Lymph Flow Transient Following Elevation of Venous Pressure in the Dog’s Hind Paw

1977 ◽  
pp. 19-26 ◽  
Author(s):  
H. I. Chen ◽  
H. J. Granger ◽  
A. E. Taylor
Keyword(s):  
Venous Pressure ◽  
Lymph Flow

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
Keyword(s):  
Heart Rate ◽  
Flow Rate ◽  
Venous Pressure ◽  
Control Period ◽  
Lymph Flow ◽  
Thoracic Duct Lymph ◽  
Acute Administration ◽  
Before And After ◽  
Estrogen Effects ◽  
Estrogen Administration

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)

Lymph flow in sheep with rapid cardiac ventricular pacing

1997 ◽  
Vol 272 (5) ◽  
pp. R1595-R1598 ◽  
Author(s):  
R. E. Drake ◽  
S. Dhother ◽  
R. A. Teague ◽  
J. C. Gabel
Keyword(s):  
Heart Failure ◽  
Flow Rate ◽  
Mediastinal Lymph Node ◽  
Venous Pressure ◽  
Lymphatic Vessels ◽  
Lymph Flow ◽  
Ventricular Pacing ◽  
Fluid Filtration ◽  
Flow Rates ◽  
Lymphatic Flow

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.

Hyaluronan flux from cat intestine: changes with lymph flow

1992 ◽  
Vol 262 (2) ◽  
pp. H457-H462 ◽  
Author(s):  
R. K. Reed ◽  
M. I. Townsley ◽  
T. C. Laurent ◽  
A. E. Taylor
Keyword(s):  
Blood Flow ◽  
Major Part ◽  
Interstitial Fluid ◽  
Venous Pressure ◽  
Lymph Flow ◽  
Fluid Flux ◽  
Control Value ◽  
One Step ◽  
Experimental Group

Isolated and autoperfused ileal segments from pentobarbital-anesthetized cats were used to study turnover of hyaluronan in the intestine. A postnodal lymphatic was cannulated, and transcapillary and interstitial fluid fluxes were increased by raising venous pressure. Lymph hyaluronan concentration in control averaged 20.2 +/- 18.8 (SD) micrograms/ml (range 4.6-50) and increased with increasing lymph flow in all experiments to peak at concentrations two to three times above control values (at 15-20 mmHg increase in venous pressure). At higher lymph flows, hyaluronan concentration fell to below 5 micrograms/ml to an average of 21.3 +/- 19.5% of control value at the highest venous pressures used (30-40 mmHg). Tissue hyaluronan content fell from 349 +/- 191 micrograms/g dry wt in control to 148 +/- 78 micrograms/g dry wt (P less than 0.05) at the end of the experiment. In a second group, vasodilators were administered before elevation of venous pressure to prevent redistribution of blood flow between mucosal and muscular layers. The results were similar to those obtained above. In a third experimental group, venous pressure was elevated in one step to 30 mmHg and maintained at this level. Again, hyaluronan concentration initially increased and later fell well below control values. We conclude that a major part of the intestinal hyaluronan is easily mobilized by increased interstitial fluid flux.

Intestinal capillary filtration in acute and chronic portal hypertension

1988 ◽  
Vol 254 (3) ◽  
pp. G339-G345 ◽  
Author(s):  
R. J. Korthuis ◽  
D. A. Kinden ◽  
G. E. Brimer ◽  
K. A. Slattery ◽  
P. Stogsdill ◽  
...  
Keyword(s):  
Blood Flow ◽  
Portal Hypertension ◽  
Capillary Pressure ◽  
Vascular Resistance ◽  
Interstitial Fluid ◽  
Venous Pressure ◽  
Fluid Pressure ◽  
Lymph Flow ◽  
Interstitial Fluid Pressure ◽  
Capillary Filtration

The impact of acute and chronic portal hypertension on the dynamics of intestinal microvascular fluid exchange was examined in anesthetized, fasted, sham-operated control rats with normal portal pressures (CON), during acute elevations in portal pressure (APH) in control rats, and in rats in which chronic portal hypertension (CPH) was produced by calibrated stenosis of the portal vein 10 days prior to the experiments. Although intestinal blood flow and vascular resistance were not altered by APH in control rats, CPH was associated with an increased intestinal blood flow and reduced intestinal vascular resistance when compared with CON and APH. Intestinal capillary pressure and lymph flow were elevated in APH and CPH relative to control values. However, the increase in both variables was greater in CPH. The capillary filtration coefficient was elevated only in CPH. The transcapillary oncotic pressure gradient was not altered by APH or CPH. Interstitial fluid pressure was increased from -1.1 mmHg in CON to 3.9 mmHg during APH and to 5.0 mmHg in CPH. The results of this study indicate that chronic elevations in portal venous pressure produce larger increments in intestinal capillary pressure and filtration rate than do acute elevations in portal venous pressure of the same magnitude. However, the potential edemagenic effects of elevated capillary pressure in both acute and chronic portal hypertension are opposed by increases in lymph flow and interstitial fluid pressure.

Vascular perfusion limits mesenteric lymph flow during anaphylactic hypotension in rats

2012 ◽  
Vol 302 (10) ◽  
pp. R1191-R1196 ◽  
Author(s):  
Wei Zhang ◽  
Toshishige Shibamoto ◽  
Yuhichi Kuda ◽  
Yasutaka Kurata ◽  
Shohei Shinomiya ◽  
...  
Keyword(s):  
Vascular Permeability ◽  
Surface Area ◽  
Venous Pressure ◽  
Lymph Flow ◽  
Arterial Flow ◽  
Vascular Perfusion ◽  
Vascular Surface ◽  
Vascular Bed ◽  
Mesenteric Lymph ◽  
Anesthetized Rats

To determine fluid extravasation in the splanchnic vascular bed during anaphylactic hypotension, the mesenteric lymph flow (Qlym) was measured in anesthetized rats sensitized with ovalbumin, along with the systemic arterial pressure (Psa) and portal venous pressure (Ppv). When the antigen was injected into the sensitized rats ( n = 10), Psa decreased from 125 ± 4 to 37 ± 2 mmHg at 10 min with a gradual recovery, whereas Ppv increased by 16 mmHg at 2 min and returned to the baseline at 10 min. Qlym increased 3.3-fold from the baseline of 0.023 ± 0.002 g/min to the peak levels of 0.075 ± 0.009 g/min at 2 min and returned to the baseline within 12 min. The lymph protein concentrations increased after antigen, a finding indicating increased vascular permeability. To determine the role of the Ppv increase in the antigen-induced increase in Qlym, Ppv of the nonsensitized rats ( n = 10) was mechanically elevated in a manner similar to that of the sensitized rats by compressing the portal vein near the hepatic hilus. Unexpectedly, Ppv elevation alone produced a similar increase in Qlym, with the peak comparable to that of the sensitized rats. This finding aroused a question why the antigen-induced increase in Qlym was limited despite the presence of increased vascular permeability. Thus the changes in splanchnic vascular surface area were assessed by measuring the mesenteric arterial flow. The mesenteric arterial flow was decreased much more in the sensitized rats (75%; n = 5) than the nonsensitized Ppv elevated rats (50%; n = 5). In conclusion, mesenteric lymph flow increases transiently after antigen presumably due to increased capillary pressure of the splanchnic vascular bed via downstream Ppv elevation and perfusion and increased vascular permeability in anesthetized rats. However, this increased extravasation is subsequently limited by decreases in vascular surface area and filtration pressure.

scholarly journals LYMPH PRESSURES IN STERILE INFLAMMATION

1932 ◽  
Vol 56 (3) ◽  
pp. 363-370 ◽  
Author(s):  
Madeleine E. Field ◽  
Cecil K. Drinker ◽  
James C. White
Keyword(s):  
Protein Concentration ◽  
Venous Pressure ◽  
Lymph Flow ◽  
Sterile Inflammation ◽  
Maximum Pressure ◽  
Anesthetized Dogs

1. The normal lymph pressure in the legs of anesthetized dogs is not measurable. 2. The maximum pressure of lymph in the quiescent leg under conditions of sterile inflammation is around 120 cm. of lymph. 3. Venous pressure rises immediately in a region subjected to sterile inflammation and then slowly returns to normal. The rise in lymph pressure follows the rise in venous pressure. 4. Changes in lymph flow, lymph pressure, and protein concentration of the lymph occur when the part producing lymph is subjected to external temperatures between 50° and 60°C.

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
Keyword(s):  
Body Weight ◽  
Lymphatic System ◽  
Venous Pressure ◽  
Ringer Solution ◽  
Lymph Flow ◽  
The Body ◽  
Intravenous Fluid ◽  
Thoracic Duct Lymph ◽  
Duct Lymph ◽  
Intestinal Lymphatics

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.

Effect of outflow pressure on liver lymph flow in unanesthetized sheep

1990 ◽  
Vol 259 (4) ◽  
pp. R780-R785 ◽  
Author(s):  
R. E. Drake ◽  
J. C. Gabel
Keyword(s):  
Hepatic Vein ◽  
Flow Rate ◽  
Lymphatic Vessel ◽  
Venous Pressure ◽  
Lymph Flow ◽  
Reference Level ◽  
Effective Pressure ◽  
Lymphatic Flow ◽  
Zero Reference ◽  
Po Delta

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.

Increased lymphatic flux of hyaluronan from cat intestine during fat absorption

1992 ◽  
Vol 263 (1) ◽  
pp. G6-G11
Author(s):  
R. K. Reed ◽  
M. I. Townsley ◽  
V. H. Pitts ◽  
T. C. Laurent ◽  
A. E. Taylor
Keyword(s):  
Oleic Acid ◽  
Venous Pressure ◽  
Fold Increase ◽  
Lymph Flow ◽  
Fat Absorption ◽  
Matrix Component ◽  
Pore Sizes ◽  
Group 2 ◽  
Lymph Sample ◽  
Group 1

During fat absorption, chylomicrons with sizes up to 5,000-10,000 A must traverse an interstitium that has estimated pore sizes of 120-200 A to reach the lacteals. The present experiments were performed to study the behavior of the interstitial matrix component hyaluronan during fat absorption from the intestine. Ileal segments were isolated and autoperfused in pentobarbital-anesthetized cats. A postnodal lymphatic was cannulated, and lymph flow, protein, and hyaluronan concentration in lymph were determined. In group 1, a mixture of oleic acid and taurocholate was infused into the ileal lumen, while in group 2 the animals were fed cream overnight. In group 1, control lymph flow and hyaluronan concentration averaged 53.3 +/- 16.0 (SD) microliters.min-1.100 g intestine-1 and 21.4 +/- 16.0 micrograms/ml, respectively. Administration of taurocholate and oleic acid increased lymph flow and lymph hyaluronan concentration by 100 and 50%, respectively, resulting in a nearly three-fold increase in hyaluronan flux. Subsequent increases in venous pressure increased lymph flow and reduced hyaluronan concentration in lymph to less than 3 micrograms/ml. Hyaluronan flux remained approximately 2 micrograms.min-1.100 g intestine-1 independent of lymph flow. In group 2, no lymph sample was available before administration of fat. Hyaluronan concentration at control venous pressure was 19.3 +/- 6.7 micrograms/ml and fell to 10 micrograms/ml at the highest lymph flow. Hyaluronan flux was approximately 10 micrograms.min-1.100 g intestine-1 at the highest lymph flow and venous pressure (P less than 0.05 compared with the same lymph flow in group 1).(ABSTRACT TRUNCATED AT 250 WORDS)

Microvascular, interstitial, and lymphatic interactions in normal heart

1985 ◽  
Vol 249 (4) ◽  
pp. H834-H842 ◽  
Author(s):  
G. A. Laine ◽  
H. J. Granger
Keyword(s):  
Plasma Protein ◽  
Protein Concentration ◽  
Venous Pressure ◽  
Left Ventricular ◽  
Lymph Flow ◽  
Normal Heart ◽  
Oncotic Pressure ◽  
Fluid Exchange ◽  
Edema Formation ◽  
Total Plasma Protein

Control of transmicrovascular fluid exchange in the heart is of critical importance in the prevention of myocardial edema formation. To quantify the absolute values for, and the interrelationships between, the forces and flows governing fluid balance within the normal heart, the following variables were measured: arterial pressure (Pa), coronary sinus pressure (Pcs), myocardial interstitial fluid pressure (Pint), plasma protein concentration (Cp), and oncotic pressure (tau cap) along with interstitial protein concentration (CL), interstitial oncotic pressure (tau int), and left ventricular lymph flow rate (Jv). All parameters were recorded under control conditions and during graded venous pressure elevations. Control values were Pa, 125 +/- 21 mmHg; Pcs, 7.3 +/- 1.3 mmHg; Pint, 14.9 +/- 3.1 mmHg; CL/Cp, 0.82 +/- 0.12; and Jv, 7.0 +/- 2.7 ml/h. As Pcs was elevated to eight times control, Pint increased from 15 to 50 mmHg and lymph flow rose sixfold. A filtration-independent value for CL/Cp could not be obtained for total plasma protein, although a washdown CL/Cp value for beta-lipoprotein of 0.04 was obtained. Our data indicate that a large surface area of myocardial exchange vessels coupled with lymphatics of relatively low sensitivity to extravascular volume expansion produce a system that relies on a large increase in interstitial hydrostatic pressure to limit edema formation.

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