Superior Pancreaticoduodenal Vein Research Articles

Anterior Tributaries of the Portal Vein at the Superior Margin of the Pancreas: Is "Tunneling" Procedure Safe During Pancreatic Surgery?

It is widely believed that using the "tunneling" procedure during pancreatoduodenectomy is a safe maneuver because the anterior tributaries of the portal vein (PV) are absent or very rare. The head of the pancreas with the duodenum and the common bile duct (CBD) was obtained from 22 autopsy cases. Three colors of silicon-polymerase dyes were injected into the pancreatic artery, PV, and bile duct. The tributaries of the PV at the superior margin of the pancreas were studied. There was no anterior branch of the intrapancreatic PV. The anterior superior pancreaticoduodenal vein (ASPDV) gave a definite branch to the anterior aspect of the PV at the superior margin of the pancreas in 4 of 22 cases. When the posterior superior pancreaticoduodenal vein (PSPDV) was located in front of the CBD (5 of 22 cases), the ASPDV and PSPDV had a thick common trunk at the right side of the PV. In these 5 cases, no individual branch from the ASPDV was found at the anterior aspect of the PV. PV sometimes has a definite anterior tributary at the superior margin of the pancreas; this must be kept in mind to perform the tunneling procedure during pancreatic surgery.

Small peripancreatic veins: improved assessment in pancreatic cancer patients using thin-section pancreatic phase helical CT.

Recent studies have shown evaluation of the small peripancreatic veins to have potential in improving pancreatic cancer staging. This study was performed to determine the effectiveness of thin-section pancreatic phase helical CT images in visualizing these veins. Seventy-two patients (30 with pancreatic adenocarcinoma and 42 with no pancreatic disease) underwent dual-phase helical CT with thin-section pancreatic phase acquisition (40-70 sec after i.v. contrast initiation at 3 ml/sec) and hepatic phase acquisition (70-100 sec). Visualization (with diameter measurement) or nonvisualization of the posterior superior pancreaticoduodenal vein (PSPDV), anterior superior pancreaticoduodenal vein (ASPDV), and gastrocolic trunk was recorded for both acquisitions. We also correlated surgical tumor resectability with the status of the small peripancreatic veins. Visualization of peripancreatic veins was significantly better on pancreatic phase images than on hepatic phase images for both healthy individuals (PSPDV, 88% of the veins visualized on the pancreatic phase images versus 50% on the hepatic phase images; ASPDV, 93% on the pancreatic phase images versus 48% on the hepatic phase images; gastrocolic trunk, 98% on the pancreatic phase images versus 76% on the hepatic phase images) and for pancreatic cancer patients (PSPDV, 97% on the pancreatic phase images versus 57% on the hepatic phase images; ASPDV, 77% on the pancreatic phase images versus 43% on the hepatic phase images) (p < .05). The exception was the gastrocolic trunk in cancer patients (83% on the pancreatic phase images versus 77% on the hepatic phase images) (p > .05). In pancreatic cancer patients, 11 dilated peripancreatic veins were identified on the pancreatic phase images compared with six on the hepatic phase images. However, only one of the 11 dilated peripancreatic veins was in a patient with surgically resectable disease. In a dual-phase helical CT protocol, thin-section pancreatic phase images provided visualization of the small peripancreatic veins that was superior to hepatic phase images, providing further support for the use of this protocol in pancreatic cancer evaluation.

Venous drainage from the posterior aspect of the pancreatic head and duodenum.

Eighty-three pancreatic head and duodenum specimens, selected from 214 specimens, were dissected minutely to clarify the configurations of the posterior superior pancreaticoduodenal vein (PSPDv) with special reference to its topographical relationship to the common bile duct (CBD) and to whether an artery accompanied the PSPDv. The PSPDv frequently (71.1%) ran postero-inferior to the CBD without the accompaniment of an artery. Moreover, several tributaries draining the second and third portions of the duodenum sometimes (28.9%) joined together without arterial association and formed a stem, the so-called dorsal pancreatic vein. Variations of PSPDv were discussed in relation to the general vascular configuration of the small intestine.

Direct quantification of norepinephrine spillover and hormone output from the pancreas of the conscious dog.

To estimate pancreatic neural activity and to assess the potential role of the pancreatic nerves in the regulation of hormone secretion, the methodology necessary to quantify neurotransmitter spillover and hormone output in the conscious dog was developed. A femoral artery and the superior pancreaticoduodenal vein (SPDV) were chronically cannulated, and a flow probe was placed on the SPDV. Hormone output was calculated using the pancreatic arteriovenous concentration difference and the SPDV plasma flow. Basal glucose levels were 103 +/- 1 mg/dl; the pancreatic outputs of insulin, glucagon, and pancreatic polypeptide (PP, an index of parasympathetic neural activity) were 2,900 +/- 700 microU/min, 1,900 +/- 400 pg/min, and 9.3 +/- 4.6 ng/min, respectively. Pancreatic norepinephrine (NE) spillover was calculated similarly; however, pancreatic extraction of epinephrine was used as an index of NE extraction. Basal NE spillover was 3,600 +/- 700 pg/min, greatly exceeding that reported using anesthetized, laparotomized dogs. Intravenous glucose infusion increased plasma glucose to 146 +/- 13 mg/dl, increased insulin output approximately twofold, and suppressed glucagon output by approximately 50%. Hyperglycemia markedly reduced PP output. Hyperglycemia failed to influence pancreatic NE spillover. Insulin-induced hypoglycemia (36 +/- 2 mg/dl) completely suppressed insulin output and stimulated glucagon output (> 10-fold). Hypoglycemia increased NE spillover and PP output to 19,900 +/- 4,600 pg/min and 117 +/- 22 ng/min, respectively. We conclude that pancreatic neurotransmitter spillover in the basal state is much higher than previously appreciated and that neural signaling to the pancreas is responsive to physiological and pathophysiological changes in the metabolic state.

Peripancreatic veins on thin-section (3 mm) helical CT.

The purpose of this study was to evaluate thin-section helical CT for the frequency of visualization of the peripancreatic veins, the venous anatomy at the head of the pancreas, and variations of the venous anatomy. We performed 30-sec helical CT of the pancreas with one breath-hold and a 3-mm scanning collimation in 50 patients. The scan was started 60 sec after injection of an i.v. contrast medium at the rate of 2 ml/sec (total amount of contrast medium, 100 ml). The axial scan data were reviewed for the following information: the frequency of CT visualization of the peripancreatic veins (anterior superior pancreaticoduodenal vein, first jejunal vein, gastrocolic trunk, inferior mesenteric vein, left gastric vein, middle colic vein, posterior superior pancreaticoduodenal vein, right colic vein, and right gastroepipolic vein) and the anatomic relationship between the large portal venous system (portal vein, superior mesenteric vein, and splenic vein) and its tributaries. The frequency of visualization on CT of each vessel was gastrocolic trunk, 100%; right gastroepiploic vein, 100%; first jejunal vein, 96%; inferior mesenteric vein, 88%; left gastric vein, 80%; posterior superior pancreaticoduodenal vein, 72%; middle colic vein, 72%; right colic vein, 64%; and anterior superior pancreaticoduodenal vein, 50%. The anatomic relationship between the large portal venous system and its tributaries was as follows: The left gastric vein drained into the splenic vein-portal vein confluence (46%), into the splenic vein (32%), and into the portal vein (22%); the inferior mesenteric vein drained into the splenic vein (46%), the splenic vein-superior mesenteric vein confluence (25%), and the superior mesenteric vein (29%). The posterior superior pancreaticoduodenal vein drained into the portal vein above the splenic vein-portal vein confluence (mean distance, 0.3 cm). The middle colic vein, gastrocolic trunk, and first jejunal vein drained into the superior mesenteric vein below the splenic vein-portal vein confluence (mean distances of 2.4 cm, 3.0 cm, and 3.7 cm, respectively). Thin-section helical CT scans provide good visualization of the peripancreatic veins.

Carcinoma of the head of the pancreas: evaluation of the pancreaticoduodenal veins with dynamic CT--potential for improved accuracy in staging.

To determine if detection of abnormal dilatation of pancreaticoduodenal veins can improve the accuracy of computed tomographic (CT) staging of pancreatic adenocarcinoma. CT scans obtained during bolus administration of contrast material in 86 patients (aged 34-85 years) with pancreatic head carcinoma were reviewed. The diameter of the small veins that surround the head of the pancreas was measured (normal diameter of gastrocolic trunk, < or = 7 mm; of anterior superior pancreaticoduodenal vein, < or = 4 mm; of posterior superior pancreaticoduodenal vein, < or = 4 mm). Twenty-nine abnormally dilated peripancreatic veins were identified in 22 patients. Twenty-two of these dilated veins were in 16 patients with other CT criteria of tumor unresectability; seven dilated veins were in six patients with tumors deemed resectable at CT. All tumors in these latter six patients were unresectable at surgery. Although dilatation of these small peripancreatic veins without other CT criteria of tumor unresectability is an unusual finding, it may be a reliable sign of unresectable pancreatic carcinoma.

Effect of C-terminal fragments of glucagon on insulin secretion in dogs

Although the insulinotropic action of glucagon is well known, which parts of the glucagon molecule play an importent role in its action remain to be elucidated. To investigate the direct effect of the C-terminal peptides of glucagon on the endocrine function of the pancreas, glucagon(17–29), (21–29), (23–29), and (25–29) were studied using an in situ local circulation system of the canine pancreas. These glucagon fragments, as well as glucagon(1–29), were infused into the superior pancreaticoduodenal artery (PA) in a dosage of 400 pmol for 10 minutes during 0.5% glucose or 0.5% arginine infusion, and plasma insulin (IRI) and glucagon (IRG) levels in the superior pancreaticoduodenal vein (PV) were determined. During the glucose infusion, plasma IRI increased significantly following the administration of glucagon(23–29), (21–29), (17–29), or (1–29), but not glucagon(25–29). In these experiments, plasma IRG increased significantly following infusion of glucagon(21–29), (17–29), or (1–29). During the arginine infusion, all of the glucagon fragments studied enhanced insulin secretion, whereas plasma IRG was increased following the administration of glucagon(21–29), (17–29), or (1–29). In these experiments with glucose or arginine infusion, blood glucose in the femoral artery (FA) did not change significantly except for glucagon(1–29), which increased the blood glucose level. In addition, the administration of graded doses of glucagon(21–29) [50, 150, and 400 pmol] during the glucose infusion elicited an increase in plasma IRI in a dose-related manner. From the present study, it is concluded that the C-terminal peptides of glucagon enhanced insulin release, and that glucagon(21–29) is the minimum structure among the C-terminal glucagon fragments to stimulate insulin secretion.

Venous anatomy of the pancreatic head: normal CT appearance in cadavers and patients.

This study was conducted to define the normal CT appearance of the four pancreaticoduodenal veins (anterior and posterior superior, and anterior and posterior inferior) in the head of the pancreas in injected cadaveric specimens and to assess the frequency with which these normal vessels are seen on dynamic contrast-enhanced CT scans. The appearance of the four pancreaticoduodenal veins was studied on CT scans of four cadavers in which the portal veins were injected in situ with radiopaque solutions. A computer-generated three-dimensional model of the pancreatic head and its venous drainage was then produced from one cadaveric examination to show the venous anatomy. After definition of the venous anatomy in the cadaveric specimen, the anterior superior pancreaticoduodenal vein, posterior superior pancreaticoduodenal vein, and gastrocolic trunk were analyzed retrospectively on dynamic bolus contrast-enhanced abdominal CT scans of 100 consecutive patients who had no evidence of pancreatic disease. The anterior and posterior superior pancreaticoduodenal veins were seen on 98% and 88% of scans, respectively. The veins had mean diameters of 2.1 mm. The gastrocolic trunk was seen on 89% of scans and had a mean diameter of 4.7 mm. The inferior pancreaticoduodenal veins are small and were not identified definitively. The anterior and posterior superior pancreaticoduodenal veins and gastrocolic trunk are routinely visualized on CT scans of patients without pancreatic disease. Consequently, assessment of the veins may be useful in staging pancreatic carcinoma.

Posterior superior pancreaticoduodenal vein: mimic of distal common bile duct at sonography.

Previous investigators have noted that the common bile duct may appear to merge with the portal vein on sagittal sonograms, mimicking a venous structure. The posterior superior pancreaticoduodenal vein courses adjacent to the distal part of the common bile duct within the pancreatic head. A prospective study was performed to assess the sonographic appearance of the posterior superior pancreaticoduodenal vein. The study included 50 consecutive subjects in whom the pancreatic head was well seen. Anatomic characteristics of the posterior superior pancreaticoduodenal vein were noted with gray-scale, duplex Doppler, and color Doppler sonography. The site of insertion of the posterior superior pancreaticoduodenal vein into the portal vein was noted. The posterior superior pancreaticoduodenal vein was visualized in all 50 cases. Although it usually (82% of cases) inserted into the posterior aspect of the portal vein, the posterior superior pancreaticoduodenal vein inserted into the anterior aspect of the portal vein in nine cases (18%), resulting in an appearance mimicking the common bile duct on sagittal sonograms. Doppler examination showed flow toward the portal vein in all obliquely oriented posterior superior pancreaticoduodenal veins, and in 40% overall. The common bile duct could always be followed into the porta hepatis and was anterior to the posterior superior pancreaticoduodenal vein in 49 cases (98%). The posterior superior pancreaticoduodenal vein can be seen routinely on sonograms when the pancreatic head is unobscured, and it can mimic the common bile duct in a significant number of cases. These structures can be distinguished by noting continuation of the common bile duct into the porta hepatis, the generally anterior position of the common bile duct, and flow in the posterior superior pancreaticoduodenal vein on Doppler examination. Awareness of the existence and anatomy of the posterior superior pancreaticoduodenal vein minimizes its confusion with the common bile duct at sonographic examination.

Insulin releasing action of N-terminal peptides of glucagon in dogs.

The relationship between the molecular structure and insulin releasing action of glucagon remains unknown. In order to investigate the direct action of N-terminal peptides of glucagon, glucagon (1-14), and glucagon (1-21) were studied using an in situ local circulation of the canine pancreas. These glucagon fragments as well as glucagon (1-29) were infused into the superior pancreaticoduodenal artery in a dose of 400 pmol for 10 min during the glucose or arginine infusion, and plasma insulin and glucagon in the superior pancreaticoduodenal vein were determined by radioimmunoassay. During the glucose infusion, glucagon (1-14) elicited a slight increase in plasma insulin, whereas glucagon (1-21) and (1-29) revealed significant changes in plasma insulin. In these experiments plasma glucagon did not change significantly following the administration of glucagon (1-14) or (1-21). During the arginine infusion all of the glucagon fragments studied enhanced insulin secretion markedly, whereas glucagon secretion was not affected. Furthermore, graded doses of glucagon (1-14) (50, 150, and 400 pmol) elicited an increase in plasma insulin in a dose-related manner. It is concluded from the present study that the N-terminal peptides of glucagon stimulate insulin release especially during the arginine infusion.

Dilated posterior superior pancreaticoduodenal vein: recognition with CT and clinical significance in patients with pancreaticobiliary carcinomas.

The authors retrospectively reviewed computed tomographic (CT) scans, angiograms, and surgical-pathologic records of 226 patients without and 64 patients with pathologically proved pancreaticobiliary carcinoma to evaluate frequency of depiction, normal range of size, and causes of dilatation of the posterior superior pancreaticoduodenal vein (PSPDV) at CT. Among the patients with pancreaticobiliary carcinoma, CT demonstrated enlarged PSPDVs (diameter, greater than or equal to 8 mm) in seven patients. CT and angiography showed that the portal-superior mesenteric vein (P-SMV) was occluded or stenotic at its confluence in three patients and was normal in four patients. Among the latter four patients, localized tumor invasion was found surgically-pathologically along the right lateral wall of the P-SMV in three. A dilated PSPDV with obliteration of the P-SMV at CT may confirm tumor extension to the P-SMV. In patients with a normal P-SMV at CT, a dilated PSPDV indicates that the tumor has extended beyond the pancreatic parenchyman and occluded other pancreaticoduodenal veins or extended to the wall of the P-SMV.

Pancreatic Release of Pancreastatin in the Pig

It is known that pancreastatin-like immunoreactivity (PLI) occurs in the secretory granules of the islet B- and D-cells in the pig pancreas, and that porcine pancreastatin inhibits insulin secretion in rats and mice. In this study, we characterized the porcine plasma PLI and examined whether PLI is released from the pig pancreas in vivo. We found that PLI in unextracted pig plasma largely consists of two high-molecular fractions, with Mr values of 80-85,000 and 300-350,000, respectively. In addition, a small peak of PLI eluted after gel filtration at the position of synthetic porcine pancreastatin. After extraction on octadecylsilyl silica, virtually all PLI disappeared except in the fraction co-eluting with porcine pancreastatin. In thiopenthal-anesthetized pigs, plasma samples were obtained from the carotid artery and the superior pancreaticoduodenal vein. By multiplying the venous-arterial concentration difference by the pancreatic venous plasma flow, a net pancreatic output of PLI of 420 +/- 120 pmol/min was found. This pancreatic PLI output was significantly reduced by electrical stimulation of the local autonomic nerves along the superior artery during atropine administration (p less than 0.001). Furthermore, the pancreatic venous PLI levels were elevated during intravenous infusion of glucose (p less than 0.01). We conclude that pig plasma PLI levels can be measured by radioimmunoassay after extraction on octadecylsilyl silica and that there is a net pancreatic output of PLI, which is reduced by sympathetic stimulation and enhanced during hyperglycemia.

The pancreas and oxygen consumption (Part 2)

In order to evaluate the effect of methylprednisolone sodium succinate (MPSS) on the alteration of pancreatic oxygen consumption (VO2) in hypovolemic shock, MPSS was administered to four normal canines and three hypovolemic animals. All were treated according to the protocol used in the initial report. (The Pancreas and Oxygen Consumption 1: Pancreatic Oxygen Consumption in Normo- and Hypovolemic Dogs.) All seven underwent a splenectomy at the beginning of the experiment. Pancreatic VO2, obtained by adding up VO2 for the head (minus the uncinate process) and tail of the pancreas, was equal to the product of regional blood flow, Q, determined electromagnetically on the gastroduodenal (GDA) and splenic (SA) arteries, times O2 extraction, (a-v)O2; O2 content (in mL%) was measured in the femoral artery (RFA), in the splenic (SV) and superior pancreaticoduodenal (SPDV) veins. Similar determinations were carried out on the right hind limb that served as a control. Recordings were made for 4 h in both groups, the first hour determinations (five in all) serving as reference values. Methylprednisolone did not appear to alter pancreatic VO2, which showed a significant increasing trend from + 77% 1 h after MPSS had been given, to + 98% 3 h later (vs + 56 and + 92%, respectively, in the control group). As in the control group, these increases were owing to augmented O2 extraction by the pancreas. No significant change was noted between the head and tail of the pancreas. In the hind limb, VO2 increased significantly the first 2 h and differed from control VO2 at the end of the first hour only.

Localization and Resection of Insulinomas and Gastrinomas

SELECTED CASES Case 1 A 45-YEAR-OLD woman with a threeyear history of epigastric pain was treated initially with cimetidine and then with ranitidine hydrochloride and antacids, with only mild relief. Her fasting serum gastrin level was elevated at 496 ng/L (496 pg/mL) (normal, 200 ng/L [>200 pg/mL]). Ultrasound, computed tomographic (CT) scan, and selective angiogram all failed to demonstrate a gastrinoma. Selective venous sampling was performed and a marked step-up in gastrin levels was found in the superior pancreaticoduodenal vein (Fig 1). The patient underwent an exploratory laparotomy, and intraoperative ultrasound demonstrated a lesion in the posterior head of the pancreas (Fig 2). After enucleation,

Extraction of epinephrine and norepinephrine by the dog pancreas in vivo

This study determined the fractional extraction of epinephrine and norepinephrine by the in situ dog pancreas. Plasma samples for epinephrine measurements were taken simultaneously from the femoral artery and the superior pancreaticoduodenal vein. Pancreatic extraction of epinephrine was 73 ± 5% when basal arterial epinephrine levels were 380 ± 93 pg/mL, 76 ± 4% when arterial levels were 896 ± 123 pg/mL (epinephrine infused intravenously at 20 ng/kg/min), and 84 ± 1% when arterial levels were 2,956 ± 414 pg/mL (epinephrine infused intravenously at 80 ng/kg/min) suggesting that the process of epinephrine extraction by the pancreas is not saturable over this range. During a similar sampling protocol, norepinephrine was infused intravenously at 4 μg/kg/min; pancreatic extraction of norepinephrine was then 65 ± 7% when arterial norepinephrine levels were 107,000 ± 28,000 pg/mL. In separate experiments, lower rates of norepinephrine (12 to 1,200 ng/min) were infused directly into the pancreatic artery and pancreatic norepinephrine extraction was calculated; it ranged between 66% and 75%. Because the pancreas produces as well as extracts norepinephrine, a third technique was required to determine pancreatic norepinephrine extraction at the lower endogenous levels of norepinephrine; 3H-norepinephrine was infused intravenously and the arteriovenous difference of 3H-norepinephrine was measured. Fractional extraction of 3H-norepinephrine was 74 ± 4% both in the basal state (arterial norepinephrine level = 202 ± 44 pg/mL) and during systemic, glucopenic, stress induced by 2-deoxy-glucose (arterial norepinephrine level = 636 ± 70 pg/mL). These data suggest that also the norepinephrine extraction process by the pancreas is not sarurable. Further, since the pancreatic extraction of norepinephrine is so avid, these data suggest that measurement of the arteriovenous concentration difference of endogenous norepinephrine alone will markedly underestimate local norepinephrine spillover. Correcting these measurements for the extraction would, however, provide an index of the endogenous activity of pancreatic adrenergic nerves. Finally, this study also determined whether pancreatic catecholamine extraction is altered by α-or β-adrenoceptor antagonists; phenoxybenzamine was found to reduce the extraction of both epinephrine ( P < .001) and norepinephrine ( P < .05) whereas propranolol did not. Thus, one must consider how changes of pancreatic catecholamine extraction might alter the interpretation of experiments using α-adrenoceptor antagonists to study local norepinephrine release or catecholamine effects on pancreatic hormone secretion. In summary, (1) at steady state 60% to 80% of either epinephrine or norepinephrine is extracted in one pass by the dog pancreas, (2) this process of extraction appears nonsaturable, and (3) the pancreatic extraction of catecholamines is impaired by the α-adrenoceptor antagonist phenoxybenzamine, but not by the β-adrenoceptor antagonist propranolol.

Preparation of the orthotopic autotransplanted pancreas for long-term exocrine studies

The operative technique for the construction of an orthotopically autotransplanted pancreas with a permanent pancreatic fistula has been described. The operation is performed in two stages, with preparation of the transplant based on the gastroduodenal artery and superior pancreaticoduodenal vein in the first stage and construction of a Herrera-type permanent pancreatic fistula in the second stage. Elimination of warm ischemic time by dividing and reanastomosing the vessels on which the transplant will be based during the first stage while the pancreas continues to be perfused by its other vessels resulted in a uniformly successful outcome. The pancreatic transplant functioned well. The dogs were neither diabetic nor exocrine pancreatic deficient. Their responses to stimulation with exogenous secretin and the cholecystokinin analogue, cerulein, were only slightly less than those of dogs without a pancreatic transplant. This preparation should enable studies to be carried out that will better define the interactions of nerves and hormones in the control of pancreatic secretion.

Immunoreactive dog C-peptide level in the pancreatic vein.

C-peptide immunoreactivity (CPR) levels were measured in dog superior pancreaticoduodenal vein using synthetic dog C-peptide and its antiserum. The basal CPR level was approximately twice as high as the basal immunoreactive insulin (IRI) level on a molar basis. Glucose (10 mg/kg/min) or arginine (250 mg/kg/min) infusion for 5 min into the superior pancreaticoduodenal artery caused a prompt, parallel increase in IRI and CPR. IRI and CPR were closely equimolar at peak secretions. One bolus administration of synthetic neurotensin (10 microgram/kg) into the same artery produced a mild hyperglycemic response and biphasic IRI and CPR responses at 30 min in the vein. The IRI and CPR increases were closely equimolar during the first phase of secretion, but during the second peak a larger increase was found in CPR than IRI. Upon infusion of synthetic substance P (50 ng/kg/min) for 30 min, IRI and CPR concentrations showed a parallel and closely equimolar fall. These results indicate that insulin and C-peptide were released from beta cells in equimolar concentrations.

イヌ膵静脈血中C-ペプチドの動態

Feedback regulation of insulin secretion from dog pancreatic B cells by exogenous insulin was demonstrated. Dog C-peptide immunoreactivity (CPR) concentration in the superior pancreaticoduodenal (pancreatic) vein was measured as an index of endogenous insulin secretion from B cells.Exogenous monocomponent (MC) insulin was administered into superior pancreaticoduodenal (pancreatic) artery of normal dogs which had various concentrations of blood glucose.When the blood glucose level was maintained at about 400 mg/dl, bolus injection of MC insulin (0.1 u/kg) into the pancreatic artery caused about 8.3% suppression of CPR level in the pancreatic vein. However, when the blood glucose concentration was approximately 180 mg/dl, suppression of the CPR level in the pancreatic vein was about 41%.With a fasting blood glucose concentration, exogenous MC insulin caused about 35% suppression of CPR level, but exogenous dog C-peptide (0.2 pM/kg/min) infusion did not affect the IRI concentration in the pancreatic vein.

Anatomy of the pancreatic veins. A post mortem and clinical phlebographic investigation.

The venous anatomy of 22 autopsy specimens of human pancreas was examined by dissection and radiography after injection of gelatin agent. The most constant findings were the posterior superior pancreaticoduodenal vein draining to the portal vein and the anterior superior pancreaticoduodenal vein draining to the gastrocolic trunk and superior mesenteric vein. Both veins were identified in 21 and 20 of 22 cases, respectively. All other pancreatic veins varied considerably in their course. The normal findings in clinical selective pancreatic phlebography based on 148 examinations are described.

The Effects of Xenopsin on Endocrine Pancreas and Gastric Antrum in Dogs

Effects of synthetic xenopsin on endocrine pancreas and gastric antrum in anesthetized dogs were studied. Synthetic xenopsin was administered into the superior pancreaticoduodenal artery and plasma insulin, glucagon and gastrin in the superior pancreaticoduodenal vein and gastrin in the right gastroepiploic vein were measured radioimmunologically. Administration of 10 microgram of xenopsin per kg of body weight brought about a hyperglycemic response and rapid and sharp elevations of the hormones in the pancreatic vein. Plasma gastrin level in the gastric vein also showed an immediate and sharp increase following xenopsin administration. Xenopsin appeared more potent inducer of the glucagon. It is concluded that xenopsin acts directly on endocrine pancreas and gastric antrum to secrete their hormones.