Estrogen effects on lymph flow as a function of outflow pressure in ewes

1990 ◽  
Vol 258 (5) ◽  
pp. H1317-H1320 ◽  
Author(s):  
G. J. Valenzuela ◽  
S. Kim

The purpose of the present study was to assess whether acute estrogen administration decreased the lymphatic vessel's "pumping" ability. An additional goal was to assess whether estrogen affected the capillary filtration (used here as the total transfer of fluid and protein across the capillaries evidenced by the thoracic duct lymph flow rate). We reasoned that if estrogen administration decreases the lymph pumping ability against outflow pressure, then this phenomenon could help to explain the interstitial fluid retention seen during chronic estrogen. In six nonpregnant ewes we studied the thoracic lymph flow rate measured at different outflow pressures, before and after the acute administration of 50 mg of Premarin (conjugated estrogenic hormones). We also continuously determined arterial and venous pressures and heart rate. The arterial pressure declined from a mean of 99 +/- 0.33 (SE) mmHg to 95.4 +/- 0.2 mmHg (P less than 0.05) after the administration of estrogen. Heart rate increased from 88.5 +/- 0.8 to 111.3 +/- 1.2 beats/min (P less than 0.01). Venous pressure, plasma and lymph protein concentrations, and hematocrit did not change significantly (P greater than 0.1). Lymph flow rate declined progressively when measured against positive outflow pressure, whereas it remained stable when measured against negative pressure. Lymph flow rate during negative outflow pressure was higher after the administration of estrogen 0.044 +/- 0.002 vs. 0.032 +/- 0.002 ml.min-1.kg-1 for the control period (P less than 0.05). The calculated outflow pressure at which lymph flow rate became zero was similar for the period before or after the estrogen administration (P greater than 0.1).(ABSTRACT TRUNCATED AT 250 WORDS)

1995 ◽  
Vol 269 (4) ◽  
pp. H1277-H1281
Author(s):  
R. A. Brace

Blood volume returns toward normal after hemorrhage much more rapidly in the fetus than in the adult due to a rapid entry of fluid and plasma proteins into the fetal circulation. One potential source of fetal fluids and plasma proteins is the lymphatic system, since basal lymph flow rate and interstitial protein concentration are high in the fetus. Furthermore, studies in adults suggest that lymph flow rate may increase following hemorrhage. To test the hypothesis that hemorrhage induces an increase in lymph flow in the fetus, 15 late-gestation ovine fetuses underwent left thoracic duct catheterization with low-resistance catheters and were studied 5 or more days after surgery at 134 +/- 1 (SE) days gestation. The protocol included three successive 30-min periods: control, hemorrhage, and recovery. During the first 5 min of the hemorrhagic period, 61 +/- 4 ml of fetal blood were removed. The blood was reinfused over the first 5 min of the recovery period. After the hemorrhage, fetal arterial pressure, venous pressure, and heart rate decreased (analysis of variance, P < 0.001). These variables significantly increased above basal levels following blood reinfusion. Fetal hematocrit (P < 0.001) and plasma protein concentration (P < 0.05) also decreased after the hemorrhage and returned to control values after the reinfusion. Fetal lymph flow rate was 0.55 +/- 0.06 (SE) ml/min before the hemorrhage and decreased by a maximum of 30.3 +/- 6.3% (P < 0.001) at 8 min after the end of the hemorrhage. Lymph flow rate was reduced by an average of 19.1 +/- 6.6% during the hemorrhagic period and returned to prehemorrhage levels following blood reinfusion.(ABSTRACT TRUNCATED AT 250 WORDS)


1987 ◽  
Vol 252 (5) ◽  
pp. R853-R858
Author(s):  
G. J. Valenzuela ◽  
C. W. Hewitt ◽  
A. D. Graham

Both pregnancy and estrogen administration are associated with a decrease in the systemic vasculature pressor response to angiotensin II infusion; however, the lymphatic vessel system response is not clear. In the present study we infused angiotensin II to nine nonpregnant splenectomized ewes with 0.1, 10, or 1,000 ng X kg-1 X min-1 for a 5-min period at each dose. At the lowest dose the mean arterial pressure increased from 10 to 20% over base line. At the highest dose, the left thoracic duct flow rate peaked at 361% 10 min after the infusion was started, whereas arterial pressure peaked at 183% of the control value. Peak lymph flow occurred 4-6 min after the maximal increase in mean systemic arterial pressure. Neither hematocrit nor venous pressure were altered at any of the doses administered. This suggests that the interstitial fluid space pressure remained unchanged and that the increase in lymph flow was not secondary to fluid transfer from the intravascular system. We postulate, therefore, that the effect of angiotensin II in the increase of lymph flow rate is by direct action on the lymphatic vessels themselves.


1990 ◽  
Vol 258 (1) ◽  
pp. R240-R244 ◽  
Author(s):  
R. A. Brace ◽  
G. J. Valenzuela

Studies have shown that lymph flow rate from several tissues depends on the pressure at the outflow end of the lymphatics. The left thoracic lymph duct is the largest lymphatic vessel and it transports a majority of the body's lymph. We varied outflow pressure for the left thoracic lymph duct independent of venous pressure in six unanesthetized, nonpregnant adult ewes with chronic lymphatic and venous catheters. When outflow pressure was negative, the thoracic duct lymph flow rate was independent of outflow pressure and averaged 0.040 +/- 0.004 (SE) ml.min-1.kg body wt-1. Lymph flow began to decrease with increasing outflow pressure only when outflow pressure was significantly greater than venous pressure. Above this breakpoint, lymph flow decreased linearly with outflow pressure and ceased at an outflow pressure of 25.6 +/- 4.2 mmHg. After vascular volume loading with lactated Ringer solution, steady-state thoracic duct lymph flow increased to 351 +/- 54% of control and was independent of outflow pressure when outflow pressure was negative. As outflow pressure was elevated, lymph flow began to decrease at the same breakpoint as before volume loading, and lymph flow ceased at the same outflow pressure as before volume loading. Thus this study shows that there is a plateau where thoracic duct lymph flow rate is independent of outflow pressure. In addition venous pressure under normal or volume-loaded conditions is not an impediment to thoracic duct lymph flow in unanesthetized sheep. Large increases in venous pressure are required to totally block thoracic duct lymph flow.


1997 ◽  
Vol 272 (5) ◽  
pp. R1595-R1598 ◽  
Author(s):  
R. E. Drake ◽  
S. Dhother ◽  
R. A. Teague ◽  
J. C. Gabel

Increases in systemic venous pressure (Pv) associated with heart failure cause an increase in microvascular fluid filtration into the tissue spaces. By removing this excess filtrate from the tissues, lymphatic vessels help to prevent edema. However, the lymphatics drain into systemic veins and an increase in Pv may interfere with lymphatic flow. To test this, we cannulated caudal mediastinal node efferent lymphatics in sheep. We used rapid cardiac ventricular pacing (240-275 beats/min) to cause heart failure for 4-7 days. Each day we determined the lymph flow rate two ways. First, we adjusted the lymph cannula height so that the pressure at the outflow end of the lymphatic was zero. After we determined the lymph flow with zero outflow pressure, we raised the cannula so that outflow pressure was equal to the actual venous pressure. We quantitated the effect of venous pressure on lymph flow rate by comparing the flow rate with outflow pressure = Pv to the flow rate with zero out low pressure. At baseline, Pv = 5.0 +/- 2.5 (SD) cmH2O and we found no difference in the two lymph flow rates. Pacing caused Pv and both lymph flow rates to increase significantly. However for Pv < 15 cmH2O, we found little difference in the two lymph flow rates. Thus increases in Pv to 15 cmH2O at the outflow to the lymphatics had little effect on lymph flow. By comparison, Pv > 15 cmH2O slowed lymph flow by 55 +/- 29% relative to the lymph flow rate with zero outflow pressure. Thus Pv values > 15 cmH2O interfere with lymph flow from the sheep caudal mediastinal lymph node.


1989 ◽  
Vol 256 (1) ◽  
pp. H16-H20 ◽  
Author(s):  
R. A. Brace

A method was developed for chronic catheterization of the left thoracic lymph duct at the base of the neck in the sheep fetus, which did not disrupt the other major lymphatic vessels that join the venous circulation at the same location. The lymphatic catheter was connected to a catheter in a jugular vein when lymph flow was not being recorded, so that the lymph continuously returned to the fetal circulation. Special consideration of catheter size to minimize flow resistance and treatment to prevent clotting were required. Individual animals were maintained up to 17 days with lymph flow continuing. In 13 fetuses averaging 128 days gestation (term = 147 days) at the time of catheterization, lymph flow rate was measured for 1 h each day for the first 7 postsurgical days with an on-line computer technique that continuously calculated lymph flow rate. Lymph flow averaged 0.64 +/- 0.17 (SD) ml/min in fetuses weighing 2.3-4 kg and tended to undergo a nonsignificant increase with time. Lymph and plasma protein concentrations did not change with time. In individual fetuses, large spontaneous variations in lymph flow rate occurred over periods of several seconds to a few minutes. Analysis showed that these variations in flow rate were not associated with fetal breathing movements. Thus the present study describes a technique for studying the dynamics of lymph flow in the unanesthetized sheep fetus in utero over a time period limited primarily by the length of gestation. In addition, it appears that thoracic duct lymph flow rate in the fetus per unit body weight averages three to four times that in the adult.


1981 ◽  
Vol 240 (5) ◽  
pp. R282-R288
Author(s):  
R. A. Brace ◽  
G. G. Power

Fluid and protein flux responses in the left thoracic duct and vasculature were measured in pentobarbital-anesthetized, nephrectomized, adult dogs before and after four successive intravascular saline infusions of 2% of body weight each. We found three main characteristics of the thoracic lymph flow and protein flux responses to the intravenous saline: 1) lymph flow reached a peak and then decreased by approximately 40% after each infusion; 2) the maximum lymph flow occurred 5-7 min after terminating each infusion; and 3) the lymph-to-plasma protein concentration ratio fell more than may be expected from the distribution of the infused saline. We were unable to explain these experimental data with a simple two-compartment mathematical model representing the vascular and interstitial spaces. To adequately explain the data, the model had to be expanded to four compartments representing a vascular compartment, two interstitial compartments each with different capillary protein permeabilities, and a lymphatic compartment. We also found it necessary to include interstitial stress relaxation, a nonlinear function curve for lymph flow versus interstitial fluid pressure, and a complaint lymphatic system.


1988 ◽  
Vol 255 (1) ◽  
pp. R149-R156 ◽  
Author(s):  
K. Sander-Jensen ◽  
J. Mehlsen ◽  
C. Stadeager ◽  
N. J. Christensen ◽  
J. Fahrenkrug ◽  
...  

Progressive central hypovolemia is characterized by a normotensive, tachycardic stage followed by a reversible, hypotensive stage with slowing of the heart rate (HR). We investigated circulatory changes and arterial hormone concentrations in response to lower-body negative pressure (LBNP) in six volunteers before and after atropine administration. LBNP of 55 mmHg initially resulted in an increase in HR from 55 +/- 4 to 90 +/- 5 beats/min and decreases in mean arterial pressure (MAP) from 94 +/- 4 to 81 +/- 5 mmHg, in central venous pressure from 7 +/- 1 to -3 +/- 1 mmHg, and in cardiac output from 6.1 +/- 0.5 to 3.7 +/- 0.11/min. Concomitantly, epinephrine and norepinephrine levels increased. After 8.2 +/- 2.3 min of LBNP, the MAP had decreased to 41 +/- 7 mmHg and HR had decreased to 57 +/- 3 beats/min. Vasopressin increased from 1.2 +/- 0.3 to 137 +/- 45 pg/ml and renin activity increased from 1.45 +/- 4.0 to 3.80 +/- 1.0 ng.ml-1.h-1 with no further changes in epinephrine, norepinephrine, and vasoactive intestinal polypeptide. A tardy rise in pancreatic polypeptide indicated increased vagal activity. After atropine. LBNP also caused an initial increase in HR, which, however, remained elevated during the subsequent decrease in MAP to 45 +/- 6 mmHg occurring after 8.1 +/- 2.4 min.(ABSTRACT TRUNCATED AT 250 WORDS)


1993 ◽  
Vol 265 (3) ◽  
pp. R703-R705 ◽  
Author(s):  
R. E. Drake ◽  
Z. Anwar ◽  
S. Kee ◽  
J. C. Gabel

Intravenous fluid infusions cause increased venous pressure and increased lymph flow throughout the body. Together the increased lymph flow and increased venous pressure (the outflow pressure to the lymphatic system) should increase the pressure within the postnodal intestinal lymphatics. To test this, we measured the pressure in postnodal intestinal lymphatics and the neck vein pressure in five awake sheep. At baseline, the neck vein pressure was 1.2 +/- 1.5 (SD) cmH2O and the lymphatic pressure was 12.5 +/- 1.7 cmH2O. When we infused Ringer solution intravenously (10% body weight in approximately 50 min), the neck vein pressure increased to 17.3 +/- 0.9 cmH2O and the lymphatic pressure increased to 24.6 +/- 3.8 cmH2O (both P < 0.05). In two additional sheep, the thoracic duct lymph flow rate increased from 0.8 +/- 0.4 ml/min at baseline to 5.5 +/- 2.0 ml/min during the infusions. Our results show that postnodal intestinal lymphatic pressure may increase substantially during intravenous fluid infusions. This is important because increases in postnodal lymphatic pressure may slow lymph flow from the intestine.


1990 ◽  
Vol 259 (4) ◽  
pp. R780-R785 ◽  
Author(s):  
R. E. Drake ◽  
J. C. Gabel

We used lymph flow rate (QL) to lymphatic vessel outflow pressure (Po) relationships to analyze lymphatic flow in five unanesthetized sheep with liver lymphatic cannulas. The olecranon was the zero reference level for pressures. Increases in Po did not change QL until Po exceeded 19 +/- 4 (SD) cmH2O. However, for Po greater than 19 +/- 4 cmH2O, QL decreased linearly with increases in Po. We fit regression lines to the QL vs. Po data for Po greater than 19 cmH2O and estimated the effective lymphatic resistance (RL) as -delta Po/delta QL. The effective pressure driving lymph (PL) was the Po at which QL = 0. At baseline, RL = 0.18 +/- 0.10 cmH2O.min.microliter-1 and PL = 29.6 +/- 3.4 cmH2O. When we increased hepatic vein pressure by 5.7 +/- 1.7 cmH2O, QL increased to 6.2 +/- 3.2 times baseline, RL decreased to 0.050 +/- 0.015 cmH2O.min.microliter-1, and PL increased to 37.1 +/- 3.5 cmH2O (P less than 0.05). Thus 1) liver lymph flow is very sensitive to increases in hepatic vein pressure, 2) there is a substantial QL vs. Po plateau for liver lymphatics, and 3) after hepatic venous pressure elevations, liver lymph flow increases as if it were driven by a higher pressure through a lower resistance.


1977 ◽  
Vol 232 (3) ◽  
pp. H236-H240
Author(s):  
D. A. Stinson ◽  
P. M. Taylor ◽  
E. P. Rees ◽  
U. Boonyaprakob

The effect of moderate hypercapnia on right-thoracic duct lymph flow, pulmonary hemodynamics, and lung water content was studied in seven 2- to 5-wk-old dogs and eleven adult dogs anesthetized with pentobarbital, paralyzed with succinylcholine, and maintained on intermittent positive-pressure ventilation. Following a 30-min control period in which arterial pH and blood gases were maintained within normal limits, the dogs were ventilated with 3-14% CO2 for 30 min; they were then returned to control conditions fro a 30-min recovery period. Hypercapnia was associated with a significant increase in lymph flow rate in both pups and adult dogs (P less than 0.05) and a significant increase in pulmonary artery and pulmonary artery wedge pressures in adult dogs (P less than 0.05). These data suggest that hypercapnia may increase the net flow of water out of the pulmonary vascular bed.


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