Functional diagrams of flow and volume for the dog's lung

1982 ◽  
Vol 52 (4) ◽  
pp. 1035-1042 ◽  
Author(s):  
D. S. Moffatt ◽  
A. C. Guyton ◽  
T. H. Adair
Keyword(s):  
Arterial Pressure ◽  
Blood Volume ◽  
Arterial Compliance ◽  
Venous Pressure ◽  
Flow Characteristics ◽  
Transpulmonary Pressure ◽  
Pulmonary Vasculature ◽  
Venous Compliance ◽  
Lung Weight ◽  
Pressure Changes

Quantitative diagrams have been constructed from data obtained in isolated perfused dog lungs for the multiple interrelationships among pressure, volume, and flow characteristics of the pulmonary vasculature. These characteristics are described in the form of functional diagrams for flows from 0.3 to 1.0 l . min-1 . 100 g wet lung weight-1 (WLW), for venous pressures from -8 to +14 Torr, and for arterial pressures from 16 to 30 Torr. The quantitative relationships were shown not to change significantly as the transpulmonary pressure changes within the range from 3 to 10 Torr. The change in blood volume with arterial pressure, called the “distributed arterial compliance,” averaged 1.5 g . Torr-1 . 100 g WLW-1. This compliance was nearly constant over the range of arterial pressure studied. On the other hand, the change in blood volume with venous pressure, called the 'distributed venous compliance” was different for different levels of venous pressures. Its maximum value was 1.04 g . Torr-1 . 100 g WLW-1 when the venous pressure was near 2 Torr. At venous pressures both above and below this pressure level this compliance decreased. These distributed compliances are described as resulting to a significant extent from changes in flow patterns through the pulmonary circulation rather than being direct indications of the true vascular compliances.

Effect of lung inflation on lung blood volume and pulmonary venous flow

1985 ◽  
Vol 58 (3) ◽  
pp. 954-963 ◽  
Author(s):  
R. Brower ◽  
R. A. Wise ◽  
C. Hassapoyannes ◽  
B. Bromberger-Barnea ◽  
S. Permutt
Keyword(s):  
Blood Volume ◽  
Transpulmonary Pressure ◽  
Left Ventricular ◽  
Respiratory Cycle ◽  
Pulmonary Vasculature ◽  
Venous Flow ◽  
Lung Inflation ◽  
Pulmonary Venous Flow ◽  
Respiratory Wave ◽  
Left Ventricular Preload

Phasic changes in lung blood volume (LBV) during the respiratory cycle may play an important role in the genesis of the respiratory wave in arterial pressure, or pulsus paradoxus. To better understand the effects of lung inflation on LBV, we studied the effect of changes in transpulmonary pressure (delta Ptp) on pulmonary venous flow (Qv) in eight isolated canine lungs with constant inflow. Inflation when the zone 2 condition was predominant resulted in transient decreases in Qv associated with increases in LBV. In contrast, inflation when the zone 3 condition was predominant resulted in transient increases in Qv associated with decreases in LBV. These findings are consistent with a model of the pulmonary vasculature that consists of alveolar and extra-alveolar vessels. Blood may be expelled from alveolar vessels but is retained in extra-alveolar vessels with each inflation. The net effect on LBV and thus on Qv is dependent on the zone conditions that predominate during inflation, with alveolar or extra-alveolar effects being greater when the zone 3 or zone 2 conditions predominate, respectively. Lung inflation may therefore result in either transiently augmented or diminished Qv. Phasic changes in left ventricular preload may therefore depend on the zone conditions of the lungs during the respiratory cycle. This may be an important modulator of respiratory variations in cardiac output and blood pressure.

Effect of hypoxic hypoxia on systemic vasculature

1984 ◽  
Vol 56 (5) ◽  
pp. 1403-1410 ◽  
Author(s):  
J. Malo ◽  
H. Goldberg ◽  
R. Graham ◽  
H. Unruh ◽  
C. Skoog
Keyword(s):  
Arterial Pressure ◽  
Inferior Vena ◽  
Superior Vena ◽  
Venous Pressure ◽  
Vena Cava ◽  
Venous Drainage ◽  
Hypoxic Hypoxia ◽  
Venous Compliance ◽  
Flow Curves ◽  
Pressure Flow

Effects of hypoxic hypoxia (HH) on cardiac output (CO), CO distribution, arterial and venous pressure-flow curves, vascular compliance, vascular time constant (tau), and resistance to venous return (RVR) were evaluated on six dogs. The vascular bed was isolated into four compartments depending on venous drainage: superior vena cava (SVC), splanchnic, renal and adrenal, and the remainder of the inferior vena cava (IVC). Low arterial O2 content and PO2 produced a threefold increase in CO at the same mean arterial pressure and a significant redistribution of CO to the SVC. Arterial pressure-flow curves decreased their slope (i.e., flow resistance) by a factor of two in the IVC and renal beds and by a factor of three in the splanchnic and SVC beds. Venous pressure-flow curves for the animal also decreased their slope significantly. HH causes a twofold increase in venous compliance and in mean venous pressure; tau did not change, but RVR halved. Seventy percent of the CO increase is explained by the increase in mean venous pressure and 30% by the reduction in RVR.

Changes in intestinal volume with hemorrhage

1960 ◽  
Vol 199 (3) ◽  
pp. 589-592 ◽  
Author(s):  
Paul C. Johnson
Keyword(s):  
Small Intestine ◽  
Blood Volume ◽  
Sympathetic Nerve Activity ◽  
Venous Pressure ◽  
Volume Changes ◽  
Local Pressure ◽  
Local Reduction ◽  
Pressure Changes ◽  
Sympathetic Discharge ◽  
Intestinal Weight

The purpose of these experiments was to study the changes in intestinal volume occurring with hemorrhage, utilizing a gravimetric technique which permitted a study of small segments of the intestine. It had been observed previously that intestinal weight often increased in the upper small intestine during hemorrhage, while in the lower small intestine it usually decreased. In studying the latter effect it was found that sympathetic nerve activity and reduction of venous pressure were both important in decreasing intestinal volume. Changes in tonus and local reduction in arterial pressure did not appear to be important. The increase in volume with hemorrhage appeared due to epinephrine discharge from the adrenal medulla since it was eliminated by adrenalectomy. Local pressure changes and alteration of tonus were eliminated as causal factors. It appears that systemic hypotension induces sympathetic discharge which in turn may cause either an increase or a decrease in intestinal blood volume. Sympathetic discharge over the vasoconstrictor fibers reduces blood volume while adrenal medullary secretion increases it. The observed response is apparently a resultant of these two antagonistic effects.

Comparison of responses to sarafotoxins 6a and 6c in pulmonary and systemic vascular beds

1992 ◽  
Vol 262 (3) ◽  
pp. H852-H861
Author(s):  
R. K. Minkes ◽  
J. A. Bellan ◽  
T. R. Higuera ◽  
P. J. Kadowitz
Keyword(s):  
Arterial Pressure ◽  
Vascular Resistance ◽  
Perfusion Pressure ◽  
Venous Pressure ◽  
Constant Flow ◽  
Flow Conditions ◽  
Arterial Perfusion ◽  
Intravenous Injections ◽  
Autonomic Reflexes ◽  
Pressure Changes

Cardiovascular and pulmonary responses to sarafotoxin (S) 6a and S6c were investigated in the anesthetized cat. Intravenous injections of the peptides in doses of 0.1-1.0 nmol/kg caused decreases or biphasic changes in arterial pressure (AP) and increases in central venous pressure, pulmonary arterial pressure (PAP), and cardiac output (CO). Secondary decreases in CO were observed in response to higher doses, and biphasic changes in systemic (SVR) and pulmonary (PVR) vascular resistances were observed. Under constant-flow conditions, the peptides only increased pulmonary lobar arterial perfusion pressure and lobar vascular resistance. AP responses to S6a, S6c, endothelin (ET)-1, ET-2, vasoactive intestinal contractor (VIC), and Lys7-ET-1 were similar, whereas AP responses to S6b and ET-3 were similar. S6a, S6b, S6c, ET-1, ET-2, ET-3, VIC, Lys7-ET-1, and big ET-1 increased PAP. S6a and S6c increased distal aortic and superior mesenteric arterial (SMA) blood flow and caused biphasic changes at the highest doses. Under constant-flow conditions, S6a and S6c produced dose-dependent biphasic changes in hindquarters perfusion pressure. Changes in SVR and PVR in response to the peptide were not affected by hexamethonium, glyburide, or meclofenamate, indicating that responses are independent of autonomic reflexes, activation of ATP-regulated K+ channels, or release of cyclooxygenase products. In contrast, N-nitro-L-arginine methyl ester decreased hindquarters vasodilator response to S6a and S6c. The present data show that S6a and S6c produce both vasodilation and vasoconstriction in the systemic vascular bed and increase lobar vascular resistance and that hindquarters vasodilator responses are mediated, in part, by the release of endothelium-derived relaxing factor.

Distributions of vascular volume and compliance in the lung

1988 ◽  
Vol 64 (1) ◽  
pp. 266-273 ◽  
Author(s):  
C. A. Dawson ◽  
D. A. Rickaby ◽  
J. H. Linehan ◽  
T. A. Bronikowski
Keyword(s):  
Arterial Pressure ◽  
Information Content ◽  
Blood Volume ◽  
Vascular Resistance ◽  
Venous Pressure ◽  
Upper Bounds ◽  
Lower And Upper Bounds ◽  
Vascular Volume ◽  
Capillary Bed ◽  
Lung Lobes

The ether- and dye-dilution methods were used to estimate the arterial, capillary, and venous volumes and compliances in isolated dog lung lobes. In the range of arterial pressure from approximately 7 to 14.5 Torr and venous pressure of 1.4 to 10.8 Torr, the total lobar blood volume ranged from approximately 2 to approximately 2.6 ml/kg body wt. About 19% of the lobar vascular volume was in the arteries, approximately 59% was in the capillaries, and approximately 22% was in the veins. The lobar vascular compliance was approximately 0.065 ml.Torr-1.kg body wt-1 with an arterial-capillary-venous distribution of approximately 30:49:21. These results suggest that the largest fractions of the intralobar blood volume and compliance are in the capillary bed. The segmental compliances along with outflow occlusion data were used to place lower and upper bounds on the arterial, capillary, and venous resistances. These bounds were 13.6 and 61.4% of the total vascular resistance for the arteries, 0 and 59.4% for the capillaries, and 5.5 and 64.9% for the veins, respectively. These bounds are rather broad, but they help to put the information content of the occlusion data under the conditions of these experiments into perspective.

Optical measurement of isolated canine lung filtration coefficients after alloxan infusion

1998 ◽  
Vol 84 (4) ◽  
pp. 1381-1387 ◽  
Author(s):  
Joseph W. Klaesner ◽  
N. Adrienne Pou ◽  
Richard E. Parker ◽  
Charlene Finney ◽  
Robert J. Roselli
Keyword(s):  
Reflection Coefficient ◽  
Blood Volume ◽  
Optical Method ◽  
Statistical Difference ◽  
Optical Measurement ◽  
Venous Pressure ◽  
Optical Technique ◽  
Lung Weight ◽  
Percent Contribution ◽  
Multiple Indicator

In this study, lung filtration coefficient ( K fc) was measured in eight isolated canine lung preparations by using three methods: standard gravimetric (Std), blood-corrected gravimetric (BC), and optical. The lungs were held in zone III conditions and were subjected to an average venous pressure increase of 8.79 ± 0.93 (mean ± SD) cmH2O. The permeability of the lungs was increased with an infusion of alloxan (75 mg/kg). The resulting K fc values (in milliliters ⋅ min−1 ⋅ cmH2O−1 ⋅ 100 g dry lung weight−1) measured by using Std and BC gravimetric techniques before vs. after alloxan infusion were statistically different: Std, 0.527 ± 0.290 vs. 1.966 ± 0.283; BC, 0.313 ± 0.290 vs. 1.384 ± 0.290. However, the optical technique did not show any statistical difference between pre- and postinjury with alloxan, 0.280 ± 0.305 vs. 0.483 ± 0.297, respectively. The alloxan injury, quantified by using multiple-indicator techniques, showed an increase in permeability and a corresponding decrease in reflection coefficient for albumin (ςf). Because the optical method measures the product of K fc and ςf, this study shows that albumin should not be used as an intravascular optical filtration marker when permeability is elevated. However, the optical technique, along with another means of measuring K fc (such as BC), can be used to calculate the ςfof a tracer (in this study, ςfof 0.894 at baseline and 0.348 after injury). Another important finding of this study was that the ratio of baseline-to-injury K fc values was not statistically different for Std and BC techniques, indicating that the percent contribution of slow blood-volume increases does not change because of injury.

Fetal cardiovascular, endocrine, and fluid responses to atrial natriuretic factor infusion

1989 ◽  
Vol 257 (3) ◽  
pp. R580-R587 ◽  
Author(s):  
R. A. Brace ◽  
L. A. Bayer ◽  
C. Y. Cheung
Keyword(s):  
Arterial Pressure ◽  
Blood Volume ◽  
Atrial Natriuretic Factor ◽  
Venous Pressure ◽  
Plasma Renin ◽  
Urine Osmolality ◽  
Urine Flow ◽  
Fetal Sheep ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

The purpose of this study was to determine the effects of atrial natriuretic factor (ANF) in the fetus and to explore the interactions among the fetal cardiovascular, endocrine, and fluid responses to ANF. In 12 chronically catheterized fetal sheep at 130 +/- 1 (SE) days gestation, ANF was infused intravenously for 30 min at 14-300 ng.min-1.kg-1. Fetal arterial plasma ANF concentration increased by 174 to 5,410 pg/ml from a preinfusion value of 163 +/- 13 pg/ml. The clearance of ANF from the circulation was 122 +/- 28 ml.min-1.kg-1 and the half-life was 0.46 +/- 0.07 min. When plasma ANF was greater than 2,000 pg/ml, fetal arterial pressure decreased, venous pressure increased transiently, and heart rate was unchanged. Plasma arginine vasopressin (AVP) concentration and plasma renin activity (PRA) increased with high ANF concentrations, while norepinephrine concentrations were unaffected. Fetal blood volume decreased in all fetuses, and urine flow increased significantly but not in every fetus. Blood and urine osmolalities did not change. On terminating the infusion, venous pressure and urine flow decreased below control, while blood volume and arterial pressure remained reduced. Plasma AVP concentration increased further, and this was accompanied by an increase in urine osmolality. Thus the most consistent effect of ANF in the fetus was a reduction in blood volume, which was independent of urine flow changes. Other cardiovascular, endocrine, and fluid responses to ANF as well as interactions among them appeared to occur largely at supraphysiological concentrations and may be secondary to the changes in blood volume.(ABSTRACT TRUNCATED AT 250 WORDS)

Pressure-volume behavior of perivascular interstitium measured in isolated dog lung

1980 ◽  
Vol 48 (6) ◽  
pp. 939-946 ◽  
Author(s):  
S. J. Lai-Fook ◽  
B. Toporoff
Keyword(s):  
Interstitial Fluid ◽  
Venous Pressure ◽  
Fluid Pressure ◽  
Transpulmonary Pressure ◽  
Interstitial Fluid Pressure ◽  
Alveolar Pressure ◽  
Lung Weight ◽  
Lung Volumes ◽  
Water Accumulation ◽  
Alveolar Surface

Pulmonary perivascular interstitial fluid pressure (Px) was measured as a function of extravascular water accumulation (W). Px was measured directly by wick catheters and open-ended needles inserted in the interstitium near the hilus of isolated perfused dog lobes. Lobes were studied at constant transpulmonary pressure (Ptp) and vascular pressure (Pv, arterial equal to venous pressure). Px-W behavior had two distinct phases: an initial low compliance phase interpreted as perivascular filling, followed sometimes by an abrupt transition to a high compliance phase interpreted as alveolar flooding. W at transition was between 20 and 50% of the initial lung weight. Perivascular compliance during filling at a Ptp of 6 cmH2O was 0.1 g.g wet lobe wt-1.cmH2O-1, which was one-sixth that during alveolar flooding and 2.5 times that at a Ptp of 25 cmH2O. At the start of alveolar flooding, estimated alveolar interstitial fluid pressure was slightly (2 cmH2O) below alveolar pressure (PAlv) at a Ptp of 6 cmH2O but considerably belov PAlv at high lung volumes. These findings support the concept that alveolar surface tension reduces the interstitial fluid pressure below PAlv.

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