Intravenous saline infusion in rat increases hyaluronan efflux in intestinal lymph by increasing lymph flow

1993 ◽  
Vol 147 (3) ◽  
pp. 329-335 ◽  
Author(s):  
G. ØSTGAARD ◽  
R. K. REED
1986 ◽  
Vol 251 (3) ◽  
pp. G321-G325 ◽  
Author(s):  
J. S. Lee

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.


2009 ◽  
Vol 10 (1_suppl) ◽  
pp. S3-S6 ◽  
Author(s):  
Neil MacGillivray

The paper reviews the work of Dr Thomas Latta who during the cholera epidemic of 1831—32 pioneered the use of intravenous saline infusion in the treatment of cholera. The reaction of the medical profession to this new therapy is described and the reasons for the profession’s failure to acknowledge the importance of this advance is analysed. The reasons why the name of Thomas Latta and his contribution did not survive his death in 1833 are discussed and the contributions of twentieth century scholars in remembering his work are highlighted.


2008 ◽  
Vol 22 (S1) ◽  
Author(s):  
G. Kim Prisk ◽  
I. Mark Olfert ◽  
Tatsuya J Arai ◽  
Richard M Hinds ◽  
Kun Lun Huang ◽  
...  

2022 ◽  
Author(s):  
Yoshitoki Yanagimoto ◽  
Yuko Ishizaki ◽  
Yoko Nakai ◽  
Miki Minami ◽  
Rinako Tamai ◽  
...  

Abstract Background: Intravenous saline infusion is considered effective for the treatment of postural tachycardia syndrome (POTS) in adults. However, few studies have assessed the efficacy of intravenous saline infusion for POTS in children and adolescents. Aim: This study aimed to evaluate the efficacy of intravenous saline infusion in children and adolescents with POTS.Methods: A total of 107 children with POTS (median age: 13 years, range: 10–15 years) were enrolled. Eighty-eight children were in the intravenous saline infusion group and 19 children were in the comparison group. Blood pressure (BP) and pulse rate (PR) were recorded before and after standing. A standing test was performed early in the morning for 2 consecutive days. A volume of 1.5 L of saline was administered intravenously to each participant in the intervention group for a mean duration of 17 hours between the two standing tests.Results: The mean change in PR was significantly lower in the intervention group than in the comparison group during the second test (36.9 vs. 52.8 beats/minute, p<0.001). Additionally, the mean change in PR was significantly lower in the second test than in the first test (44.7 beats/minute) in the intervention group (p<0.001). However, the mean change in systolic BP was not different before and after intravenous saline infusion between the two groups or between the two tests in each group.Conclusion: Intravenous saline infusion reduces the increased PR on standing in children with POTS. Intravenous saline infusion improves tachycardia in children with POTS when standing.


1996 ◽  
Vol 271 (4) ◽  
pp. G714-G721 ◽  
Author(s):  
M. I. Townsley ◽  
C. Erlanson-Albertsson ◽  
A. Ohlsson ◽  
C. Rippe ◽  
R. K. Reed

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.


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.


1989 ◽  
Vol 257 (3) ◽  
pp. G438-G446 ◽  
Author(s):  
H. G. Bohlen ◽  
J. L. Unthank

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.


2009 ◽  
Vol 297 (4) ◽  
pp. H1319-H1328 ◽  
Author(s):  
H. Glenn Bohlen ◽  
Wei Wang ◽  
Anatoliy Gashev ◽  
Olga Gasheva ◽  
Dave Zawieja

Multiple investigators have shown interdependence of lymphatic contractions on nitric oxide (NO) activity by pharmacological and traumatic suppression of endothelial NO synthase (eNOS). We demonstrated that lymphatic diastolic relaxation is particularly sensitive to NO from the lymphatic endothelium. The predicted mechanism is shear forces produced by the lymph flow during phasic pumping, activating eNOS in the lymphatic endothelium to produce NO. We measured [NO] during phasic contractions using microelectrodes on in situ mesenteric lymphatics in anesthetized rats under basal conditions and with an intravenous saline bolus (0.5 ml/100 g) or infusion (0.5 ml·100 g−1·h−1). Under basal conditions, [NO] measured on the tubular portions of the lymphatics was ∼200–250 nM, slightly higher than in the adjacent adipocyte microvasculature, whereas [NO] measured on the lymphatic bulb surface was ∼400 nM. Immunohistochemistry of eNOS in isolated lympathics indicated a much greater expression in the lymph valves and surrounding bulb area than in the tubular regions. During phasic lymphatic contractions, the valve and tubular [NO] increased with each contraction, and during intravenous saline infusion, [NO] increased in proportion to the contraction frequency and, presumably, lymph flow. The partial blockade of eNOS over ∼1 cm length with Nω-nitro-l-arginine methyl ester lowered the [NO]. These in vivo data document for the first time that both valvular and tubular lymphatic segments increase NO generation during each phasic contraction and that [NO] summated with increased contraction frequency. The combined data predict regional variations in eNOS and [NO] in the tubular and valve areas, plus the summated NO responses dependent on contraction frequency provide for a complex relaxation mechanism involving NO.


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