Filtration Surface Area, Salt Intake and Hypertension

Author(s):  
Barry M. Brenner ◽  
Sharon Anderson
1990 ◽  
Vol 68 (4) ◽  
pp. 1581-1589 ◽  
Author(s):  
T. Shibamoto ◽  
J. C. Parker ◽  
A. E. Taylor ◽  
M. I. Townsley

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.


1982 ◽  
Vol 52 (5) ◽  
pp. 1324-1329 ◽  
Author(s):  
T. A. Jones ◽  
M. I. Townsley ◽  
W. J. Weidner

Elevation of intracranial pressure (ICP; 50–150 Torr) in sheep produces an increase in protein-rich lymph flow (QL) from the lung. This may be attributed to either microvascular permeability changes or increases in filtration surface area through recruitment. To eliminate increases in surface area, we recruited potential filtration beds by increasing left atrial pressure (Pla; 27–35 Torr) prior to elevating ICP in sheep anesthetized with pentobarbital sodium or halothane. Under these conditions, increased pulmonary microvascular permeability would be expected to produce an increased QL, lymphatic protein flux (CL), and plasma clearance of protein (CP). The results of ICP elevation following a period of steady-state Pla hypertension showed no such change in QL, CL or CP (n=8) compared with prior period of increased Pla. ICP elevation alone (n=6) produces a significant increase in CP manifested as an increase in QL (73%), with little change in the lymph-to-plasma ratio of protein concentration. These results suggest that a change in pulmonary microvascular surface area (not permeability) is the primary mechanism underlying increases in protein-rich QL following the elevation of ICP alone.


1988 ◽  
Vol 65 (1) ◽  
pp. 343-349 ◽  
Author(s):  
M. A. Gropper ◽  
J. Bhattacharya ◽  
N. C. Staub

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.


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