Gastroduodenal Vein Research Articles

Description of the arterial supply and venous drainage of the abdominal viscera in the puma (Puma concolor) (Linnaeus, 1771).

Detailed descriptions of the abdominal vasculature have not been reported on Puma concolor; thus, herein we provided a thorough description. Our findings include the following: a celiac artery branching into the hepatic and gastrolienal arteries, and this latter further branched into the left gastric, the left gastroepiploic, the lienal and three more arteries that supplied the greater omentum. We also found a cystic artery that derived from the right gastroduodenal artery; a right gastric artery that derived from the right hepatic artery; and an antimesenteric ileal artery that derived from the lateral cecal artery. The right gastric vein did not form the gastroduodenal vein as in other species, but it drained directly into the portal vein. Also, a middle pancreaticoduodenal vein was identified as the last branch of the cranial mesenteric vein. Finally, the left caudal phrenic vein drained into the left renal vein. The abdominal blood supply described herein corresponds to a single individual; further reviews are desirable to corroborate our observations and to detect potential intraspecific anatomical variations.

Early partial portal venous contrast enhancement in canine CT‐Angiography

Early partial portal vein contrast enhancement (EPoVE) during the late arterial phase is seen in CT angiography of dogs. Previously, it has been a finding attributed to arterioportal vascular anomalies. However, EPoVE may be a normal feature of venous return from abdominal organs. This prospective, descriptive study investigated the origin of EPoVE using four-dimensional CT (4D-CT). Sixteen dogs undergoing 4D-CT for disease of the cranial abdomen were prospectively collected. Regions of interest were placed in the hepatic artery (HA), gastroduodenal vein (GV), extrahepatic portal vein (EHPV) cranial and caudal to the GV, and splenic vein (SV) caudal to its EHPV entry. Times to earliest, partial, full, and maximal vascular enhancement were recorded. A mixed model analysis of variance was used to compare time-to-contrast enhancement between vessels. The number, origin, and time of EPoVE were recorded if visible. A total of 24 EPoVE areas were observed in all dogs. Most dogs had either one (10/16) or two (5/16) areas of EPoVE. The origin of EPoVE was identified in 14 of 24 areas: the GV in five areas, cranial mesenteric vein in four areas, pancreatic branch of SV in three areas, and SV in two areas. The time-to-contrast-enhancement was significantly different for the individual veins compared to the HA. EPoVE during the late arterial phase is a common phenomenon of early portal venous drainage of abdominal organs; it should not be interpreted as pathognomonic for arterioportal vascular anomalies, which should be diagnosed based on additional criteria.

<b>Microvascularization of the Pancreas in Larval and Adult </b><i><b>Xenopus laevis</b></i><b> – Histomorphology and Scanning Electron Microscopy of Vascular Corrosion </b><b>Casts </b>

The microvascularization of the pancreas of larval and adult South African Clawed Toads Xenopus laevis, was studied by scanning electron microscopy of vascular corrosion casts and light microscopy of paraplast embedded Goldner-stained serial tissue sections. We showed that branches of left and right gastric artery, hepatic artery and anterior intestinal artery, namely anterior pancreatic, anterior middle pancreatic, posterior middle pancreatic and caudal pancreatic arteries supply and pancreatic veins drain the adult pancreas into hepatic portal vein, anterior and middle gastric vein, gastroduodenal vein, and anterior duodenal vein. In premetamorphosis the pancreas showed a dense but immature vascular bed with signs of ongoing sprouting and non-sprouting angiogenesis (=intussusceptive microvascular growth; IMG). During metamorphic climax the pancreas shrinked dramatically paralleled by vascular regression.The larval pancreas had an underdeveloped ductal system which in the course of pancreas remodeling during metamorphic climax developed into a complex ductal system. In adult Xenopus laevis the pancreas showed intralobular islets of Langerhans only and an insuloacinar portal vessel system as described sofar in reptiles, birds and mammals. Islets in Xenopus located superficially and within deeper regions and emitted both insulo-acinar portal vessels and insulo-venous efferent vessels. Intrainsular microvascular patterns found suggest that in Xenopus islets blood flows first to β-cells and subsequently to the other endocrine cells present in the endocrine pancreas. Key words: Xenopus, pancreas, microvascularization, vascular casts, histomorphology

Veia porta do preá (Galea spixii Wagler, 1831)

O preá é um roedor pertencente à família Caviidae. O objetivo deste artigo, considerando a inexistência de informações na literatura, é descrever a origem da veia porta no preá. Foram utilizados 10 espécimes que vieram a óbito por causas naturais no Centro de Multiplicação de Animais Silvestres, Mossoró-RN, Brasil. Esses animais foram incisados medianamente e a veia porta foi canulada inicialmente em sentido cranial e depois em sentido caudal para injeção de solução de látex corado de azul. Em seguida, os animais foram fixados em solução de formol a 10% e dissecados após 72 h. As tributárias da veia porta no preá foram as veias gastrolienal e gastroduodenal, assim como as veias mesentéricas cranial e caudal.

Computed tomography findings in portal vein aneurysm of dogs

In this retrospective study, the appearances of extrahepatic and intrahepatic portal vein aneurysms (PVAs) in dogs were evaluated using multidetector computed tomography (CT). Data from 3060 dogs that underwent abdominal CT were reviewed for focal portal vein dilatation. PVAs were detected in 15/3060 (0.49%) dogs. The bodyweights of dogs with PVAs were significantly higher than the bodyweights of dogs without aneurysms (P=0.0001). Male sex was also significantly associated with PVAs (OR=6.23). Boxers were predisposed to the development of PVA (OR=11.88). Extrahepatic PVAs were always located in the portal vein at the level of the gastroduodenal vein insertion and were saccular in 10/15 dogs and fusiform in 5/15 dogs. One dog had an additional intrahepatic aneurysm of the umbilical part of the left intrahepatic portal branch. No dogs had clinical signs related to the PVA(s), although one dog developed a portal vein thrombosis in the site of the aneurysm.

Contrast-enhanced computed tomography angiography and volume-rendered imaging for evaluation of cellophane banding in a dog with extrahepatic portosystemic shunt

A 4-year-old, 1.8 kg, male, castrated Maltese was presented for evaluation of urolithiasis. Urinary calculi were composed of ammonium biurate. Preprandial and postprandial bile acids were 44.2 and 187.3 micromol/l, respectively (reference ranges 0-10 and 0-20 micromol/l, respectively). Single-phase contrast-enhanced computed tomography angiography (CTA) with volume-rendered imaging (VRI) was obtained. VRI revealed a portocaval shunt originating just cranial to a tributary of the gastroduodenal vein and draining into the caudal vena cava at the level of the epiploic foramen. CTA revealed a 3.66 mm-diameter shunt measured at the level of the termination of the shunt and a 3.79 mm-diameter portal vein measured at the level between the origin of the shunt and the porta of the liver. Surgery was performed using cellophane banding without attenuation. Follow-up single-phase CTA with VRI was obtained 10 weeks after surgery. VRI revealed no evidence of portosystemic communication on the level of a cellophane band and caudal to the cellophane band. CTA demonstrated an increased portal vein diameter (3.79-5.27 mm) measured at the level between the origin of the shunt and the porta of the liver. Preprandial and postprandial bile acids were 25 and 12.5 micromol/l, respectively (aforementioned respective reference ranges), 3 months post-surgery. No problems were evident at 6 months.

A macroscopical investigation of the portal veins of the Van cat

In this study veins that constituted the portal vein were investigated in eight adult Van cats. The portal vein of the Van cat was composed of five peripheral branches which supplied the abdominal organs and two intrahepatic branches at the hepatic porta. The peripheral branches were cranial mesenteric, splenic, gastroduodenal, right gastric and cystic veins. The cranial mesenteric vein was the largest vessel that joined to the portal vein, and was constituted by the caudal pancreaticoduodenal, ileal, ileocolic and jejunal veins. The splenic vein was formed by the left gastric, left gastroepiploic, pancreatic and short gastric veins. The gastroduodenal vein was formed by the cranial pancreaticoduodenal and right gastroepiploic veins. The right gastric vein separately joined to the portal vein. The caudal mesenteric vein joined to the portal vein either alone or by a common trunk receiving either the caudal pancreaticoduodenal vein or ileocolic vein. The caudal mesenteric vein also opened rarely into the splenic vein. Intrahepatic branches were the right branch which gave off the ramus caudatus and ramus dexter lateralis, and the left branch which gave off the ramus dexter medialis, ramus quadratus, ramus sinister lateralis and ramus sinister medialis.

Dual-phase CT angiography of the normal canine portal and hepatic vasculature.

A dual-phase computed tomography (CT) angiographic technique was developed to image the hepatic and portal vascular systems using a nonselective peripheral injection of contrast medium. The arterial phase of the dual-phase scan imaged the hepatic arteries and veins, and the portal phase imaged the portal vein as well as its tributaries and branches. There were three steps involved in acquiring the dual-phase scan: a survey helical scan for orientation, a dynamic scan for timing, and finally the dual-phase helical scan. Five normal dogs were imaged using a helical scan technique. The timing of the arterial and portal phases of the scan was calculated using time vs. attenuation graphs generated from a dynamic scan. The median time of appearance of contrast medium in the cranial abdominal aorta was 8.6 s and the median time of appearance of contrast medium in the hepatic artery occurred 0.4 s later. The median time of peak enhancement in the cranial abdominal aorta was 12.0 s. The median time of appearance of contrast medium in the portal vein was 14.6 s and median time of peak enhancement was 33.0 s. The dual-phase scans provided excellent vascular opacification. The hepatic arteries, hepatic veins, cranial and caudal mesenteric veins, splenic vein, gastroduodenal vein, and portal vein branches were all consistently well defined. Dual-phase CT angiography is a minimally invasive technique which provides an excellent three-dimensional representation of portal and hepatic vascular anatomy.

Ultrasonographic assessment of hemodynamic changes in the portal vein during surgical attenuation of congenital extrahepatic portosystemic shunts in dogs.

To determine portal hemodynamic changes associated with surgical shunt ligation and establish ultrasonographic criteria for determining the optimal degree of shunt narrowing and predicting outcome. Case series. 17 dogs, each with a single congenital extrahepatic portosystemic shunt. Pre- and postligation flow velocities and flow directions were determined by Doppler ultrasonography intraoperatively in the shunt and in the portal vein cranial and caudal to the shunt origin. Outcome was evaluated 1 month after surgery by measuring blood ammonia concentration and performing abdominal ultrasonography. Hepatofugal flow was detected in 9 of 17 dogs before shunt attenuation in the portal segment that was between the shunt origin and the entering point of the gastroduodenal vein. If hepatofugal flow became hepatopetal after shunt ligation, hyperammonemia resolved. Hepatofugal portal flow was caused by blood that flowed from the gastroduodenal vein toward the shunt. Shunt attenuation converted hepatofugal flow to hepatopetal in the shunt in 12 of 17 dogs. Chronic portal hypertension developed or perioperative death occurred when the portal congestion index caudal to the shunt origin increased by > 3.6 times. After hepatopetal flow in the cranial portal vein and the shunt is established, further shunt narrowing is contraindicated. Increase of the portal congestion index caudal to the shunt > 3.5 times should be avoided. Poor outcome because of severe hypoplasia of the portal branches can be expected if the flow direction remains hepatofugal after shunt occlusion cranial to the shunt origin.

Repeated intraportal hepatocyte transplantation in analbuminemic rats

The optimal site for implantation of isolated hepatocytes has not been established. We have developed a novel technique which allows repeated infusion of hepatocytes into the portal system via an indwelling catheter. Seven Nagase Analbuminemic rats (NAR) underwent single intraportal infusion of 2 × 10 7 isolated normal albumin-producing rat hepatocytes. Another seven NAR rats underwent placement of indwelling catheters into the portal venous system via the gastroduodenal vein. Each of them received six batches of 5 × 10 6 normal albumin producing hepatocytes. Seven control NAR rats were infused repeatedly (intraportally) with saline only. Plasma albumin (ELISA) showed significant increase in experimental animals and was more pronounced ( p < 0.05) in rats transplanted repeatedly than in those given a single dose of cells. Immunohistochemical staining of the liver sections confirmed the presence of transplanted albumin producing hepatocytes. Rats transplanted with a single large batch of isolated hepatocytes showed liver tissue damage, whereas those subjected to repeated cell infusions had normal liver histology. We have developed a novel intraportal transplantation method which allows successful engraftment of a large number of isolated hepatocytes.

Repeated intraportal hepatocyte transplantation in analbuminemic rats.

The optimal site for implantation of isolated hepatocytes has not been established. We have developed a novel technique which allows repeated infusion of hepatocytes into the portal system via an indwelling catheter. Seven Nagase Analbuminemic rats (NAR) underwent single intraportal infusion of 2 x 10(7) isolated normal albumin-producing rat hepatocytes. Another seven NAR rats underwent placement of indwelling catheters into the portal venous system via the gastroduodenal vein. Each of them received six batches of 5 x 10(6) normal albumin producing hepatocytes. Seven control NAR rats were infused repeatedly (intraportally) with saline only. Plasma albumin (ELISA) showed significant increase in experimental animals and was more pronounced (p < 0.05) in rats transplanted repeatedly than in those given a single dose of cells. Immunohistochemical staining of the liver sections confirmed the presence of transplanted albumin producing hepatocytes. Rats transplanted with a single large batch of isolated hepatocytes showed liver tissue damage, whereas those subjected to repeated cell infusions had normal liver histology. We have developed a novel intraportal transplantation method which allows successful engraftment of a large number of isolated hepatocytes.

Gross Anatomy of the Canine Portal Vein

The gross anatomy of the portal vein of 21 dogs was studied by venous portography, corrosion casting, and gross dissection. The portal vein in all specimens originated by confluence of the cranial and caudal mesenteric veins. Its large tributaries were the splenic and gastroduodenal veins, which entered the portal vein between its origin and the hepatic porta. At the hepatic porta, the portal vein divided into a short right branch and a larger left branch. The right branch ramified in the caudate process of the caudate lobe and in the right lateral lobe of the liver. The left branch was essentially the continuation of the portal vein from which successive branches passed to each of the remaining lobes of the liver and the papillary process of the caudate lobe.

Selective intraportal hepatocyte transplantation in analbuminemic and Gunn rats.

Although significant progress has been achieved in isolated hepatocyte transplantation, the optimal site of cell implantation has not yet been determined. We have developed a novel experimental method of intraportal hepatocyte transplantation that allows easy assessment of the morphology and function of transplanted hepatocytes. Donor hepatocytes were harvested from Sprague-Dawley rats by in situ EDTA/collagenase perfusion. Fifteen recipient Nagase analbuminemic rats (NAR) underwent cannulation of the gastroduodenal vein under ether anesthesia. Either the posterior or anterior liver lobes were selectively infused with cells by occluding the portal venous supply of the nontransplanted liver lobes. Normal donor hepatocytes (2 x 10(7)) suspended in normal saline were infused over 1 min (4 ml). Recipients were treated with cyclosporine for the duration of the experiment. Plasma albumin levels were determined by ELISA, before and at various intervals after transplantation. In NAR rats transplanted with normal hepatocytes, there was a significant (P < 0.003) and sustained (12 weeks) increase in plasma albumin levels. Control NAR rats transplanted with NAR hepatocytes (n = 8) showed no significant changes in plasma albumin levels. Similarly, normal Wistar hepatocytes were infused intraportally into the posterior lobes of Gunn rats (n = 4), which lack the ability to conjugate bilirubin. Pre- and posttransplantation bile was collected following bile duct cannulation. Bile analysis by HPLC, demonstrated a significant (P = 0.04) increase in the level of bilirubin conjugates following transplantation and a corresponding decrease in total serum bilirubin (P = 0.04). Our experimental data demonstrate that direct selective intraportal infusion of hepatocytes is an effective technique of hepatocyte transplantation in the rat.

Diversion of the gastroduodenal vein: an in situ model of systemic insulin drainage

A technique of diversion of the gastroduodenal vein in a canine model is described to compare long-term metabolic effects of systemic versus portal pancreatic endocrine drainage. The vein was transected at its entrance into the portal vein and either diverted to the inferior vena cava (systemic group) or reanastomosed to the portal vein (portal group). All remaining venous drainage of the pancreas was interrupted. An additional group of animals underwent laparotomy without manipulation of pancreatic vasculature (sham group). Fasting peripheral insulin and glucose values were determined 3 months postoperatively. Fasting insulin values were significantly higher in the systemic group (mean 10.7 ± 1.06 U/ml) than in the portal (5.8 ± 0.70, P = 0.002) and sham (6.4 ± 0.68, P = 0.01) groups. Fasting glucose values were not significantly different in the three groups. At sacrifice, venous thrombosis was noted in one systemically diverted dog (6.7%). All other anastomoses were patent. No significant collateralization was apparent in any group. No significant complications were noted. This procedure simulates the hormonal milieu created by heterotopic pancreatic transplantation while preserving pancreatic innervation and exocrine function, and serves as an excellent model for investigating the effects of systemic hyperinsulinemia on protein, carbohydrate, and lipid metabolism.

Splenic and gastro-duodenal vein occlusion—influence on the pancreatic gland and on the outcome of experimental pancreatitis

The observation that splenic vein thrombosis results in pancreatic changes similar to haemorrhagic pancreatitis initiated the present investigation. The influence of splenic and/or gastroduodenal vein occlusion on the pancreatic gland was evaluated and compared to that obtained after induction of experimental pancreatitis (EP). The influence of splenic vein occlusion on EP was also investigated. An approximately 4-fold increase in serum amylase activity was obtained after simultaneous ligation of the splenic and gastroduodenal veins. This increase was comparable to that obtained after EP. On the other hand, amylase activity in ascites was considerably lower after vein occlusion than after EP. Splenic vein occlusion in rats with EP more moderately increased the amylase activity but did not influence mortality rate 24 h postoperatively. Venous thromboses were observed in all groups with occluded veins but not in rats with EP. Vein occlusion alone did not result in fat necroses. Although occlusion of the splenic and gastroduodenal veins results in macromorphologic and biochemical changes resembling those in EP, the microscopic findings of the two conditions differ. Thus, the results do not support the hypothesis that pancreatic vein thromboses are of etiologic significance for the development of acute haemorrhagic pancreatitis.

Canine pancreaticoduodenal autotransplantation: a preparation for human pancreatic transplantation.

This canine pancreaticodunodenal autotransplantation model includes virtually the entire pancreas attached to a duodenal cuff (second portion). The blood supply is based on the superior pancreaticoduodenal artery and the venous outflow on the gastroduodenal vein. The vascular anastomoses are end-to-side to the external iliac artery and vein. Exocrine drainage is channeled through the bladder from the transplanted duodenum. This technique closely resembles whole-organ pancreas transplant in humans with a cystoduodenostomy. The bowel reconstruction consists of a Billroth I gastroduodenostomy and a cholecystoduodenostomy. The entire procedure is relatively free of major complications and may be performed in less than 4 hours.

Control of traumatic liver hemorrhage in the cirrhotic rat by intraportal infusion of norepinephrine.

The effect of intraportal infusion of norepinephrine (NE) on primary hemostasis in the cirrhotic rat was investigated at standardized liver trauma. Cirrhosis was induced by simultaneous administration of increasing amounts of carbontetrachloride (CCl4) and phenobarbitone. Infusion of norepinephrine took place after cannulation of the gastroduodenal vein. Intraportal infusion of NE resulted in a significant increase in arterial blood pressure and portal pressure in all animals. No difference was observed between cirrhotic and control rats. Cirrhotic animals bled longer and more profusely as compared with the controls. Infusion of NE resulted in significant decrease in bleeding time and blood loss. NE did not affect hematocrit, hemoglobin, platelet, or white cell count. Platelet aggregation was not influenced by the compound. In conclusion, intraportal infusion of NE proved effective in decreasing hemorrhage at liver trauma in cirrhotic rats.

Bilateral carotid occlusion and the sympathetic regulation of insulin secretion

After a 2-min bilateral carotid arterial occlusion (BCO) in puppies, a centrally originating, sympathetic discharge takes place which increases heart rate and blood pressure. We examined the specificity of this sympathetic neural outflow by determining whether it also caused a direct neurally mediated inhibition of insulin release from the pancreas. The effects of this BCO on portal venous insulin concentrations, as well as on heart rate and blood pressure, were examined during i.v. glucose infusions of 0 (saline), 5 and 15 mg/kg · min 1. To determine changes in splanchnic blood flow and to more closely estimate pancreatic insulin secretion rates, a major vein draining the pancreas, the gastroduodenal, was catheterized. Blood flows and the amount of insulin transversing this vein per min (insulin flow rate) were followed before, during and after BCO. BCO decreased portal vein insulin concentrations during i.v. glucose infusions of 5 and 15 mg/kg · min 1, but not when saline was infused. Since bilateral splanchnicotomy altered this result little and since BCO increased blood flow and the insulin flow rate in the gastroduodenal vein, it appears that the lower portal venous insulin concentrations during BCO are secondary, not to sympathetically induced decrease in insulin secretion rates but, to dilution of pancreatic effluent blood. We conclude that while BCO causes appropriate changes in heart rate and blood pressure, this central stimulus to the sympathetic system does not provide a direct neuroendocrine reflex change in insulin secretion. BCO alters portal venous insulin concentration indirectly, and the alteration depends on the plasma glucose concentration and an enhancement in the splanchnic blood flow.

Effects of portacaval shunt on the rat stomach

In portacaval-shunted rats, basal but not pentagastrin-stimulated acid secretion was higher than in sham-operated controls. The basal serum gastrin concentration was unchanged and the postprandial serum gastrin concentration lowered following portacaval shunt. Thus, gastrin is not responsible for the elevated basal acid secretion. The present study provides evidence that there is no trophic effect on the oxyntic mucosa as a whole and that there is no change in parietal cell-associated gastrin receptors after portacaval shunting. Interestingly, however, endocrine cells in the oxyntic mucosa (the histamine-containing ECL cells) proliferated greatly and the pentagastrin- and cholecystokinin octapeptide-induced activation of the histamine-forming enzyme, histidine decarboxylase, in these cells was much greater than in control rats. Analysis of the dose-response curves for the enzyme-activating effect of pentagastrin and cholecystokinin-octapeptide indicated that the D50 values for these two stimulants were not altered by shunting but that the maximal enzyme activation was greatly elevated. The enhanced enzyme activation can be partly, but not fully, explained by the fact that the ECL cells were increased in number. The enhanced response following portacaval shunt probably reflects also an increased number of gastrin receptors per ECL cell. The effect of portacaval shunting on gastric ECL cells can perhaps be explained by impaired degradation in the liver of intestinal substance(s) exerting a highly specific trophic effect on the ECL cells or, alternatively, causing an enrichment of gastrin receptors on these cells, thereby making them more sensitive to the trophic effect of gastrin. The ECL cell hyperplasia is manifest about 4 weeks after the shunting. A modified procedure for portacaval shunting which left the gastroduodenal vein (otherwise ligated) drained to the liver produced the same trophic effect as conventional portacaval shunt, suggesting an intestinal rather than gastroduodenal origin of the agent(s) responsible for the trophic action.

Origin and distrubition of portal blood in the cat and the rabbit.

AbstractThe portal vein in the rabbit is formed by union of the gastrosplenic vein, which extends caudally and to the right, and the relatively larger and cranially directed mesenteric vein, formed from cranial and caudal mesenteric and caudal pancreaticoduodenal tributaries. The gastroduodenal vein, which receives blood from the distal pylorus, greater omentum, pancreas and duodenum, joins the rabbit portal vein opposite the branch to the caudate lobe. In the cat, the portal vein is formed by the junction of the gastrosplenic, which is directed transversely or cranially, and the mesenteric, and receives two main tributaries: the gastroduodenal, which is the main vein from the stomach, and the cranial pancreaticoduodenal.When 131I‐rose bengal was injected into the spleen of conscious standing cats and entered the portal vein in the gastrosplenic, it was distributed preferentially to the right branch and the left lateral ramus of the left branch. In the rabbit, there was no evidence for preferential distribution of splenic blood, but blood from the cranial mesenteric vein was distributed preferentially to the right and caudate branches and that from the caudal mesenteric to the caudate. This distribution was affected by the entry of blood in the gastrosplenic vein. Although statistically significant differences did occur in the intrahepatic distribution of blood derived from the portal tributaries, the absolute differences were small.