Jejunal Vein Research Articles

Air in the portal vein: sonographic and Doppler manifestations.

Three patients with portal venous gas (one with radiographic and computed tomographic findings) had similar sonographic and Doppler patterns in the portal vein (PV). These patterns consisted of hyperechogenic foci moving within the lumen of the PV, producing sharp bidirectional spikes superimposed on the usual Doppler tracing of the PV. An injection of 0.25-0.50 cm3 of air, oxygen, nitrogen, and carbon dioxide into the jejunal vein of nine dogs yielded identical portal venous sonographic and Doppler patterns. In addition, the liver parenchyma of the dogs became hyperechogenic after the injection of gas. Gas in the PV is accompanied by the following signs: echogenic, moving foci within the lumen of the PV; sharp spikes on Doppler spectral display; and hyperechogenic foci within the liver parenchyma.

Effect of left hepatic vein ligation on hepatic circulation, function, and microanatomy in dogs

SUMMARY Eighteen healthy dogs were allotted to 3 groups (n = 6 dogs each). All dogs were evaluated at the beginning of the study by complete physical examination; total and differential WBC counts; serum biochemical analysis (alanine transaminase and alkaline phosphatase activities and bilirubin and albumin concentrations); sulfobromophthalein excretion, ammonia tolerance, and glucagon response testing; portal and intraparenchymal pressure determinations; operative mesenteric portography; and histologic assessment of hepatic biopsy specimens. The left hepatic vein was ligated completely in dogs of groups 1 and 2. Group-3 (control) dogs had a ligature placed loosely around the left hepatic vein. Dogs of groups 1 and 3 were reevaluated 24 hours after surgery by use of the aforementioned hematologic and biochemical tests. Group-1 dogs were reevaluated by use of portal and intraparenchymal pressure determinations, jejunal vein portography, and complete necropsy at 48 hours after surgery. At 4 weeks after surgery, dogs of groups 2 and 3 were reevaluated by use of all aforementioned tests. Results indicated transient hepatic congestion, which resolved by the fourth postoperative week. Longstanding effect on hepatic structure, circulation, or function was not found. We concluded that left hepatic vein ligation in clinically normal dogs does not cause severe or permanent liver damage.

スルファジメトキシンの腸管吸収に及ぼす血清蛋白結合の置換効果

The displacing effect of serum protein binding on the intestinal absorption of sulfadimethoxine (SDM) in rabbits was examined by using N4-acetylsulfadimethoxine (N4-AcSDM), a major metabolite of SDM, as a displacing drug. N4-AcSDM markedly decreased the in vitro serum protein binding of SDM, while many drugs including phenylbutazone and salicylic acid did not display such a marked decreasing-effect. The intravenous administration of N4-AcSDM clearly decreased the in situ intestinal absorption of SDM. As expected, the intravenously administered N4-AcSDM enhanced the serum concentration of unbound SDM in the common jejunal vein. However, the intravenously administered N4-AcSDM caused no change in the transfer of SDM across the intestinal membrane. These results indicate that the displacement of serum protein binding can become one of factors decreasing the intestinal absorption of SDM.

Absorption of Etoposide (VP-16-213) from the Small Intestine of the Rat. The Potential Role of Mucus as an Absorption Rate Limiting Barrier.

The absorption of etoposide (VP-16-213) was investigated in a perfused intestinal loop. The absorbed amount of drug was determined by collecting the blood draining the loop via cannulation of the efferent jejunal vein. The absorption rate of VP-16-213 strongly depended on the composition of the perfusion medium. The addition of taurocholate to an aqueous etoposide solution enhanced the absorption rate. When N-acetylcysteine was added to an aqueous solution, the absorption rate dropped significantly.

The effect of catecholamines on intestinal glucose and oxygen uptake in the dog.

Using the anaesthetized dog, continuous recording was made of the oxygen and glucose contents of the artery and the vein draining the upper jejunum. Flow was also measured and results expressed as differences in oxygen and glucose between the aorta and the jejunal vein (a-v), also as oxygen consumption and glucose uptake. Resting glucose uptake was greater than could be accounted for on the basis of oxidation. When adrenaline (1 microgram/kg. min) or noradrenaline (2 micrograms/kg. min) was infused intravenously, oxygen uptake rose by about 50% whereas glucose uptake rose by 300-500%; moreover, the rise in glucose uptake was apparent before the rise in oxygen uptake. The beta-blocking agent, propranolol (0 X 5 mg/kg. min) had no effect on oxygen uptake but caused a three-fold rise in glucose uptake. Subsequently infusion of adrenaline had no effect on oxygen uptake and no effect on glucose uptake. However, on stopping the infusion there was a marked drop in glucose uptake, which was not maintained. It is suggested that the effects of catecholamines may be due to altered arterial blood glucose levels and that the jejunum may play a role in glucose homeostasis which requires the action of beta receptors.

Regional differences in electrical and mechanical properties of guinea-pig mesenteric vessels.

Regional differences in electrical and mechanical properties of guinea-pig mesenteric vessels were investigated using microelectrode and isometric tension recording methods. The amplitude of membrane potentials differed according to region and in the following order; branch of jejunal artery (BJA) > cranial mesenteric artery (CMA) > jejunal artery (JA) greater than or equal to jejunal vein (JV) not equal to portal vein (PV). There were also regional differences in the muscle membrane potential with various concentrations of [K]o or [Na]o, while no differences were observed with applications of various concentrations of [Ca]o or [Cl]o. ACh produced hyperpolarization of the muscle membrane in the CMA, JA and JV but not in the PV and BJA. Hyperpolarization in the JA mainly followed increase in the K-permeability, and a reversal potential for ACh was distributed at about -70mV. In the JV, the ACh-induced hyperpolarization accompanied tension development. Phenylephrine depolarized the muscle membranes of the CMA, JA and PV but not of the BJA and JV. Low concentrations of phenylephrine produced contractions with no depolarization of the membrane in the JA and CMA. Isoprenaline-induced hyperpolarization was smaller in arteries than in veins, and this hyperpolarization was reduced in amplitude with repeated applications. The ACh-induced relaxation and phenylephrine-induced contraction were larger in the JA than in the CMA. Regional differences of the muscle property in response to application of different agents were discussed in relation to the physiological roles.

Comparison of renal responses to 5% saline infusions into vena portae and vena cava in conscious dogs.

Indwelling catheters were placed in conscious dogs into the vena portae via a jejunal mesenteric vein several weeks prior to actual experiments. To compare a possible different response to different pathways of administration, 5% saline solution was infused either into vena portae or into vena cava at a rate of 0.05 ml/min/kg BW for 40 min. 1. Infusion of 5% sodium chloride into the vena portae, as well as into the vena cava caused a significant increase in urine flow, serum osmolality, sodium excretion rate and heat rate. The increase in urine flow was always due to an increase in osmolal clearance whereas free water clearance decreased consistantly. In some experiments plasma renin activity (PRA) was measured by radioimmunoassay. For both routes of administration the hypertonic saline infusion caused a decrease in PRA. At no time did any of these parameters display significant differences depending on route of application. 2. This means that the calculated differences between infused and excreted amounts of water and of sodium did not depend on the route of infusions. 3. A close relationship was found between initial urine osmolality and the length of the periods during which peak values of urine flow were observed.

Localization of mesenteric hyperemia during digestion in dogs.

For localization of the site of post-prandial mesenteric hyperemia, low-fat, low-protein food was placed in either the stomach, duodenum, or jejunum while blood flow was measured in the celiac artery, superior mesenteric artery (SMA), or jejunal vein of anesthetized dogs. Distribution of flow in the jejunal wall was also measured. After intragastric placement of food, celiac arterial flow increased within 5 min and remained elevated for 30-60 min; SMA flow increased within 30 min and stayed up for at least 3 h. Intra-duodenal infusion of digested food increased SMA flow but did not alter celiac flow or flow to an isolated jejunal segment. Placement of digested food into one jejunal segment increased flow to that segment did not affect flow was localized to the mucosal layer. These studies indicate that during digestion, blood flow increases in the mucosa of the intestine when exposed to chyme and is not changed in other areas of the gastrointestinal tract. Postprandial mesenteric hyperemia induced by low-fat, low-protein food is a local phenomenon.

Effect of Blood Glucose on Glucagon Secretion in Anesthetized Dogs

Insulin induced hypoglycemia and tolbutamide administration accompanied by much smaller falls in blood glucose were associated with increased pancreatic vein IRG concentrations in laparotomized dogs under barbiturate anesthesia. Hyperglycemia may have diminished pancreatic IRG release. Changes in IRG levels in peripheral and jejunal veins during hypoglycemia were unremarkable. In dogs, pancreatectomy was associated with no change in IRG release into a jejunal vein. Very small doses of glucagon administered intraportally during hyperglycemia were effective in promoting IRI release. It is concluded that a fall in blood glucose from the basal state is a stimulus, and hyperglycemia is an inhibitor, of pancreatic IRG release. It is possible that glucagon may act in the basal state to deliver repeated small pulses of glucose and insulin into the circulation.

Pathway and form of absorption of palmitic acid in the chicken

The ratio of lipid C14 in plasma of portal vein blood to that in plasma of systemic blood was determined in chickens killed 30, 60, 90, and 150 min after injection of palmitic acid-1-C14 into their gizzards. In other experiments other ratios were determined: (a) lipid C14 in plasma of pancreaticoduodenal blood to that in portal vein blood in chickens killed 30 min after fatty acid administration; and (b) lipid C14 in jejunal vein to that in portal vein plasma in birds killed 90 and 150 min after the injection. The results demonstrated that the portal system is a significant pathway for the absorption of fatty acid from the intestines of the bird, and that during the early period absorption from the duodenum takes place. Measurement of the C14 remaining in the digestive tract contents indicated that up to 96% of the injected labeled palmitic acid was absorbed in 90 min. Analysis of ultracentrifugally-separated plasma lipoproteins in blood drawn from the pancreaticoduodenal vein half an hour after introduction of the labeled palmitic acid into the gizzard revealed that the palmitic acid was absorbed from the intestines into the bloodstream principally as triglycerides in the very low density (Sf > 20) lipoproteins.