delta Pt due to reduction in the resistance of extra-alveolar vessels followed by an increase in delta Pt due to a volume-dependent increase in the resistance of all vessels. In conclusion, we provided for the first time evidence that lung inflation results in a volume-dependent increase in the resistance of both alveolar and extra-alveolar vessels. The data suggest that while the volume-related changes in PVR are identical with PPI and NPI, there are pressure-related changes that can be different between the two modes of inflation.

Effect of hematocrit on vascular pressure profile in dog lungs

1985 ◽  
Vol 58 (3) ◽  
pp. 743-748 ◽  
Author(s):  
M. Julien ◽  
T. S. Hakim ◽  
R. Vahi ◽  
H. K. Chang
Keyword(s):  
Vascular Resistance ◽  
Lower Lobe ◽  
Blood Flow Rate ◽  
Pressure Profile ◽  
Venous Occlusion ◽  
Longitudinal Distribution ◽  
Middle Segment ◽  
Pressure Drops ◽  
Occlusion Technique

We studied the effect of blood hematocrit (Hct) on the longitudinal distribution of pulmonary vascular pressure profile in an in situ isolated left lower lobe preparation of dog lung using the arterial and venous occlusion technique. The total arteriovenous pressure drop (delta PT) across the lobe was partitioned into pressure drops across an arterial (delta Pa), a venous (delta Pv), and a middle segment (delta Pm). Three levels of Hct were studied: low (18 +/- 5%), normal (41 +/- 4%), and high (66 +/- 5%). Arterial and venous occlusions were performed under constant-flow or constant-pressure perfusion. When flow was maintained constant, the increase in delta PT between low and normal Hct was due to increases in delta Pa, delta Pm, and delta Pv; however, between normal and high Hct, the increase in delta PT was primarily due to an increase in delta Pm. When delta PT was kept constant by adjusting flow, changes in delta Pa and delta Pv were in the same direction as changes in blood flow rate but in opposite direction to changes in Hct. In contrast, changes in delta Pm were in the same direction as changes in Hct. The results showed that the vascular resistance of the middle segment ranged from 7% of total pulmonary vascular resistance at low Hct to 53% at high Hct, suggesting that the vessels within this segment offer the greatest impairment to the transit of blood cells.

Segmental pulmonary vascular resistance in progressive hydrostatic and permeability edema

1985 ◽  
Vol 59 (1) ◽  
pp. 242-247 ◽  
Author(s):  
C. G. Wang ◽  
T. S. Hakim ◽  
R. P. Michel ◽  
H. K. Chang
Keyword(s):  
Vascular Resistance ◽  
Venous Pressure ◽  
Lower Lobe ◽  
Venous Occlusion ◽  
Longitudinal Distribution ◽  
Edema Formation ◽  
Small Rise ◽  
Occlusion Technique ◽  
Isolated Lungs

We used the in situ blood-perfused left lower lobe preparation of the dog to examine the effect of hydrostatic and permeability edema on the slope and intercept of the vascular pressure-flow (P/Q) relationship and on the longitudinal distribution of vascular resistance with the arterial and venous occlusion technique. Hydrostatic edema (HE) was induced by raising the venous pressure, and permeability edema (PE) was induced with alpha-naphthylthiourea. When the hematocrit (Hct) of the perfusate was kept normal (approximately 40%), HE had no significant effect on either the slope or the intercept of the P/Q relationship or on the distribution of vascular resistance. PE caused a small increase in the intercept of the P/Q relationship and a small rise in the resistance of the vessels in the middle segment. In another series of HE experiments in which Hct was allowed to increase during edema formation, there was a marked increase in vascular resistance. We conclude that edema per se does not increase vascular resistance significantly and that the increases in vascular resistance which were observed previously by other investigators in the isolated lungs may be due to increases in blood hematocrit.

Effects of anaphylaxis mediators on partitioned pulmonary vascular resistance during ragweed shock in dogs

1998 ◽  
Vol 84 (3) ◽  
pp. 782-790 ◽  
Author(s):  
S. N. Mink ◽  
A. Becker ◽  
H. Unruh ◽  
W. Kepron
Keyword(s):  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Anaphylactic Shock ◽  
Arterial Occlusion ◽  
Relative Increase ◽  
Longitudinal Distribution ◽  
Lipoxygenase Pathway ◽  
Pressure Drops ◽  
Occlusion Technique ◽  
Pulmonary Arterial

We examined the effect of anaphylactic shock on the longitudinal distribution of pulmonary vascular resistance (PVR) in ragweed-sensitized dogs in which PVR was partitioned into an upstream arterial component (Rus) and a downstream venous and capillary component (Rds). We also assessed whether Rus and Rds would be reduced by pretreatment with histamine H1- and H2-receptor blocking agents and with cyclooxygenase and lipoxygenase pathway inhibitors. Anesthetized animals were examined on separate occasions 3 wk apart in which one of the treatments was randomly given. The pulmonary arterial occlusion technique was used to determine segmental pressure drops. During ragweed challenge, PVR increased ≈4 times compared with the preshock value (3.04 vs. 12.07 mmHg ⋅ l−1⋅ min; P< 0.05). Although both Rus and Rds increased postshock, the greatest relative increase occurred in Rds. None of the treatments reduced partitioned resistances compared with no treatment. Our results show that, under conditions of anaphylactic shock, increases in Rus and Rds could not be ascribed to release of histamine or products of the cyclooxygenase and lipoxygenase pathways.

Ventilatory effects on left atrium and pulmonary vascular resistance

1963 ◽  
Vol 18 (1) ◽  
pp. 117-122
Author(s):  
K. Kuramoto ◽  
S. Rodbard
Keyword(s):  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Negative Pressure ◽  
Left Atrial ◽  
Venous Pressure ◽  
Negative Resistance ◽  
Lung Inflation ◽  
Intrapleural Pressure ◽  
Ventilatory Effects ◽  
Isolated Lungs

Pulmonary vascular resistance was studied in thoracotomized dogs enclosed in a respirator. The lung was inflated by respirator pressure, the trachea being open to the atmosphere. Blood flow through the lung was held constant. “Intrapleural” and left atrial pressures fell equally during inspiration; the pulmonary arterial pressure fell to a lesser extent. Calculated resistance increased during the midinspiratory phase and became maximal at end-inspiration and early expiration. Negative-pressure lung inflation had only small effects on resistance at minimal negative respirator pressures; resistance increased markedly as “intrapleural” pressure became progressively more negative. Resistance returned to control values at each end-expiration, regardless of the previous degree of negative-pressure inflation. Resistance increased in isolated lungs under constant flow perfusion when pulmonary venous and “intrapleural” pressures oscillated together; resistance fell when pulmonary venous pressure was held constant with respect to atmospheric pressure. The results suggest that previous disagreements on pulmonary vascular resistance may have been due to failure to evaluate the effect of “intrapleural” pressure on left atrial pressure. The increased resistance during negative-pressure inflation may result from a negative transmural pressure in the collapsible vessels of the lung. Submitted on July 18, 1962

Site of pulmonary hypoxic vasoconstriction studied with arterial and venous occlusion

1983 ◽  
Vol 54 (5) ◽  
pp. 1298-1302 ◽  
Author(s):  
T. S. Hakim ◽  
R. P. Michel ◽  
H. Minami ◽  
H. K. Chang
Keyword(s):  
Flow Rate ◽  
Airway Pressure ◽  
Lower Lobe ◽  
Blood Flow Rate ◽  
Venous Occlusion ◽  
Smooth Muscle Contraction ◽  
Vasoactive Drugs ◽  
Pressure Drops ◽  
Hypoxic Vasoconstriction ◽  
Occlusion Technique

We applied the arterial and venous occlusion technique in an in situ, isolated left lower lobe preparation of a dog lung to compare the effects of hypoxia with the effects of airway pressure elevation, and the infusion of serotonin, norepinephrine, and histamine. The total arteriovenous pressure drop across the lobe was partitioned longitudinally into pressure drops across the relatively indistensible arteries (delta Pa) and veins (delta Pv) and across the middle distensible vessels (delta Pm). Hypoxia increased primarily delta Pm, as did elevation of airway pressure, whereas the vasoactive drugs increased either delta Pa or delta Pv. The increases in pulmonary arterial pressure (Pa) caused by hypoxia and by elevation of airway pressure were independent of blood flow rate, but increases in Pa induced by the vasoactive drugs were dependent on flow rate. We conclude that in the dog hypoxia acts primarily on small distensible vessels, whereas pulmonary vasoactive drugs constrict the relatively indistensible arteries and veins. It is possible that the increase in pulmonary vascular resistance during hypoxia did not involve smooth muscle contraction.

Partitioning of pulmonary vascular resistance in dogs by arterial and venous occlusion

1982 ◽  
Vol 52 (3) ◽  
pp. 710-715 ◽  
Author(s):  
T. S. Hakim ◽  
R. P. Michel ◽  
H. K. Chang
Keyword(s):  
Flow Rate ◽  
Venous Pressure ◽  
Venous Occlusion ◽  
Pulmonary Vasculature ◽  
Pressure Drops ◽  
Lower Lung ◽  
Arterial Inflow ◽  
Arteries And Veins ◽  
Lung Lobes

We perfused in situ isolated left lower lung lobes at a steady flow rate in zone 3 condition. When the lobar arterial inflow was suddenly occluded, the arterial pressure (Pa) fell rapidly and then more slowly. When the lobar venous outflow was suddenly occluded, the venous pressure (Pv) rose rapidly and then continued to rise more slowly. The rapid changes in Pa and Pv with inflow and outflow occlusion, respectively, represent the pressure drops across the arterial (delta Pa) and venous (delta Pv) relatively indistensible vessels. The total arteriovenous pressure difference (delta Pt) minus delta Pa + delta Pv gives the pressure drop across the vessels in the middle (delta Pm) that are much more distensible. Serotonin and histamine infusion increased delta Pa and delta Pv, respectively, but left delta Pm unchanged. delta Pa and delta Pv, but not delta Pm, increased as flow rate was increased. The studies with varying flow rate and venous pressures suggested that the arteries and veins became resistant to distension when their transmural pressures exceeded 10--5 Torr, respectively. Under the conditions studied, the middle nonmuscular segment contributed a major fraction of the vascular compliance and less than 16% of the total resistance. The muscular arteries and veins contributed equally to the remaining resistance. We conclude that the arterial and venous occlusion method is a useful technique to describe the resistance and compliance of different segments of the pulmonary vasculature.

Intrinsic control of colonic blood flow and oxygenation

1980 ◽  
Vol 238 (6) ◽  
pp. G478-G484
Author(s):  
P. R. Kvietys ◽  
T. Miller ◽  
D. N. Granger
Keyword(s):  
Blood Flow ◽  
Vascular Resistance ◽  
Perfusion Pressure ◽  
Reactive Hyperemia ◽  
Venous Pressure ◽  
Arterial Occlusion ◽  
Venous Occlusion ◽  
Colonic Blood Flow ◽  
O2 Extraction ◽  
O2 Delivery

In a denervated autoperfused dog colon preparation, arterial perfusion pressure, venous outflow pressure, blood flow, and arteriovenous O2 difference were measured during graded arterial pressure alterations, arterial occlusion, venous pressure elevation, venous occlusion, and local intra-arterial infusion of adenosine. As perfusion pressure was reduced from 100 to 30 mmHg, colonic blood flow decreased and arteriovenous O2 difference increased. Although blood flow was not autoregulated O2 delivery was maintained within 10% of control between 70 to 100 mmHg and then decreased with further reduction in perfusion pressure. Arterial occlusion (15, 30, and 60 s) resulted in a postocclusion reactive hyperemia; the magnitude of the hyperemia was directly related to the duration of occlusion. Venous occlusion resulted in a postocclusion reactive hypoemia. Elevation of venous pressure from 0 to 20 mmHg increased vascular resistance, O2 extraction, and the capillary filtration coefficient, but decreased O2 delivery. Infusion of adenosine decreased vascular resistance and O2 extraction, but increased O2 delivery. These data suggest that both metabolic and myogenic mechanisms are involved in the control of colonic blood flow and oxygenation.

Effects of Hct and norepinephrine on segmental vascular resistance distribution in isolated perfused rat livers

2004 ◽  
Vol 286 (1) ◽  
pp. H121-H130 ◽  
Author(s):  
Chiaki Kamikado ◽  
Toshishige Shibamoto ◽  
Minoru Hongo ◽  
Shozo Koyama
Keyword(s):  
Blood Flow ◽  
Vascular Resistance ◽  
Venous Pressure ◽  
Regression Line ◽  
Venous Occlusion ◽  
Portal Venous Pressure ◽  
Venous Resistance ◽  
Four Levels ◽  
Rat Livers ◽  
Line Analysis

We studied the effects of blood hematocrit (Hct), blood flow, or norepinephrine on segmental vascular resistances in isolated portally perfused rat livers. Total portal hepatic venous resistance ( Rt) was assigned to the portal ( Rpv), sinusoidal ( Rsinus), and hepatic venous ( Rhv) resistances using the portal occlusion (Ppo) and the hepatic venous occlusion (Phvo) pressures that were obtained during occlusion of the respective line. Four levels of Hct (30%, 20%, 10%, and 0%) were studied. Rpv comprises 44% of Rt, 37% of Rsinus, and 19% of Rhv in livers perfused at 30% Hct and portal venous pressure of 9.1 cmH2O. As Hct increased at a given blood flow, all three segmental vascular resistances of Rpv, Rsinus, and Rhv increased at flow >15 ml/min. As blood flow increased at a given Hct, only Rsinus increased without changes in Rpv or Rhv. Norepinephrine increased predominantly Rpv, and, to a smaller extent, Rsinus, but it did not affect Rhv. Finally, we estimated Ppo and Phvo from the double occlusion maneuver, which occluded simultaneously both the portal and hepatic venous lines. The regression line analysis revealed that Ppo and Phvo were identical with those measured by double occlusion. In conclusion, changes in blood Hct affect all three segmental vascular resistances, whereas changes in blood flow affect Rsinus, but not Rpv or Rhv. Norepinephrine increases mainly presinusoidal resistance. Ppo and Phvo can be obtained by the double occlusion method in isolated perfused rat livers.

Effect of increased alveolar surface tension on segmental pulmonary vascular resistance

1988 ◽  
Vol 64 (1) ◽  
pp. 154-161 ◽  
Author(s):  
G. F. Nieman ◽  
T. S. Hakim ◽  
C. E. Bredenberg
Keyword(s):  
Surface Tension ◽  
Pressure Gradient ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Lower Lobe ◽  
Normal Lung ◽  
Pressure Flow ◽  
Constant Flow Rate ◽  
Alveolar Surface ◽  
Surfactant Depletion

The site of change in pulmonary vascular resistance (PVR) after surfactant displacement with the detergent diocytl sodium sulfosuccinate (OT) was studied in the isolated canine left lower lobe preparation. Changes in PVR were assessed using the arterial and venous occlusion technique and the vascular pressure-flow relationship. Changes in alveolar surface tension were confirmed from measurements of pulmonary compliance as well as from measurements of surface tension of extracts from lung homogenates. After surfactant depletion (the perfusion rate constant) the total pressure gradient (delta PT) across the lobe increased from 13.4 +/- 1 to 17.1 +/- 0.8 mmHg. This increase in delta PT was associated with a significant increase in the arterial and venous gradients (3.7 +/- 0.3 to 4.9 +/- 0.4 and 5.7 +/- 0.5 to 9.4 +/- 0.6 mmHg, respectively) and a decrease in middle pressure gradient (4.1 +/- 0.8 to 2.9 +/- 0.6 mmHg). The vascular pressure-flow relationship supported these findings and showed that the mean slope increased by 52% (P less than 0.05), whereas the pressure intercept decreased slightly but not significantly (3.7 +/- 0.7 to 3.2 +/- 0.8 mmHg). These results suggest that the resistance of arteries and veins increases, whereas the resistance of the middle segment decreases after surfactant depletion. These effects were apparently due to surface tension that acts directly on the capillary wall. Direct visualization of subpleural capillaries supported the notion that capillaries become distended and recruited as alveolar surface tension increases. In the normal lung (perfused at constant-flow rate) changes in alveolar pressure (Palv) were transmitted fully to the capillaries as suggested by equal changes in pulmonary arterial pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

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