Intestinal lymphatic pressure increases during intravenous infusions in awake sheep

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 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.


1963 ◽  
Vol 204 (2) ◽  
pp. 284-288 ◽  
Author(s):  
René Wégria ◽  
Horst Zekert ◽  
Kenneth E. Walter ◽  
Richard W. Entrup ◽  
Christian De Schryver ◽  
...  

In acute experiments on the anesthetized dog, partial or complete occlusion of the left innominate vein resulting in a rise of pressure in the venous territory into which the thoracic duct drains, commensurate with the venous pressure rise seen in congestive heart failure, reduces the flow of lymph in the thoracic duct. This decrease in thoracic duct lymph flow is due, at least partially, to the accumulation of lymph in the lymphatic system and possibly the intercellular spaces. The present acute experiments suggest the possibility that this factor may play a role in the genesis of the systemic edema of chronic congestive heart failure, although only chronic experiments now under way will permit definitive conclusions.


1983 ◽  
Vol 245 (6) ◽  
pp. R785-R791
Author(s):  
R. A. Brace ◽  
G. G. Power

To test whether whole-body lymph flow responses to vascular volume loading depend on osmolality, we measured left thoracic duct lymph flow rate and protein concentration, plasma protein concentration, plasma osmolality, hematocrit, and arterial and venous pressures in pentobarbital-anesthetized, acutely nephrectomized dogs. Hypo- (100 mosmol), iso- (309 mosmol), and hypertonic (600 mosmol) saline, isotonic lactated Ringer solution, and 5% glucose in lactated Ringer solution (580 mosmol) were infused into the jugular vein (20 ml/kg per infusion over 5 min at 30-min intervals). Changes in blood, interstitial, and cellular volumes were calculated from the infused volume and from the hematocrit and plasma osmolality. The hypotonic fluid increased lymph flow about half as much as the isotonic fluid, whereas the hypertonic fluids increased lymph flow about twice as much as the isotonic infusions. Responses appeared independent of the osmotic agent, because hypertonic NaCl was as effective as hypertonic glucose in increasing lymph flow. Responses were not altered appreciably after lowering arterial pressure by 25 mmHg. The major finding of this study is that for every condition we explored, the excess lymph flow over 30 min (ELF in ml X kg-1 X 30 min-1) correlated with the change in interstitial fluid volume (delta ISFV in ml/kg); ELF = 0.076 delta ISFV (r = 0.909). These data suggest that cellular fluid that enters the interstitium is equally effective in increasing thoracic duct lymph flow as is vascular fluid that filters into the interstitium.


1986 ◽  
Vol 250 (6) ◽  
pp. R1095-R1098 ◽  
Author(s):  
G. Valenzuela ◽  
L. L. Woods ◽  
R. A. Brace

Left thoracic duct lymph flow rate averaged 0.077 +/- 0.003 (SD) and 0.078 +/- 0.003 ml X min-1 X kg-1 in near-term pregnant and nonpregnant sheep (P greater than 0.5). Lymph and plasma protein concentrations were unaltered in the pregnant compared with the nonpregnant animals. The thoracic duct lymph flow responses to three serial intravenous infusions of lactated Ringer solution were essentially the same in the pregnant and nonpregnant animals. Blood volume and vascular pressure changes during and after volume loading were essentially the same in both groups. In addition, terbutaline administration after volume loading caused no change in thoracic duct lymph flow rates. Thus the present study suggests that basal lymph flow rates, lymphatic function, and vascular as well as interstitial compliances are largely unaltered late in pregnancy in the sheep. In addition, beta-mimetic stimulation with terbutaline does not appear to suppress lymph flow rate.


Neonatology ◽  
1993 ◽  
Vol 64 (5) ◽  
pp. 325-330 ◽  
Author(s):  
Alfred L. Gest ◽  
Derek Bair ◽  
Mary C. Vander Straten

1983 ◽  
Vol 145 (1) ◽  
pp. 126-130 ◽  
Author(s):  
Michael Last ◽  
Lewis Kurtz ◽  
Theodore A. Stein ◽  
Leslie Wise

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)


1996 ◽  
Vol 271 (3) ◽  
pp. R601-R609 ◽  
Author(s):  
V. L. Tucker

The relationship between plasma immunoreactive atrial natriuretic peptide (irANP) and radiolabeled albumin clearance (CBSA) in multiple tissues after graded volume stimuli was examined. To obtain a pure volume stimulus, pentobarbital sodium-anesthetized rats (5 or 6 per group) were equilibrated with a reservoir of blood by a femoral arteriovenous shunt, and volume expansion (VE) was produced by adjusting reservoir outflow. Peak increases in central venous pressure (CVP) during VE equal to 2 and 4% of the body weight over 5 min were 3.6 +/- 0.2 and 7.0 +/- 0.3 mmHg, and plasma irANP levels measured at 40 min post-VE were elevated 1.9- and 4.1-fold above baseline, respectively. Graded increases in CBSA measured between 5 and 35 min post-VE occurred in selective tissues, including intestine, visceral fat, lung, and muscle (P < or = 0.05). In separate animals, the level of VE was maintained after 2% VE by slower administration of an additional 2% VE for the remaining 30 min. This resulted in a more sustained CVP elevation and larger increases in irANP levels and CBSA compared with either 2 or 4% VE. Furthermore, equations derived from previous work in this laboratory involving intravenous administration of ANP predicted the magnitude of CBSA elevation during maintained VE. These findings support a role for ANP in regulating transcapillary protein distribution during acute intravascular expansion.


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.


1990 ◽  
Vol 259 (6) ◽  
pp. R1205-R1213 ◽  
Author(s):  
J. Valenzuela-Rendon ◽  
R. D. Manning

The roles of the transvascular fluid flux and lymph flow in the distribution of extracellular fluid volume during angiotensin II (ANG II) hypertension were evaluated in 11 conscious dogs. Similarly, the factors regulating the distribution of plasma protein across the microvasculature were assessed. By the second day of ANG II infusion, the thoracic duct lymph flow had increased 58% above control, transcapillary fluid flux had increased 45%, and plasma volume, sulfate space, and interstitial fluid volume remained close to control. In addition, the thoracic duct lymph protein transport had increased 34%, and the accompanying increase in transcapillary protein flux prevented any change in plasma protein mass. Also, at this time, the lymph flow and protein transport from subcutaneous tissue in the hind limb were not increased, and the permeability-surface area product of this region decreased 40%. The origin of the increased thoracic duct lymph flow on day 2 probably was from the splanchnic bed. In conclusion, the increased lymph flow during ANG II hypertension compensated for the increase in transcapillary fluid flux, thus preventing edema formation.


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