Effects of pressure on water and solute transport by dog intestinal mucosa in vitro

Hakim, A A; Lifson, Nathan

doi:10.1152/ajplegacy.1969.216.2.276

Cited by 107 publications

(48 citation statements)

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“…These results indicate that a different mechanism could account for the increased alkaline responses induced by PGE2 and hypertonic NaCI. The dependence of PGE2 action on the intact organ perfusion is also supported by our previous findings (10) that the reduction of mucosal blood flow by hemorrhagic shock significantly impaired the increased alkaline response caused by PGE2 as well as basal HCO3 Output A number of mechanisms could account for the rise in alkaline secretion from the duo denal mucosa, including the direct stimulation of HCO3 output by enhancing either cellular transport or mucosal permeability (3,(11)(12)(13). In fact, passive diffusion of HCO3 via shunt pathways contributes substantially to luminal alkalinization by this tissue in vitro (13).…”

Section: Discussionsupporting

confidence: 71%

Stimulation by Prostaglandin E2 of Alkaline Secretion in the Rat Duodenum: Comparative Study with Hypertonic NaCI

Takeuchi

Niida

Takinami

et al. 1990

Japanese Journal of Pharmacology

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Section: Discussionsupporting

confidence: 71%

Stimulation by Prostaglandin E2 of Alkaline Secretion in the Rat Duodenum: Comparative Study with Hypertonic NaCI

Takeuchi

Niida

Takinami

et al. 1990

Japanese Journal of Pharmacology

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“…The positive relation between estimated capillary pressure and secretary fluxes has been observed in other experiments and was suggested as being due to passive ultrafiltration across the mucosal epithelium (MIailman & Jordan, 1975;Hakim & Lifson, 1969 Over-all, the primary effect of pentagastrin appeared to be on the Na+ fluxes because the changes, or lack thereof, in the net Na+ flux were effected through changes in the secretary Na+ fluxes in fed and fasted dogs with or without guanethidine or atropine. Because the small intestine is very permeable to H20, the lumenal solution remains isotonic and the net H20 flux is osmotically obligated by the net Na+ flux.…”

Section: Discussionsupporting

confidence: 55%

Effects of pentagastrin on intestinal absorption and blood flow in the anaesthetized dog.

Mailman¹

1980

The Journal of Physiology

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SUMMARY1. Pentagastrin (1, 10/tg/min) was infused i.v. into fed and fasted anaesthetized dogs and the intestinal absorption of NaCl and H20 and blood flow were determined. The influence of pentagastrin-induced cardiovascular changes on absorption was investigated.2. 22Na and 3H20 were used to determine the unidirectional Na and H20 fluxes from saline perfused through the ileal lumen and the clearances of 3H20 were used to calculate total and absorptive site blood flow.3. Ileal absorption of Na and H20 was reduced by 10 tg/min pentagastrin due primarily to significant increases in the secretary flux of Na and decreases in the absorptive flux of H20 in both fed and fasted animals.4. Neither total intestinal blood flow, arterial nor mesenteric vein pressure were changed by pentagastrin but absorptive site blood flow was decreased in fasted but not in fed dogs.5. Pretreatment with atropine reduced the effects of pentagastrin but pretreatment with guanethidine potentiated the effects of pentagastrin.6. Absorptive site blood flow was positively linearly correlated with the absorptive fluxes of both Na and H20. The relationships between the secretary fluxes of Na and H20 and estimated capillary pressure were changed from a positive relationship in control periods to a less positive or negative relationship following pentagastrin.7. It was concluded that pentagastrin reduces intestinal absorption through both a cardiovascular effect and an effect on the intestinal epithelium. Also, there is a strong autonomic component in the effects of pentagastrin on intestinal absorption.

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“…In vitro, a transmural pressure difference of only 4-6 cm H20 results in a rather abrupt increase in the hydraulic permeability of the mucosa and the onset of a passive secretory stream (28). It seems probable that a similar process occurs in vivo.…”

Section: Discussionmentioning

confidence: 96%

“…Suggestions as to the identity of the channels for secretory filtration include, besides the most likely one of the intercellular spaces (28,39) as shown in Fig. 10, the defects left at the tips of the villi by shedding cells (28), and large areas of individual villi denuded of epithelium (8).…”

Section: Discussionmentioning

confidence: 99%

Mechanism of production of intestinal secretion by elevated venous pressure.

Yablonski¹,

Lifson²

1976

J. Clin. Invest.

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A B S T R A C T A study was carried out to elucidate the physiological mechanisms responsible for the intestinal secretion produced by venous pressure elevation. In dogs, measurements were made of the rate and composition of small intestinal secretion, rate of flow and composition of intestinal lymph, plasma composition, and mucosal water content, all in response to elevations of intestinal venous pressure. Venous pressure elevations above a threshold value of 30-35 cm H20 produce secretion at a rate approximately proportional to the value of the pressure minus the threshold value. Above the threshold value, there were large increases in the rates of lymph flow and net sustained transcapillary filtration. These rates were also roughly proportional to the incremental venous pressure.

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Effects of pressure on water and solute transport by dog intestinal mucosa in vitro

Cited by 107 publications

References 0 publications

Stimulation by Prostaglandin E2 of Alkaline Secretion in the Rat Duodenum: Comparative Study with Hypertonic NaCI

Stimulation by Prostaglandin E2 of Alkaline Secretion in the Rat Duodenum: Comparative Study with Hypertonic NaCI

Effects of pentagastrin on intestinal absorption and blood flow in the anaesthetized dog.

Mechanism of production of intestinal secretion by elevated venous pressure.

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