Microcirculation of the intestinal mucosa

Granger, D. Neil; Kvietys, Peter R.; Korthuis, Ronald J.; Premen, A. J.

doi:10.1002/cphy.cp060139

Cited by 35 publications

(70 citation statements)

References 274 publications

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“…In the present study there was still some flow in the intes tinal vein at a venous pressure of 50 mm Hg, which means that the capillary hydrostatic pressure must have been above 50 mm Hg. An increase in capillary pressure in excess of 15 mm Hg causes edema [20], High capillary pressure therefore explains the edema of the intestinal wall observed in our experiment. It also explains the marked exudation of fluid into the peritoneal cavity and the increased hematocrit in the intestinal vein blood.…”

Section: Discussionmentioning

confidence: 54%

“…Acute elevation of intestinal venous pressure normally results in increased lymph flow in the small intestine [19][20][21]. However, in the present experimental model, and probably also in clinical closed-loop intestinal obstruc tion, the lymph vessels are exposed to high extrinsic pres sure which probably reduces or inhibits the lymph flow.…”

Section: Discussionmentioning

confidence: 71%

“…However, in the present experimental model, and probably also in clinical closed-loop intestinal obstruc tion, the lymph vessels are exposed to high extrinsic pres sure which probably reduces or inhibits the lymph flow. This contributes to increasing the interstitial fluid pres sure and the filtration secretion [20].…”

Section: Discussionmentioning

confidence: 99%

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Hemodynamic Changes Associated with Strangulation Obstruction in Cats

Fevang

Fevang²,

Gíslason³

et al. 1995

Int J Microcirc

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While changes in blood flow associated with simple intestinal obstruction have been studied extensively, little is known about blood flow changes associated with strangulation obstruction. Closed loop strangulation was produced in anesthetized cats by means of a baby pressure gasket. Intestinal blood flow was measured by transit time flowmetry. Blood pressure was measured in a carotid artery and in veins of a closed loop of small intestine. The gasket pressure was increased stepwise in 10 mm Hg increments after which the intestinal venous pressure was kept constant at 50 mm Hg for 5 h. Increasing gasket pressure was followed by a corresponding increase in venous pressure in the closed bowel loop. Blood flow in the closed loop decreased with increasing venous pressure and was closely related to the arteriovenous perfusion pressure under stepwise increase of the gasket pressure and during prolonged periods with increased venous pressure. At constant elevated venous pressure the intestinal blood flow was determined by the arterial pressure. The vascular resistance in the closed loop increased exponentially with increasing venous pressure and especially at very low blood flow. In conclusion, we have found that strangulation obstruction is associated with increased venous pressure in the closed loop which contributes to maintaining intestinal blood flow during the obstruction.

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Section: Discussionmentioning

confidence: 54%

Section: Discussionmentioning

confidence: 71%

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Hemodynamic Changes Associated with Strangulation Obstruction in Cats

Fevang

Fevang²,

Gíslason³

et al. 1995

Int J Microcirc

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“…A dilution of 1:20 represents an underestimate of the plasma dilution that is present in myocardial interstitial fluid. 26 The decrease in myocyte beating rate was transient, ie, recovery to control beating rate occurred within 24 hours of removal of the septic plasma. In another set of experiments, myocytes were incubated with septic plasma obtained 2, 4, or 6 hours after the induction of CLP (diluted 1:20 in M199) for 4 hours, washed, and then incubated with M199 for an additional 60 minutes.…”

Section: Characterization Of the In Vitro Modelmentioning

confidence: 99%

Cardiac Myocytes Activated by Septic Plasma Promote Neutrophil Transendothelial Migration

Madorin

Tao

Sugimoto

et al. 2004

Circulation Research

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Abstract-Cardiac myocytes isolated from rats with peritonitis (cecal ligation and perforation; CLP) promote PMN transendothelial migration. Herein, we assessed (1) the mechanisms involved in cardiac myocyte activation during peritonitis and (2) the means by which these activated myocytes promote PMN transendothelial migration. Plasma obtained from mice subjected to CLP (septic plasma) activated isolated cardiac myocytes as evidenced by (1) increased nuclear levels of nuclear factor-B (NF-B) and (2) their ability to promote PMN migration across endothelial cell monolayers. Pretreatment of septic plasma with an antibody against tumor necrosis factor-␣ (TNF-␣), but not interleukin-1␤ (IL-1␤), blunted the ability of septic plasma to activate the myocytes. However, septic plasma obtained from TNF-␣-deficient mice could still activate the myocytes; an effect attenuated by an antibody against IL-1␤. If the myocytes were pretreated with a proteasome inhibitor (MG 132) to prevent NF-B activation, the myocyte-induced PMN transendothelial migration was compromised. The activated myocytes released platelet-activating factor (PAF), and myocyte-induced PMN migration was abrogated by a PAF receptor antagonist (WEB 2086

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“…Vascular smooth muscle of splanchnic arterioles contracts intensely in response to stretch (inducing a sudden elevation in portal pressure). The intense dilation of arterioles observed in chronic portal hypertension likely reflects the accumulation of vasodilators [e.g., increased nitric oxide (NO) production, increased blood levels of glucagons] that overcome intrinsic myogenic vasoconstrictor factors (8).…”

Section: Structure and Function Of The Splanchnic Vasculaturementioning

confidence: 99%

Anatomy and Vascular Biology of the Cells in the Portal Circulation

Pinzani

Vizzutti

Clinical Gastroenterology

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Microcirculation of the intestinal mucosa

Cited by 35 publications

References 274 publications

Hemodynamic Changes Associated with Strangulation Obstruction in Cats

Hemodynamic Changes Associated with Strangulation Obstruction in Cats

Cardiac Myocytes Activated by Septic Plasma Promote Neutrophil Transendothelial Migration

Anatomy and Vascular Biology of the Cells in the Portal Circulation

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