Ileal Vein Research Articles

Acquisition of Protein S Deficiency by Liver Transplantation

Purpose: Liver transplantation is a life-saving procedure for patients with end-stage liver disease. Post-transplantation complications that threaten the longevity of the graft, such as rejection and recurrent disease, are well-recognized. However, the acquisition of systemic disease from a transplanted liver is rare. Methods: Case report and review of the literature. Results: A 62 year old Caucasian male with a history of hereditary hemochromatosis received a liver transplant in June 2004. The patient had no history of thrombotic events prior to transplantation or a family history of hypercoagulability. In fact, prior to an elective splenectomy in 1998 for thrombocytopenia, his bleeding time was 10 minutes (normal <7.5 minutes) and he bled significantly during surgery. The donor, a 29 year old woman, similarly had no prior history of thrombotic events and had not used any oral contraceptives. There were no findings of thromboses intraoperatively during organ recovery. The patient's immediate post-operative course was unremarkable with no bleeding complications. At month 9 post-transplantation, the patient developed a left lower extremity thrombosis and at month 17 post-transplantation, an ileal vein thrombus developed resulting in resection of 12 cm of necrotic ileum and ileostomy. Work-up following his ileal resection revealed protein S deficiency, suspected to be an acquired deficiency from his transplanted liver. His protein C, antithrombin 3 levels were normal and anticardiolipin antibody, prothrombin mutation and Factor V Leyden studies were negative. A review of the literature reveals one prior case of acquired protein S deficiency after liver transplantation.1 Conclusions: With the limited availability of donors for liver transplantation and the inability to obtain rapid test results to evaluate for hypercoagulable states in donors, the pre-transplant diagnosis of conditions such as protein S deficiency will continue to rely upon clinical history. However, as highlighted by our case, the development of thrombosis post-transplantation should prompt a work-up for acquired hypercoagulable conditions, recognizing the role of the transplanted liver as a potential source.

Metabolic and microbial responses in western crossbred and Meishan growing pigs fed a high-fiber diet.

Four Duroc x White composite crossbred (21.8 +/- 1.0 kg BW) and four 12-wk-old Meishan purebred (20.7 +/- 1.6 kg BW) growing barrows were used to determine the relative breed differences in metabolic and microbial responses to a high-fiber diet. The pigs were trained to consume 700 g of a diet containing 35% (as-fed basis) dehydrated alfalfa meal once daily. The pigs' daily intakes of DM, N, GE, NDF, and ADF were 610 g, 16.6 g, 2.64 Mcal, 150 g, and 88 g, respectively. On d 12 after surgical catheterization of the portal vein, ileal vein, and carotid artery, a 3-d total urine and feces collection was conducted. On d 24 after surgery, each pig was placed in an open-circuit calorimeter, and its catheters were connected to a system for simultaneous measurements of oxygen consumption by portal-drained viscera and by whole body, and the net portal absorption of VFA after a 24-h fasting and during a 5-h postprandial period. The VFA measured included acetic, propionic, isobutyric, butyric, isovaleric, and valeric acids. A second 3-d total urine and feces collection was conducted on d 30 after surgery. There were no differences (P = 0.13) between the first and second collections in apparent total-tract digestibility coefficients for nutrients and N retention of pigs. Compared with Duroc x White composite crossbred pigs, Meishan pigs had lower (P = 0.05) apparent digestibility coefficients for DM, N, NDF, hemicellulose, and N retention, but their portal-drained viscera used a greater (P = 0.05) fraction of whole-body oxygen consumption. No differences (P = 0.12) were found between Duroc x White composite crossbred and Meishan pigs in total viable bacteria and cellulolytic bacteria from fecal samples, in vitro digestibility of alfalfa NDF fractions by fecal inocula, whole-body oxygen consumption, net portal absorption of VFA, total energy of absorbed VFA, and the potential of absorbed VFA for meeting the energy needs for whole-body heat production. These results indicate that, in contrast to previous beliefs, the ability of Meishan growing pigs to utilize a high-fiber diet is not superior to that of Duroc x White composite crossbred growing pigs.

Splanchnic metabolism during gut ischemia and short-term endotoxin and hemorrhagic shock as evaluated by intravasal microdialysis.

The splanchnic area is of considerable interest in different types of shock. To characterize the metabolic changes in the splanchnic region in response to different types of shock we used a model where shock-induced metabolic changes in the splanchnic region were studied by the use of intravasal microdialysis. 23 anesthetized domestic pigs were randomized into four groups: Group I, serving as controls (n = 5); Group II, mesenteric ischemia for 180 followed by 120 min of reperfusion (n = 5); Group III, endotoxin shock for 5 h (n = 5); and Group IV, hemorrhagic shock for 180 min followed by re-transfusion of shed blood (n = 8). Microdialysis catheters were placed in the left femoral artery, portal vein and a small ileal mesenteric vein. Samples of the perfusate were continuously collected in micro-vials and analyzed for glucose, lactate, pyruvate and glycerol. In gut ischemia and endotoxin shock the outflow-pattern of lactate, lactate/pyruvate ratio and glucose in the mesenteric vein differed significantly from controls and hemorrhage whereas an increase in glycerol was only noted in the ischemic group. The most prominent differences were detected in lactate/pyruvate ratio, a marker of tissue ischemia with the most pronounced changes during mesenteric ischemia/reperfusion. During endotoxin shock increases in microdialysate metabolites were only noted in the splanchnic region suggesting a specific vulnerability in the region. Studying the lactate/pyruvate ratio may provide additional information when interpreting increased blood lactate levels. In addition glycerol may prove to be a useful marker of splanchnic ischemia. Intravasal microdialysis represents a potentially useful method for monitoring regional metabolic events.

Difference in rates of net portal absorption between crystalline and protein-bound lysine and threonine in growing pigs fed once daily1

Net portal absorption of AA during the 6-h postprandial period was measured in eight gilts (48.5 ± 1.6 kg BW) in a crossover design. The pigs had chronic catheters placed in the portal vein, carotid artery, and ileal vein, and were trained to consume 1.2 kg of a standard grower diet once daily. Blood samples were taken every 30 min for 4 h and then hourly until 6 h after feeding. The first set of blood samples was taken after pigs were fed a meal of the test 16% CP corn–soybean meal diet (16% CP) or the test 12% CP corn–soybean meal diet supplemented with crystalline lysine, threonine, and tryptophan (12% CP + AA) to equal the three AA levels in the 16% CP diet. Pigs were then fed the standard diet for 2 d. Following that, blood samples were again taken after the pigs were fed a meal of the test diet that was not given to them at the first sampling period. Net portal AA absorption was calculated by multiplying porto-arterial plasma AA concentration difference by portal vein plasma flow rate (PVPF), estimated by an indicator-dilution technique employing p-aminohippuric acid as the indicator infused into the ileal vein. Plasma concentrations of lysine and threonine of pigs were affected by the diet × time interaction (P < 0.01). Portal and arterial plasma lysine and threonine concentrations in pigs attained the maximal level by 1 h postprandial when the 12% CP + AA diet was fed, but reached the peak level at 2.5 h postprandial when the 16% CP diet was given. The PVPF of pigs over the 6 h postprandial was less (P < 0.01) when the 12% CP + AA diet was given than when the 16% CP diet was fed. Net portal absorptions of lysine and threonine also were affected (P < 0.05) by time × diet interaction. The peak portal absorption of both lysine and threonine in pigs appeared at 0.5 h postprandial when the 12% CP + AA diet was given, but at 2.5 h postprandial with the feeding of the 16% CP diet. The early appearance of peak portal absorption of lysine and threonine from feeding the 12% CP + AA compared with the 16% CP diet indicates that crystalline lysine and threonine are absorbed more rapidly than protein-bound lysine and threonine in pigs fed once daily.

Difference in rates of net portal absorption between crystalline and protein-bound lysine and threonine in growing pigs fed once daily.

Net portal absorption of AA during the 6-h postprandial period was measured in eight gilts (48.5 +/- 1.6 kg BW) in a crossover design. The pigs had chronic catheters placed in the portal vein, carotid artery, and ileal vein, and were trained to consume 1.2 kg of a standard grower diet once daily. Blood samples were taken every 30 min for 4 h and then hourly until 6 h after feeding. The first set of blood samples was taken after pigs were fed a meal of the test 16% CP corn-soybean meal diet (16% CP) or the test 12% CP corn-soybean meal diet supplemented with crystalline lysine, threonine, and tryptophan (12% CP + AA) to equal the three AA levels in the 16% CP diet. Pigs were then fed the standard diet for 2 d. Following that, blood samples were again taken after the pigs were fed a meal of the test diet that was not given to them at the first sampling period. Net portal AA absorption was calculated by multiplying porto-arterial plasma AA concentration difference by portal vein plasma flow rate (PVPF), estimated by an indicator-dilution technique employing p-aminohippuric acid as the indicator infused into the ileal vein. Plasma concentrations of lysine and threonine of pigs were affected by the diet x time interaction (P < 0.01). Portal and arterial plasma lysine and threonine concentrations in pigs attained the maximal level by 1 h postprandial when the 12% CP + AA diet was fed, but reached the peak level at 2.5 h postprandial when the 16% CP diet was given. The PVPF of pigs over the 6 h postprandial was less (P < 0.01) when the 12% CP + AA diet was given than when the 16% CP diet was fed. Net portal absorptions of lysine and threonine also were affected (P < 0.05) by time x diet interaction. The peak portal absorption of both lysine and threonine in pigs appeared at 0.5 h postprandial when the 12% CP + AA diet was given, but at 2.5 h postprandial with the feeding of the 16% CP diet. The early appearance of peak portal absorption of lysine and threonine from feeding the 12% CP + AA compared with the 16% CP diet indicates that crystalline lysine and threonine are absorbed more rapidly than protein-bound lysine and threonine in pigs fed once daily.

High basal gastric acid secretion in somatostatin receptor subtype 2 knockout mice

Background & Aims: Somatostatin receptor subtype 2 (sst 2) agonists inhibit gastric secretion. The role of sst 2 in the regulation of acid secretion was assessed using sst 2 knockout mice and urethane to induce somatostatin release. Methods: Acid secretion was monitored every 10 minutes by gastric perfusion and backtitration of perfusates in fasted, urethane-anesthetized C57/129 sst 2 (−/−) mice and wild-type (+/+) mice. The ileal vein was cannulated for drug injection. Intragastric pH and serum gastrin were monitored 1 hour after anesthesia without perfusion. Results: Gastric pH values were lower in sst 2 (−/−) mice (3.8 ± 0.3) than in wild-type mice (7.1 ± 0.1, P < 0.05), and there was no difference in gastrin levels. Basal acid output per 2 hours was 10-fold higher in sst 2 knockout mice compared with wild-type mice. The gastrin antibody abolished the high basal acid secretion in sst 2 (−/−) mice and had no effect in wild-type mice. The somatostatin antibody increased basal secretion by 4-fold in wild-type and had no effect in knockout mice. Somatostatin 14 or the sst 2 agonist DC 32-87 inhibited pentagastrin-stimulated acid secretion in wild-type mice, but did not alter basal secretion in knockout mice. Conclusions: These results indicate that sst 2 is the main subtype whereby endogenous somatostatin suppresses gastric acid secretion through inhibition of gastrin action. GASTROENTEROLOGY 1998;114:1125-1132

Effects of high-copper feeding on portal ammonia absorption and on oxygen consumption by portal vein-drained organs and by the whole animal in growing pigs1

Growing gilts that had catheters inserted into the portal vein, ileal vein, and carotid artery and that were trained to consume 1.2 kg of a 16% CP corn-soybean meal basal diet once daily were used. In Trial 1, hourly simultaneous measurements of the O2 consumption by portal vein-drained organs (PVDO) and by the whole animal during the 24- to 30-h postprandial period were conducted in eight pigs (33.8 +/- .6 kg). After initial measurements, four pigs continued to receive the basal diet and four pigs were fed a basal diet +250 ppm of Cu. Following a 7-d acclimation period, the second series of measurements were made. In pigs fed the diet supplemented with Cu, the PVDO and whole-animal O2 consumptions and the fraction of whole-animal O2 consumption used by PVDO were not different (P > .05) between the initial and second series. In Trial 2, seven gilts (38.5 +/- .9 kg) were used for measurements of net portal NH3 absorption and the O2 consumption by PVDO and by the whole animal during the 0- to 6-h postprandial period. The second series of measurements were made 7 d after four pigs were fed the diet supplemented with Cu. For pigs fed the diet supplemented with Cu, during the second series of measurements, the net portal NH3 absorption was lowered (P < .05). No differences (P > .05) in PVDO and whole-animal O2 consumptions and the fraction of whole-animal O2 consumption used by PVDO were found between the initial and second series.(ABSTRACT TRUNCATED AT 250 WORDS)

Influence of carbadox on fasting oxygen consumption by portal vein-drained organs and by the whole animal in growing pigs.

Fasting O2 consumption by the whole animal (W) and by portal vein-drained organs (PVDO) during the 24- to 30-h postprandial period were measured in seven growing pigs (36.1 +/- 2.3 kg) with catheters chronically placed in the hepatic portal vein, ileal vein, and carotid artery trained to consume 1.2 kg of a 16% CP corn soybean meal basal diet (B) once daily. The pigs were placed individually into an open-circuit, indirect calorimeter and connected to an arteriovenous (A-V) O2 difference analyzer for hourly simultaneous measurements of O2 consumption by W and PVDO. The PVDO O2 consumption was calculated by multiplying the A-V O2 difference by the portal vein blood flow rate derived from constant infusion of a p-aminohippuric acid solution into the ileal vein. After the initial series of hourly measurements, four pigs remained on the B diet and three pigs were fed a B + 55 ppm carbadox diet. Seven days later, the second series of measurements was made. In pigs fed the diet with carbadox added, the hourly W O2 consumptions were not different (P greater than .05) between the initial and second series and averaged 7.5 mL.min-1.kg of BW-1. However, the A-V O2 differences (mL/dL) were reduced (P less than .05) from 4.6 to 4.0 at 24 h, 4.8 to 4.0 at 25 h, and 4.6 to 4.0 at 29 h postprandial and the fractions of W O2 consumption used by PVDO (percentage) were reduced (P less than .05) from 28.6 to 21.6 at 26 h and 25.2 to 18.2 at 27 h postprandial.(ABSTRACT TRUNCATED AT 250 WORDS)

Potential contribution of absorbed volatile fatty acids to whole-animal energy requirement in conscious swine1

Chronic cannulas were placed in the hepatic portal vein, ileal vein, and carotid artery in seven crossbred growing gilts trained to consume once daily 1.2 kg of a 16% CP corn-soybean meal diet. Eleven days after surgery, each pig (37.4 kg BW) was placed in an open-circuit calorimeter and its cannulas were connected to a system for determining portal absorption of nutrients. The whole-animal heat production and net portal absorption of gut VFA were measured simultaneously for 12 h after the pig was fed 1.2 kg of feed. Plasma concentrations of VFA, including acetic, propionic, isobutyric, butyric, isovaleric, and valeric acids, in portal and arterial samples were determined by gas chromatography after a cleanup by ion-exchange chromatography. The net portal absorption of VFA was calculated by multiplying the porto-arterial plasma concentration difference of the VFA by portal vein plasma flow. Plasma flow was estimated by the indicator-dilution technique using p-aminohippuric acid as the indicator. The energy value of absorbed VFA was the sum of products of each individual VFA multiplied by its corresponding value of the heat of combustion. The mean hourly energy value of absorbed VFA during the 12-h postprandial period was .65 +/- .03 kcal.h-1.kg BW-1. The mean hourly whole-animal heat production was 2.70 +/- .04 kcal.h-1.kg BW-1. Thus, in our 37.4-kg pigs, which were trained to consume 1.2 kg of a 16% CP corn-soybean meal diet once daily, the gut VFA absorbed into the portal vein could contribute 23.8 +/- 1.1% to whole-animal heat production if all of the absorbed VFA were combusted to CO2.

Effect of carbadox on net absorption of ammonia and glucose into hepatic portal vein of growing pigs1

Chronic cannulas were placed into the hepatic portal vein, ileal vein and carotid artery of growing pigs trained to consume their daily allowance of 1.2 kg of feed (16% protein corn-soybean meal basal diet) in a single meal. The average preoperative BW of pigs was 44.7 kg for Trial 1 (three pigs) and 35.3 kg for Trial 2 (seven pigs). In Trial 1, net absorption of ammonia (NH3) and glucose into the portal vein was determined three times at weekly intervals. The net portal absorptions were derived by multiplying the porto-arterial plasma concentration difference of NH3 and glucose by portal vein plasma flow rate estimated with the p-aminohippuric acid indicator-dilution technique. Differences in the net portal absorptions of NH3 and glucose among the three weekly measurements were small (P greater than .05). In Trial 2, the first sequence of net portal absorption measurements was conducted when pigs were fed the basal diet, and the second sequence of measurements was conducted after the pigs had been fed the diet supplemented with 55 ppm of carbadox for 7 d. Carbadox supplementation reduced (P less than .05) plasma NH3 concentration in portal plasma during the 2.5-h to 5-h postprandial period and decreased (P less than .05) net portal absorption of NH3 during the 2.5-h to 4-h postprandial period. Carbadox, however, did not affect (P greater than .05) net portal absorption of glucose. We suggest that carbadox suppresses the production of cell-toxic NH3 by intestinal microorganisms and, thus, reduces the injury and turnover of intestinal cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Oxygen consumption by portal vein-drained organs and by whole animal in conscious growing swine.

A method was developed to measure simultaneously the O2 consumption (VO) by the whole animal and by the hepatic portal vein-drained organs (PVDO), including the gastrointestinal tract, spleen, and pancreas in conscious 3.5- to 4-month-old swine. The method was used to determine (i) the effect of feeding on hepatic portal vein blood flow rate (Qpv) and VO by PVDO and by the whole animal, and (ii) the significance of PVDO on the oxidative demand in the pig. Chronic cannulas were placed in the hepatic portal vein, carotid artery, and ileal vein. The Qpv was determined by an indicator dilution technique employing continuous constant infusion of 1% p-aminohippuric acid into the ileal vein. The VO2 by PVDO was estimated by multiplying Qpv by arterial-portal vein O2 difference measured with an arterial-venous O2 difference analyzer connected to the carotid artery and portal vein cannulas. Whole animal VO2 was measured with an open circuit indirect calorimeter. In seven pigs (3.5- to 4-month-old, 37.4 +/- 0.8 kg) trained to be fed once daily, feeding (1.2 kg of feed mixed with 1.2 liter of H2O) caused postprandial (6 hr) Qpv to increase more than 34 +/- 15% above the preprandial value of 34.5 +/- 4.2 ml.min-1.kg-1 body wt. The postprandial VO2 by PVDO was elevated more than 46 +/- 12% above the value of 1.52 +/- 0.20 ml.min-1.kg-1 body wt observed during the preprandial period. Whole animal VO2 increased 45 +/- 9 and 33 +/- 7% above the preprandial value of 6.23 +/- 0.57 ml.min-1.kg-1 body wt for the first 6 hr and the 7 to 12 hr after feeding, respectively. Although PVDO represent only 5% of body weight, they used 25% of whole body VO2. The study clearly illustrates the significance of PVDO on the whole animal oxidative demand in conscious growing swine.

A simple method for chronic cannulation of the portal vein in intact unrestrained rats.

A simple new method is described for chronic cannulation of the portal vein in rats. A Silastic catheter (0.64 mm OD) with an internal metallic leader is directly inserted in the junction of the two small ileal veins. The catheter is advanced into the mesenteric vein to the portal vein. Then the leader is removed and the catheter tunneled out the back of the neck. This method allows for the measurement of portal vein pressure, direct injection of substances in the portal vein, or blood samples for at least 1 wk in intact unrestrained rats. Validation included the presence of elevated portal vein pressure in portal hypertensive rats compared with normal rats and the absence of clot development in the portal vein. This method should help provide a better understanding of hepatic physiology and pharmacology in normal and disease states.

A method for chronically quantifying net absorption of nutrients and gut metabolites into hepatic portal vein in conscious swine.

Surgical procedures are described for chronic cannulation of portal vein, ileal vein, abdominal aorta, and carotid artery in pigs. Silastic or Micro-Renathane tubing was used for cannulating portal vein and ileal vein, while carotid artery was cannulated with Micro-Renathane tubing. The lumen of Micro-Renathane tubing was coated with tri-dodecylmethyl ammonium chloride (TDMAC)-heparin complex. The abdominal aorta was cannulated via saphenous artery with vinyl tubing. This allows simultaneous collection of blood samples from hepatic portal vein and systemic artery (carotid or abdominal aorta) and continuous infusion of p-aminohippuric acid (PAH) into ileal vein. The constant PAH infusion provided an indicator-dilution method for estimating the blood flow rate in portal vein. In 13 pigs weighing 54 +/- 2.8 kg, the mean portal vein blood flow rate during the 8-h postprandial period was estimated to be 1,979 ml X min-1 X pig-1 or 37.8 ml X min-1 X kg-1 body weight. By simultaneously measuring the concentration of nutrients and metabolites in the portal and systemic arterial blood and multiplying porto-arterial differences by the estimated portal vein blood flow rate, the net absorption of nutrients (except long-chain fatty acids) and metabolites into hepatic portal system in conscious swine can be quantified.

The Venous Supply of the Cecum, Ileum, and the Proximal Loop of the Ascending Colon in the Ox*

AbstractThe present study describes in detail the venous supply to the bovine cecum, ileum, and the proximal loop of the ascending colon. The cecum was supplied by branches from the cecal and accessory cecal veins. The accessory cecal vein was observed in the majority of the specimens examined. The cecal and accessory cecal veins were joined by 7–10 short oblique anastomoses. The ileum was supplied by the ileal branches of the cecal vein, and from the mesenteric ileal and first ileal (cranial mesenteric) veins. The ileal branches of the cecal vein formed a row of antimesenteric ileal arches in the ileal part of the ileocecal fold. The mesenteric ileal vein, in some cases, detached a collateral branch. The first ileal and the mesenteric ileal veins anastomosed on the ventral surface of the ileum. The initial loop of colon was supplied by branches from the ileocolic vein. In the majority of specimens, the common colic, a branch of the cranial mesenteric vein, supplied the first colic branch to the third part of the initial colon. In such cases, the ileocolic vein gave off only the second and third colic branches. However, in one case, the proximal loop of the ascending colon was supplied by three colic branches of the ileocolic vein and by the first colic branch of the common colic vein. In specimens in which the common colic vein was absent, the colic branches to the initial colon were all given off by the ileocolic vein. The third (or fourth) colic branch of the ileocolic vein and the first cecal branch of the cecal vein united on the lateral surface of the ileocecocolic junction to form an ileocecocolic arch. The veins on the medial surface of the ileocecocolic junction did not form an arch.The colic and ileal lymph nodes were supplied by twigs from the colic branches of the ileocolic vein and first ileal vein of the cranial mesenteric, respectively. The small cecal lymph nodes seen only in the specimen from the calf were supplied by fine branches from the cecal vein.

Effect of intralumenal cation-exchange resin on excretion of ammonia in rat ileum.

Ammonia excretion was studied in rat ileal segments during perfusion of the animal through the saphenous vein. In the first 10 min during and after intravenous infusion of L-glutamine (116 mg/kg to double arterial glutamine concentration) average net change in lumenal ammonia was 13 +/- 8 (S.E.) nmole NH3/min/g ileum; average net change in ileal venous ammonia was 28 +/- 9 nmole NH3/min/g ileum; and average net change in total ammonia (lumen + ileal vein) was 41 +/- 13 compared to -5 +/- 10 nmole/min/g ileum for animals infused with saline P less than 0.025. These data suggest that ileal metabolism of arterial glutamine liberates ammonia to both ileal venous blood and intestinal lumen. When a cation-exchange resin which binds ammonia was infused intralumenally, average net change in lumenal ammonia in the first 10 min during and after intravenous infusion of 116 mg/kg L-glutamine was 415 +/- 156 nmole NH3/min/g ileum (p less than 0.01 compared to value during perfusion of Earle's solution alone). During the first 10 min during and after glutamine infusion net change in ileal venous plasma ammonia was -8 +/- 14 when resin was being perfused through the lumen compared to +28 +/- 9 nmole/min/g ileum during perfusion of Earle's solution alone without resin P less than 0.05. Thus resin in the small intestine can trap very large amounts of ammonia.

634 EFFECT OF INTRALUMENAL CATION-EXCHANGE RESIN ON EXCRETION OF AMMONIA IN RAT ILEUM

Ammonia excretion was studied in rat ileal segments during perfusion of the animal through the saphenous vein. Average net change in lumenal ammonia in the first 10 mins following intravenous infusion of L-glutamine (116 mg/kg to double arterial glutamine concentration) was 13 ± 8 nmol NH3/min/g ileum. Average net change in ileal venous ammonia post-glutamine was 28 ± 9 nmol NH3/min/g ileum. Average net change in total ammonia (lumen + ileal vein) post-glutamine was 41 ± 13 compared to -5 ± 10 nmol/min/g ileum for animals infused with saline p <0.025. These data suggest that ileal metabolism of arterial glutamine liberates ammonia to both ileal venous blood and intestinal lumen. When a cation-exchange resin which binds ammonia was infused intralumenally, average net change in lumenal ammonia in the first 10 minutes following intravenous infusion of 116 mg/kg L-glutamine was 415 ± 156 nmol NH3/min/g ileum (p<0.01 compared to value during perfusion of Earle's solution alone). During the first 10 minutes following glutamine infusion net change in ileal venous plasma ammonia was -8 ± 14 when resin was being perfused through the lumen compared to 28 ± 9 nmol/min/g ileum during perfusion of Earle's solution alone without resin p <0.05. Thus resin in the small intestine can trap very large amounts of ammonia & may be useful in treating hyperammonemia.

Gastric A-Cell Function in Insulin-Deprived Depancreatized Dogs1

To determine if gastric A-cells are a major source of the glucagonemia of insulin-deprived depancreatized dogs and to examine their secretory behavior, immunoreactive glucagon (IRG) was measured simultaneously in plasma from the inferior vena cava (VC) and from a gastric vein (GV) draining the fundus. Basal GV IRG averaged 205 +/- 35 pg/ml, significantly above the VC level of 71 +/- 30 (P less than 0.001) and rose to 1417 +/- 498 1.5 minutes after the start of an arginine infusion, exceeding VC IRG at all points (P less than 0.01). Measurement of IRG in gastric, jejunal, and ileal veins and vena cava revealed an IRG gradient only across the stomach. Measurement of glucagon-like immunoreactivity (GLI) revealed no gradient across the stomach, jejunum, or ileum, thus excluding cross-reaction with GLI as the cause of the GV hyperglucagonemia. Intragastric arginine elicited a near doubling of GV IRG within 1.5 minutes and this persisted for at least 120 minutes, ranging from 142 to 623 pg/ml above the VC level. Infusion of insulin at a physiologic rate lowered GV IRG from 665 +/- 66 to 151 +/- 49 pg/ml in 20 minutes and abolished the GV-VC gradient within 60 minutes, whereas intravenous and intragastric glucose administration without insulin did not alter GV IRG. It is concluded that: 1) in the insulin-deprived depancreatized dog, the stomach is a major source of IRG; 2) gastric IRG secretion is somehow stimulated by intravenous and intragastric arginine administration; 3) it is not influenced by intravenous or intragastric glucose administration; and 4) its release is suppressed by physiologic levels of insulin.

Experimental thrombus formation in mesenteric microvessels: Evaluation of a method

Platelet thrombi in rats are produced at sites of electrically induced damage in mesenteric venules. The thrombus formation response is dependent on the temperature of the bathing fluid and varies with electrode polarity. Cathodal stimulation causes vasoconstriction and induces platelet aggregation after a slight delay, while anodal stimulation induces the rapid formation of aggregates containing some white cells and erythrocytes, without any vasoconstriction. The effects of cathodal and anodal stimulation can be simulated by topical application of isotonic saline adjusted to high or low pH, respectively. Ultrastructural studies showed that aggregated platelets remaining at the stimulation site lose some of their organelles after 10 min (platelet emboli were found in liver venules of gerbils after thrombi had been produced in the ileal veins). The thrombus formation response cannot be satisfactorily quantified by measuring either rate or duration of embolisation, but recording the number of thrombi produced by a group of “threshold” stimuli is a simple, semi-objective means of assessment, and gives reproducible results in control animals.