scholarly journals Intestinal Lymph Flow, and Lipid and Drug Transport Scale Allometrically From Pre-clinical Species to Humans

2020 ◽  
Vol 11 ◽  
Author(s):  
Natalie L. Trevaskis ◽  
Given Lee ◽  
Alistair Escott ◽  
Kian Liun Phang ◽  
Jiwon Hong ◽  
...  
Keyword(s):  
Drug Transport ◽  
Lymph Flow ◽  
Intestinal Lymph

Enterostatin efflux in cat intestinal lymph: relation to lymph flow, hyaluronan, and fat absorption

1996 ◽  
Vol 271 (4) ◽  
pp. G714-G721 ◽  
Author(s):  
M. I. Townsley ◽  
C. Erlanson-Albertsson ◽  
A. Ohlsson ◽  
C. Rippe ◽  
R. K. Reed
Keyword(s):  
Oleic Acid ◽  
Lymph Flow ◽  
Separate Group ◽  
Intestinal Lumen ◽  
Fat Absorption ◽  
Intestinal Lymph ◽  
Exocrine Secretions ◽  
Pancreatic Exocrine ◽  
Activation Peptide

The question addressed in this study was whether enterostatin, the pancreatic procolipase activation peptide, modulates intestinal hyaluronan turnover via lymph. In anesthetized cats, segments of ileum were surgically isolated from the proximal and distal gut, the draining lymphatic was cannulated, and the segment was autoperfused in situ. In several groups, concentrations of immunoreactive enterostatin in lymph were compared with that in plasma at baseline and elevated lymph flow and in the absence and presence of fat absorption. The baseline ratio of lymph enterostatin to that in plasma (L/P) in the absence of fat absorption was 1.44 +/- 0.29 compared with 4.93 +/- 0.42 after cream feeding (P < 0.05). In a separate group, when the intestinal lumen was perfused for 2 h with a mixture of oleic acid and taurocholate, enterostatin L/P doubled compared with baseline. At high lymph flows, enterostatin concentrations fell in all groups, resulting in an L/P of 0.47 +/- 0.09 (P < 0.05) in the absence of fat absorption, 0.77 +/- 0.35 after oleic acid, and 1.26 +/- 0.13 in the cream-fed group. These changes correlate with the pattern of hyaluronan efflux from the ileum into lymph after fat absorption [R.K. Reed, M.I Townsley, V.H. Pitts, T.C. Laurent, and A.E. Taylor. Am. J. Physiol, 263 (Gastrointest. Liver Physiol. 26): G6-G11, 1992] However, in separate groups when enterostatin was introduced into ileum, either as a close intra-arterial bolus or via the intestinal lumen, there were no resultant changes in efflux of hyaluronan from the intestine into lymph. In conclusion, despite the fact that delivery of pancreatic exocrine secretions to the ileal lumen was blocked in this model, enterostatin concentration in lymph increased after fat absorption. Nonetheless, it seems clear that enterostatin does not modify intestinal hyaluronan turnover.

Rat intestinal lymph osmolarity during glucose and oleic acid absorption

1989 ◽  
Vol 257 (3) ◽  
pp. G438-G446 ◽  
Author(s):  
H. G. Bohlen ◽  
J. L. Unthank
Keyword(s):  
Oleic Acid ◽  
Glucose Concentration ◽  
Intestinal Motility ◽  
Bowel Wall ◽  
Lymph Flow ◽  
Rat Jejunum ◽  
Bowel Motility ◽  
Acid Absorption ◽  
Intestinal Lymph ◽  
All Solutions

The two major purposes of this study were to determine 1) how glucose and oleic acid absorption by the intestinal villi influenced the osmotic composition of lymph as it exited the villus base and 2) what if any changes in lymph osmolarity occurred as the lymph traversed through the bowel wall. The rat jejunum was used in all studies and lymph was collected from individual lymphatics at 0.5-1 nl/min during control states and luminal exposure to 35-550 mg% glucose solutions (isotonic in saline) and 5 and 20 mM oleic acidtaurocholate solutions. Lymph collected from the base of villi during vigorous motility had an osmolarity of 403 +/- 15 mosM at rest and was only increased 30-50 mosM more except during exposure to 550 mg% glucose, where osmolarity increased over 100 mosM. Under comparable conditions, the submucosal lymph osmolarity at rest was 302 +/- 3.5 mosM and increased to 330-350 mosM during exposure to all of the solutions tested. When intestinal motility was virtually stopped, the submucosal lymph osmolarity was isotonic for all solutions tested. These observations indicate that absorption of glucose and oleic acid increased the osmolarity of lymph, leaving the villus only 30-50 mosM unless a glucose concentration of 550 mg% was present. Furthermore, the increased flow of villus lymph during absorption raised the osmolarity of the submucosal lymph when bowel motility assisted the lymph propulsion. This movement of materials from the villus to the submucosa by venular blood and lymph flow provides an opportunity for the villus tissue to influence the composition of the submucosal interstitial environment.

The effects of cholecystokinin and cholecystokinin-octapeptide on intestinal lymph flow in the rat

1977 ◽  
Vol 55 (6) ◽  
pp. 1393-1396 ◽  
Author(s):  
S. G. Turner ◽  
J. A. Barrowman
Keyword(s):  
Blood Flow ◽  
Protein Transport ◽  
Lymph Flow ◽  
Intestinal Blood Flow ◽  
Concomitant Increase ◽  
Cholecystokinin Octapeptide ◽  
Intestinal Lymph

Intravenous cholecystokinin and its synthetic C-terminal octapeptide were found to cause a transient augmentation of intestinal lymph flow in the rat. Concomitant increase in lymph protein transport suggests that this reflects the increase in intestinal blood flow which is known to occur in response to these agents.

scholarly journals EFFECT OF SECRETIN ON INTESTINAL LYMPH FLOW AND COMPOSITION IN THE RAT

1981 ◽  
Vol 66 (3) ◽  
pp. 297-305 ◽  
Author(s):  
J.-A. Lawrence ◽  
D. Bryant ◽  
K. B. Roberts ◽  
J. A. Barrowman
Keyword(s):  
Lymph Flow ◽  
Intestinal Lymph

Lymph flow, lymph protein concentration, and protein output from rat small intestine

1985 ◽  
Vol 248 (6) ◽  
pp. G670-G675
Author(s):  
J. S. Lee
Keyword(s):  
Small Intestine ◽  
Water Absorption ◽  
Protein Concentration ◽  
Capillary Permeability ◽  
Lymph Flow ◽  
Rat Small Intestine ◽  
Capillary Filtration ◽  
Intestinal Lymph ◽  
Lymph Duct ◽  
Protein Output

Lymph flow (JL), lymph protein concentration (CL), and protein output (JP) from the main intestinal lymph duct were determined. The basal JL from the mesenteric pedicle alone was the same as that from the mesenteric pedicle attached with a segment of the nonabsorbing intestine, indicating that the basal JL does not originate from the intestine but is totally from the region of the mesenteric pedicle. The basal CL was 3.5-3.8 g/100 ml. When the intestine was absorbing water, JL increased and CL decreased, but JP increased above the basal JP in the initial 20 min of water absorption and then decreased progressively with time. Furthermore, it was estimated that CL in the "excess lymph" (formed during water absorption) was 1.4 +/- 0.2 g/100 ml in the initial 10 min of water absorption and was zero or nearly so in the later periods. From this and other evidence, it is concluded that under various conditions without net water absorption rat small intestine does not produce lymph and that during water absorption there is no significant increase in capillary permeability or capillary filtration. Therefore, the excess lymph could be mostly derived from the fluid absorbed from the lumen of the intestine.

Lymph pressure in rat intestinal lymph duct with lymphatic obstruction

1986 ◽  
Vol 251 (3) ◽  
pp. G321-G325 ◽  
Author(s):  
J. S. Lee
Keyword(s):  
Lymph Flow ◽  
Saline Infusion ◽  
Pressure Waves ◽  
Fluid Absorption ◽  
Intestinal Lymph ◽  
Intravenous Saline ◽  
Intestinal Lymphatics ◽  
Lymph Duct ◽  
Rhythmical Contractions ◽  
Lymphatic Obstruction

Lymph pressure (PL) in the main intestinal lymph duct with obstruction of lymph flow was determined. Under various conditions, the rate of lymph flow (JL) was essentially the same in either A rats (with communications between hepatic and intestinal lymphatics) or B rats (without such communications), but PL of A rats was significantly lower (P less than 0.01) than that of B rats. When the intestine was in the basal state, JL of A and B rats was 0.2-0.3 ml/h per rat, and PL was 1.5 +/- 0.2 and 3.3 +/- 0.2 mm/Hg, respectively. During fluid absorption, JL of A and B rats increased to 0.8-0.9 ml/h, and PL was 2.1 +/- 0.4 and 6.4 +/- 0.7 mmHg, respectively. During intravenous saline infusion, JL of A and B rats increased greatly to approximately 14 ml/h, and PL was 3.1 +/- 0.3 and 10.4 +/- 1.1 mmHg, respectively. The lower PL in A rats is apparently due to the possibility that during lymphatic obstruction most lymph could be drained off by the hepatic lymphatics. In A rats, luminal distension pressure had no effect on PL but in B rats PL decreased when distension pressure was 20 mmHg or higher. Furthermore, lymph pressure waves indicate the occurrence of rhythmical contractions of the lymph duct or its surrounding tissues, which may play a role in the propulsion of lymph.

Pathways of lymph flow through intestinal lymph nodes in the horse

1992 ◽  
Vol 232 (1) ◽  
pp. 126-132 ◽  
Author(s):  
Stephen A. Nikles ◽  
Trevor J. Heath
Keyword(s):  
Lymph Nodes ◽  
Lymph Flow ◽  
Intestinal Lymph ◽  
Flow Through

Effects of bradykinin on intestinal transcapillary fluid exchange

1981 ◽  
Vol 59 (8) ◽  
pp. 786-789 ◽  
Author(s):  
J. A. Barrowman ◽  
M. A. Perry ◽  
P. R. Kvietys ◽  
M. Ulrich ◽  
D. N. Granger
Keyword(s):  
Pressure Gradient ◽  
Capillary Pressure ◽  
Protein Concentration ◽  
Fluid Pressure ◽  
Lymph Flow ◽  
Oncotic Pressure ◽  
Fluid Exchange ◽  
Intestinal Lymph ◽  
Pressure Exchange ◽  
Exchange Vessel

Bradykinin (50 μg∙L−1) increases intestinal lymph flow sixfold when infused intraarterially into the cat ileum. The capillary filtration coefficient and capillary pressure increase and interstitial fluid pressure rises from negative to positive values. A slight increase in lymph:plasma protein concentration occurs with a resulting fall in the transcapillary oncotic pressure gradient. These results indicate that the effect of bradykinin on intestinal lymph flow is attributable, at least in part, to increased capillary pressure, exchange vessel surface area, and a reduction in the effective transcapillary oncotic pressure gradient.

Effect of increased neck vein pressure on intestinal lymphatic pressure in awake sheep

1992 ◽  
Vol 262 (5) ◽  
pp. R892-R894 ◽  
Author(s):  
R. E. Drake ◽  
R. D. Abbott
Keyword(s):  
Thoracic Duct ◽  
Lymphatic Vessels ◽  
Ringer Solution ◽  
Lymph Flow ◽  
The Other ◽  
Flow Rates ◽  
Intestinal Lymph ◽  
Other Hand ◽  
Intestinal Lymphatics ◽  
Increased Pressure

Lymphatic vessels from the intestines drain into the thoracic duct, and the thoracic duct empties into veins in the neck. Thus increases in neck vein pressure (PNV) might slow intestinal lymph flow, provided the increased pressure is reflected upstream through the lymphatic vessels. To test the effect of increases in PNV on lymphatic pressure, we cannulated intestinal lymphatics in the direction of flow in six sheep. After the sheep recovered from surgery, we measured the pressure in the lymphatics (Px) as we increased PNV in steps. Px increased only slightly (but significantly) from 7.4 +/- 2.0 to 11.4 +/- 5.2 (SD) cmH2O when we increased PNV from baseline (0.8 +/- 2.4 cmH2O) to 37.4 +/- 4.1 cmH2O. However, when we simulated an increased lymph flow by infusing Ringer solution into the lymphatics at 1,000 microliters/min, Px increased to 24.6 +/- 7.0 cmH2O at PNV equal to 37.1 +/- 5.3 cmH2O. These results indicate that, at normal lymph flow rates, increases in neck vein pressure cause only small increases in intestinal lymphatic pressure. On the other hand, when lymph flow is elevated, increases in neck vein pressure may substantially increase lymphatic pressure and thus slow intestinal lymph flow.

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