Filtration profile in isolated zone 1 and zone 3 dog lungs at constant high alveolar pressure

1988 ◽  
Vol 65 (1) ◽  
pp. 343-349 ◽  
Author(s):  
M. A. Gropper ◽  
J. Bhattacharya ◽  
N. C. Staub
Keyword(s):  
Surface Area ◽  
Filtration Rate ◽  
Vascular System ◽  
Alveolar Pressure ◽  
Abrupt Increase ◽  
Filtration Fraction ◽  
Lung Weight ◽  
Exchange Surface ◽  
Filtration Surface ◽  
Lung Lobes

We measured the rate of liquid filtration in isolated dog lung lobes inflated to a constant alveolar pressure of 25 cmH2O and with all open vessels filled with plasma. We measured lung weight gain at vascular pressures ranging from 5 to 40 cmH2O relative to pleural pressure. We confirmed that under zone 1 conditions the "arterial" and "venous" extra-alveolar segments have essentially the same filtration characteristics. Using the combined extra-alveolar vascular system, we determined when recruitment of filtration surface area occurred as we increased vascular pressure from 0 to 40 cmH2O. Based on an abrupt increase in filtration rate as vascular pressure approached the zone 1/3 boundary, we infer that a sudden recruitment of exchange surface area occurred at that point. Based on the slopes of the zone 1 and zone 3 filtration profiles, we conclude that extra-alveolar vascular segments contribute approximately 25% of total to filtration in the lung under zone 3 conditions, although the exact vessels filtering under zone 1 conditions have yet to be determined. Our analysis of the data supports the concept that there is a difference in the perimicrovascular pressure around alveolar and extra-alveolar vessels, which in part may account for the apparent high filtration fraction apportioned to extra-alveolar vessels.

Erythrocytes reduce liquid filtration in injured dog lungs

1989 ◽  
Vol 256 (2) ◽  
pp. H515-H519 ◽  
Author(s):  
M. Onizuka ◽  
T. Tanita ◽  
N. C. Staub
Keyword(s):  
Whole Blood ◽  
Filtration Rate ◽  
Ringer Solution ◽  
Red Cells ◽  
Barrier Effect ◽  
Alveolar Pressure ◽  
Dramatic Decrease ◽  
Oxygen Metabolites ◽  
Filtration Surface ◽  
Lung Lobes

In isolated, dog lung lobes with pulmonary vessels filled with different liquids, we measured the rate of weight gain for 5 or 10 min at constant alveolar and vascular pressures under zone 1 conditions (alveolar pressure greater than vascular pressure). We used six different liquids: syngeneic plasma, whole blood (hematocrit = 38 +/- 4%), 4% albumin in Krebs-Ringer solution, washed red blood cells in Krebs-Ringer solution (hematocrit = 37 +/- 6%), and platelet-rich or platelet-poor plasma. We studied the lobes under three conditions: immediate perfusion after removal (less than 30 min), delayed perfusion (2 h or more), or immediate perfusion after removal from air-embolized animals. In lobes that showed low-filtration rate using plasma [less than 0.5 g/(min x 100 g)] substitution of whole blood had no effect on the filtration rate. In lobes that showed high-filtration rates using plasma (delayed perfusion or deliberately injured using air emboli) substitution of whole blood caused a dramatic decrease in the filtration rate, restoring it to the level obtained in uninjured lobes. Platelets had no effect. Thus the red cells specifically reduced abnormally high filtration but did not affect normal filtration. There appear to be three possible mechanisms: 1) red cells physically blocking large leaks; 2) red cells settling on the filtration surface area (osmotic-barrier effect); 3) red cells acting as reducing agents against active oxygen metabolites.(ABSTRACT TRUNCATED AT 250 WORDS)

Continuity of arterial and venous extra-alveolar interstitium in excised rabbit lungs

1987 ◽  
Vol 63 (2) ◽  
pp. 634-638 ◽  
Author(s):  
W. J. Lamm ◽  
R. K. Albert
Keyword(s):  
Weight Gain ◽  
Filtration Rate ◽  
Hydrostatic Stress ◽  
Alveolar Pressure ◽  
Initial Weight ◽  
Lung Weight ◽  
Fluid Filtration ◽  
Single Compartment ◽  
Pulmonary Arterial ◽  
Lung Base

We studied the interdependence of arterial and venous extra-alveolar vessel (EAV) leakage on the rate of pulmonary vascular fluid filtration (measured as the change in lung weight over time). Edema was produced in continually weighed, excised rabbit lungs kept in zone 1 (alveolar pressure = 25 cmH2O) by increasing pulmonary arterial (Ppa) and/or venous (Ppv) pressure from 5 to 20 cmH2O (relative to the lung base) and continuing this hydrostatic stress for 3–5 h. Raising Ppa and Ppv simultaneously produced a lower filtration rate than the sum of the filtration rates obtained when Ppa and Ppv were raised separately, while the lung gained from 20 to 95% of its initial weight. When vascular pressure was elevated in either EAV segment, fluid filtration always decreased rapidly as the lung gained up to 30–45% of its initial weight. Filtration then decreased more slowly. The lungs became isogravimetric at 60 and 85% weight gain when the Ppa or Ppv was elevated, respectively; when Ppa and Ppv were raised simultaneously substantial fluid filtration continued even after 140% weight gain. We conclude that the arterial and venous EAV's share a common interstitium in the zone 1 condition, this interstitium cannot be represented as a single compartment with a fixed resistance and compliance, and arterial and venous EAV leakage influences leakage from the other segment.

Perivascular interstitial fluid pressure measured by micropipettes in isolated dog lung

1982 ◽  
Vol 52 (1) ◽  
pp. 9-15 ◽  
Author(s):  
S. J. Lai-Fook
Keyword(s):  
Interstitial Fluid ◽  
Fluid Pressure ◽  
Transpulmonary Pressure ◽  
Alveolar Pressure ◽  
Lung Weight ◽  
Lung Inflation ◽  
Water Accumulation ◽  
The Right ◽  
Alveolar Surface ◽  
Lung Lobes

Micropipettes in conjunction with a servo-nulling system were used to measure fluid pressure (Pf) in the interstitium around the partially exposed vein near the hilus of the right upper lung lobes of the dog. Lobes were studied at constant transpulmonary pressure (Ptp). In the absence of extravascular water accumulation, Pf was -1.5 cmH2O relative to pleural pressure at Ptp of 6 cmH2O and vascular pressure (Pv) of 0 cmH2O and was more negative in lobes tested at higher Ptp values. In five lobes made edematous with plasma at Ptp of 6 cmH2O and Pv of 15 cmH2O, mean Pf increased from -1 to 4.4 cmH2O as lung weight increased up to 400% of the initial excised weight. In four other lobes, at Ptp of 15 cmH2O and Pv of 20 cmH2O, Pf increased from -2.4 to 8.8 for a similar increase in weight. In lobes degassed and filled with saline or plasma, Pf always equilibrated to alveolar pressure (PA). Results suggest that alveolar surface tension (tau) in air-filled lobes with gross edema prevented Pf from reaching PA. Reduction in Pf below PA was larger at higher Ptp, consistent with increased tau with lung inflation.

Derecruitment of filtration surface area in paraquat-injured isolated dog lungs

1990 ◽  
Vol 68 (4) ◽  
pp. 1581-1589 ◽  
Author(s):  
T. Shibamoto ◽  
J. C. Parker ◽  
A. E. Taylor ◽  
M. I. Townsley
Keyword(s):  
Blood Flow ◽  
Surface Area ◽  
Vascular Resistance ◽  
High Flow ◽  
Base Line ◽  
Flow Rates ◽  
Blood Flows ◽  
Capillary Filtration Coefficient ◽  
Specific Index ◽  
Filtration Surface

The capillary filtration coefficient (Kf,c) is a sensitive and specific index of vascular permeability if surface area remains constant, but derecruitment might affect Kf,c in severely damaged lungs with high vascular resistance. We studied the effect of high and low blood flow rates on Kf,c in papaverine-pretreated blood-perfused isolated dog lungs perfused under zone 3 conditions with and without paraquat (PQ, 10(-2) M). Three Kf,cs were measured successively at hourly intervals for 5 h. These progressed sequentially from isogravimetric blood flow with low vascular pressure (I/L) to high flow with low vascular pressure (H/L) to high flow with high vascular pressure (H/H). The blood flows of H/L and H/H were greater than or equal to 1.5 times that of I/L. There were no significant changes in Kf,c in lungs without paraquat over a 50-fold range of blood flow rates. At 3 h after PQ, I/L-Kf,c was significantly increased and both isogravimetric capillary pressure and total protein reflection coefficient were decreased from base line. At 4 and 5 h, H/L-Kf,c was significantly greater than the corresponding I/L-Kf,c (1.01 +/- 0.22 vs. 0.69 +/- 0.09 and 1.26 +/- 0.19 vs. 0.79 +/- 0.10 ml.min-1.cmH2O-1.100 g-1, respectively) and isogravimetric blood flow decreased to 32.0 and 12.0% of base line, respectively. Pulmonary vascular resistance increased to 12 times base line at 5 h after PQ. We conclude that Kf,c is independent of blood flow in uninjured lungs. However, Kf,c measured at isogravimetric blood flow underestimated the degree of increase in Kf,c in severely damaged and edematous lungs because of a high vascular resistance and derecruitment of filtering surface area.

Renal hemodynamic responses to increased renal venous pressure: role of angiotensin II

1982 ◽  
Vol 243 (3) ◽  
pp. F260-F264 ◽  
Author(s):  
P. R. Kastner ◽  
J. E. Hall ◽  
A. C. Guyton
Keyword(s):  
Angiotensin Ii ◽  
Filtration Rate ◽  
Enzyme Inhibitor ◽  
Venous Pressure ◽  
Renin Secretion ◽  
Ang Ii ◽  
Converting Enzyme ◽  
Filtration Fraction ◽  
A Value

Studies were performed to quantitate the effects of progressive increases in renal venous pressure (RVP) on renin secretion (RS) and renal hemodynamics. RVP was raised in 10 mmHg increments to 50 mmHg. Renin secretion rate increased modestly as RVP was increased to 30 mmHg and then increased sharply after RVP exceeded 30 mmHg. Glomerular filtration rate (GFR), renal blood flow (RBF), and filtration fraction (FF) did not change significantly when RVP was elevated to 50 mmHg. GFR and RBF were also measured after the renin-angiotension system (RAS) was blocked with the angiotensin converting enzyme inhibitor (CEI) SQ 14225. After a 60-min CEI infusion, RBF was elevated (32%), GFR was unchanged, FF was decreased, and total renal resistance (TRR) was decreased. As RVP was increased to 50 mmHg, GFR and FF decreased to 36.3 and 40.0% of control, respectively, RBF returned to a value not significantly different from control, and TRR decreased to 44.8% of control. The data indicate that the RAS plays an important role in preventing reductions in GFR during increased RVP because blockade of angiotensin II (ANG II) formation by the CEI results in marked decreases in GFR at high RVPs. The decreases in GFR after ANG II blockade and RVP elevation were not due to lack of renal vasodilation, since TRR was maintained below while RBF was maintained either above or at the pre-CEI levels.

Glomerular Mesangial Cells: Electrophysiology and Regulation of Contraction

1998 ◽  
Vol 78 (3) ◽  
pp. 723-744 ◽  
Author(s):  
JAMES D. STOCKAND ◽  
STEVEN C. SANSOM
Keyword(s):  
Surface Area ◽  
Filtration Rate ◽  
Mesangial Cells ◽  
Signal Transduction Pathway ◽  
Equilibrium Potential ◽  
Glomerular Mesangial Cells ◽  
Voltage Gated ◽  
Functional Studies ◽  
Regulation Of Contraction ◽  
Phosphatase 2A

Stockand, James D., and Steven C. Sansom. Glomerular Mesangial Cells: Electrophysiology and Regulation of Contraction. Physiol. Rev. 78: 723–744, 1998. — Mesangial cells are smooth muscle-like pericytes that abut and surround the filtration capillaries within the glomerulus. Studies of the fine ultrastructure of the glomerulus show that the mesangial cell and the capillary basement membrane form a biomechanical unit capable of regulating filtration surface area as well as intraglomerular blood volume. Structural and functional studies suggest that mesangial cells regulate filtration rate in both a static and dynamic fashion. Mesangial excitability enables a homeostatic intraglomerular stretch reflex that integrates an increase in filtration pressure with a reduction in capillary surface area. In addition, mesangial tone is regulated by diverse vasoactive hormones. Agonists, such as angiotensin II, contract mesangial cells through a signal transduction pathway that releases intracellular stores of Ca2+, which subsequently activate nonselective cation channels and Cl− channels to depolarize the plasma membrane. The change in membrane potential activates voltage-gated Ca2+ channels, allowing Ca2+ cell entry and further activation of depolarizing conductances. Contraction and entry of cell Ca2+ are inhibited only when Ca2+-activated K+ channels (BKCa) are activated and the membrane is hyperpolarized toward the K+ equilibrium potential. The mesangial BKCa is a weak regulator of contraction in unstimulated cells; however, the gain of the feedback is increased by atrial natriuretic peptide, nitric oxide, and the second messenger cGMP, which activates protein kinase G and decreases both the voltage and Ca2+ activation thresholds of BKCa independent of sensitivity. This enables BKCa to more effectively counter membrane depolarization and voltage-gated Ca2+ influx. After hyperpolarizing the membrane, BKCa rapidly inactivates because of dephosphorylation by protein phosphatase 2A. Regulation of ion channels has been linked casually to hyperfiltration during early stages of diabetes mellitus. Determining the signaling pathways controlling the electrophysiology of glomerular mesangial cells is important for understanding how glomerular filtration rate is regulated in health and disease.

Extent of glomerular injury in active and resolving lupus nephritis: a theoretical analysis

1991 ◽  
Vol 260 (5) ◽  
pp. F717-F727 ◽  
Author(s):  
B. D. Myers ◽  
A. Chagnac ◽  
H. Golbetz ◽  
L. Newton ◽  
S. Strober ◽  
...  
Keyword(s):  
Lupus Nephritis ◽  
Marked Reduction ◽  
Filtration Rate ◽  
Pore Density ◽  
Glomerular Injury ◽  
Biopsy Tissue ◽  
Structural Recovery ◽  
Proliferative Lupus Nephritis ◽  
Conventional Tests ◽  
Filtration Surface

Patients with diffuse, proliferative lupus nephritis (DPLN) were subjected to differential solute clearances (n = 22) and serial renal biopsy (n = 11) before and again after 6-12 mo of immunosuppressive therapy. Glomerular sieving of dextrans of graded size was analyzed with a heteroporous membrane model. This revealed active DPLN to be associated with 1) a reduction of overall pore density accompanied by a 53% depression of glomerular filtration rate (GFR), and 2) appearance of a subset of large, nondiscriminatory pores, which accounted for the observed nephrotic level of proteinuria. Morphometric analysis of biopsy tissue provided evidence of reduced filtration surface area due to global or segmental occlusion of capillary loops in glomerular tufts. Activity of DPLN resolved posttreatment. A computed increase in pore density was associated with a 24% increment in GFR; a marked reduction in the fraction of shuntlike pores was accompanied by a parallel reduction of proteinuria into a subnephrotic range. Repeat biopsy revealed diminished glomerular cellularity, fewer immune deposits, and an ensuing increase in the fraction of tuft area occupied by patent loops. Epithelial filtration slit frequency also increased. Neither functional nor structural recovery was complete, however. Residual pore density approximated only 23-35% of that in healthy controls, and corresponding shuntlike pores were threefold more prominent. We conclude that severe DPLN is only partially reversible by current modalities of treatment and that the ensuing residual injury is far more severe than suggested by conventional tests of renal function.

Intrapulmonary blood flow redistribution during hypoxia increases gas exchange surface area

1982 ◽  
Vol 52 (6) ◽  
pp. 1575-1580 ◽  
Author(s):  
R. L. Capen ◽  
W. W. Wagner
Keyword(s):  
Carbon Monoxide ◽  
Blood Flow ◽  
Cardiac Output ◽  
Gas Exchange ◽  
Surface Area ◽  
Vascular Resistance ◽  
Diffusing Capacity ◽  
Capillary Recruitment ◽  
Blood Flow Redistribution ◽  
Exchange Surface

We have previously shown that airway hypoxia causes pulmonary capillary recruitment and raises diffusing capacity for carbon monoxide. This study was designed to determine whether these events were caused by an increase in pulmonary vascular resistance, which redistributed blood flow toward the top of the lung, or by an increase in cardiac output. We measured capillary recruitment at the top of the dog lung by in vivo microscopy, gas exchange surface area of the whole lung by diffusing capacity for carbon monoxide, and blood flow distribution by radioactive microspheres. During airway hypoxia recruitment occurred, diffusing capacity increased, and blood flow was redistributed upward. When a vasodilator was infused while holding hypoxia constant, these effects were reversed; i. e., capillary “derecruitment” occurred, diffusing capacity decreased, and blood flow was redistributed back toward the bottom of the lung. The vasodilator was infused at a rate that left hypoxic cardiac output unchanged. These data show that widespread capillary recruitment during hypoxia is caused by increased vascular resistance and the resulting upward blood flow redistribution.

Effect of lung inflation on fluid flux in zone 1 lungs

1988 ◽  
Vol 64 (1) ◽  
pp. 285-290 ◽  
Author(s):  
R. K. Albert ◽  
W. J. Lamm ◽  
D. L. Luchtel
Keyword(s):  
Positive Pressure ◽  
Alveolar Pressure ◽  
Fluid Flux ◽  
Lung Weight ◽  
Fluid Filtration ◽  
Lung Inflation ◽  
Dependent Part ◽  
Autologous Whole Blood ◽  
New Zealand White Rabbits ◽  
Pulmonary Arterial

Because of conflicting data in the literature, we studied the effect of positive-pressure inflation on transvascular fluid filtration in zone 1 lungs. Lungs from New Zealand White rabbits (n = 10) were excised, perfused with saline and autologous whole blood (1:1), ventilated, and continuously weighed. Pulmonary arterial and venous pressures (Pvas) were referenced to the most dependent part of the lung. A change in vascular volume (delta Vvas) and a fluid filtration rate (FFR) were calculated from the change in lung weight that occurred from 0 to 30 s and from 3 to 5 and 5 to 10 min, respectively, after changing alveolar pressure (PA). FFR's and delta Vvas's were measured with Pvas equal to 2 or 10 cmH2O and PA changing from 15 to 30 cmH2O when the lungs were normal and after they were made edematous. When Pvas = 2 cmH2O, increasing PA increased the Vvas and the FFR in both normal and edematous lungs. However, when Pvas = 10 cmH2O, increasing PA only slightly changed the Vvas and reduced the FFR in the normal lungs, and decreased Vvas and markedly decreased the FFR in the presence of edema. Inflating zone 1 lungs by positive pressure has an effect on transvascular fluid flux that depends on the Pvas. The results suggest that the sites of leakage in zone 1 also vary depending on Pvas and PA.

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