Bile Oleic Acid Research Articles

Effects of micellar oleic acid on canine jejunal blood flow and neurotensin release.

The purpose of this study was to evaluate the role of neurotensin in the local regulation of the lipid-induced jejunal hyperemia. Total blood flow and the arteriovenous hormone concentration difference were measured in isolated jejunal loops of anesthetized dogs with either saline, bile (10% in normal saline), oleic acid (40 mM in normal saline), or oleic acid and bile in the lumen. The bile-oleic acid mixture produced a sustained increase (+25 +/- 3%) in jejunal blood flow, whereas neurotensin release reached a maximum (1.14 +/- 0.34 pmol X min-1 X 100 g-1) 2 min after initiation of the response and then returned to control. Venous neurotensin concentrations also reached a maximum (51 +/- 17 pmol/l) at 2 min. There were no significant changes in either blood flow or neurotensin release in response to the other test solutions. Intra-arterial infusion of neurotensin did not significantly decrease jejunal vascular resistance (-12 +/- 3%) until venous concentrations of 478 +/- 101 pmol/l were attained. It seems unlikely, then, that neurotensin plays any role in the regulation of the lipid-induced jejunal hyperemia.

Vasoactive intestinal polypeptide, cholecystokinin, glucagon, and bile-oleate-induced jejunal hyperemia.

The purpose of this study was to evaluate the roles of vasoactive intestinal polypeptide (VIP), cholecystokinin (CCK), and glucagon in the local regulation of the lipid-induced intestinal hyperemia. Total blood flow and the arteriovenous hormone concentration gradient were measured in isolated jejunal loops of anesthetized dogs with either saline, bile (10% in normal saline), oleic acid (40 mM in normal saline), or oleic acid and bile in the lumen. The bile-oleic acid mixture increased both blood flow (+21 +/- 7%) and VIP release (+118 +/- 7%), while CCK release was considerably less. There was a transient rise in glucagonlike immunoreactivity but no change in pancreatic glucagon release. Neither bile nor oleic acid alone altered either local blood flow or hormone release. Infusion of VIP into the arterial circulation of the jejunum significantly reduced vascular resistance (-11 +/- 4%) but at a dose (150 ng . min-1 X 100 g-1) 10 times that released in response to the bile-oleic acid mixture. This study indicates that oleic acid increases both blood flow and intestinal hormone production only when present in the lumen in micellar form and suggests that VIP could play a role in the jejunal vascular response to fat.

Permeability of intestinal capillaries: effects of fat absorption and gastrointestinal hormones.

The purpose of this study was to determine whether the postprandial increase of intestinal lymphatic protein flux is due to an increased capillary permeability. Intestinal lymph flow and lymph (L) and plasma (P) protein concentrations were measured at various venous pressures under control conditions, after cream feeding, and during intraluminal perfusion with a bile-oleic acid solution. The osmotic reflection coefficient (sigma d), a measure of capillary permeability that is independent of surface area, was estimated under all conditions, assuming sigma d = 1 - L/P at high capillary filtration rates. The results acquired indicate that cream feeding and intraluminal perfusion with bile-oleic acid significantly increases intestinal capillary permeability. Pretreatment with indomethacin and antihistamines did not alter the permeability increase induced by intraluminal bile-oleic acid. Intra-arterial infusion of cholecystokinin and secretin did not increase intestinal capillary permeability. These studies indicate that the postprandial increase in intestinal lymphatic protein flux is due at least in part, to an increase in capillary permeability. Cholecystokinin, secretin, histamine, and prostaglandins do not appear to mediate the increased intestinal capillary permeability during fat absorption.

Effect of atropine on bile-oleic acid-induced alterations in dog jejunal hemodynamics, oxygenation, and net transmucosal water movement

The effects of intraluminal bile-oleic acid on jejunal blood flow, oxygen uptake, net transmucosal fluid flux, and mucosal infrastructure were studied in isolated autoperfused jejunal segments before and after cholinergic blockage with atropine. Bile-oleic acid increased jejunal blood flow (40%), decreased oxygen extraction (24%), and increased oxygen uptake (15%). Cholinergic blockade did not abolish the bile-oleic acid-induced changes in these parameters. Bile-oleic acid induced net fluid secretion or significantly depressed absorption. Cholinergic blockade reversed net volume secretion to absorption or attenuated the depression of absorption produced by bile-oleic acid. Ultrastructural analyses of tissue samples taken during bile-oleic acid-induced secretion indicate major structural damage to the mucosal membrane which was not affected by cholingergic blockade. The physiologic and ultrastructural data acquired in this study suggest that: (a) the effects of bile-oleic acid on net transmucosal water movement are reversed by cholinergic blockade and (b) the hyperemia, increased oxygen consumption, and morphologic alterations induced by bile-oleic acid are not affected by cholinergic blockade. The results of this study may have important implications in steatorrheal diseases in that, atropine may alleviate the diarrhea induced by the presence of excess lipid in chyme without compromising the intestinal hyperemia and enhanced oxygen delivery required to meet the increased metabolic demands during nutrient absorption.