Subclinical ammonia toxicity in steers: effects on hepatic and portal-drained visceral flux of metabolites and regulatory hormones

Four calves (avg wt 161 kg) were surgically fitted with indwelling catheters in the femoral artery and femoral, portal, hepatic and mesenteric veins to study the effects of subclinical ammonia toxicity on portal-drained viscera (PDV) and hepatic (HEP) net flux of key metabolites and pancreatic hormones. Hyperammonemia was induced via administration of ammonium chloride (NH4Cl; 12 mumol.kg BW-1.min-1) via the femoral vein catheter for 240 min; infusions were preceded (PRE) and followed (POST) by 60- and 180-min control periods, respectively. Blood samples were obtained from the arterial catheters, and portal and hepatic vein catheters. Net flux rates were calculated by multiplying venoarterial differences by blood flow. Arterial plasma ammonia N peaked (P less than .01) at 327 micrograms/dl; hepatic ammonia extraction increased (P less than .01) from 10 to 23% during NH4Cl infusion. Arterial plasma glucose concentrations increased (P less than .05) during NH4Cl infusion (90.5 vs 82.6 mg/dl) concomitant with trends toward a reduction in net HEP glucose output. Portal-drained visceral release of insulin did not increase (P greater than .10) during NH4Cl infusion despite the steady rise in circulating glucose concentration; however, cessation of NH4Cl infusion resulted in a 109% increase (P less than .05) in PDV insulin release at +60 min POST. Plasma L-lactate, nonesterified fatty acids, urea N and glucagon concentrations and net fluxes were variable throughout the experiment. Results tend to indicate that hyperammonemia reduced hepatic glucose output and glucose-mediated pancreatic insulin release.     

Gross and histopathological observations of long-term catheterized vessels in experimental sheep

Chronic indwelling central vessel catheters provide vascular access for compartmental infusion or sampling. However, complications with catheter patency during the postoperative and/or experimental period often arise. In order to identify physiological occurrences common with such complications, 10 multicatheterized sheep (61.8 +/- 7.8 kg BW), obtained from a previous nutrient flux study were used for gross and histopathological investigation. Catheters had been surgically placed in a hepatic portal vein (PVC), a hepatic vein (HVC), a distal mesenteric vein (MVC) and a mesenteric artery (MAC). In the previous study, catheters (PVC, HVC and MAC) were used to collect blood samples or infuse (MVC) p-aminohippurate. Catheters were maintained for a total of 58 days prior to necropsy. Histopathological findings indicated that catheter failures were associated with the following tissue responses: (i) thromboses with frequent focal vasculitis; (ii) euplastic tissues associated with extensive fibrosis; (iii) granulomas; (iv) neo-vascularization of the media; (v) calcification processes; and (vi) micro-abscesses. Additional studies are needed that address and incorporate improvement of catheter design and placement to minimize irritation of endothelium, improvement of catheter treatments and therapeutic regimes, and development and use of alternative anti-coagulants. A greater understanding of the mechanisms leading to failure will help researchers improve catheter performance and patency.     

Effects of dietary monensin and sodium propionate on net nutrient flux in steers fed a high-concentrate diet

Four Holstein steers (mean body weight, 211 +/- 20 kg) were utilized in a Latin-square design with a 2 X 2 factorial arrangement of treatments to investigate the effects of monensin (0 or 220 mg/d) and sodium propionate (0 or 450 g/d) on net nutrient flux. Steers were surgically prepared with hepatic portal and mesenteric venous catheters and an elevated carotid artery, after which they were adjusted to their basal diet (85% concentrate) and initial treatment over 19 d. Samples of arterial and portal venous blood were taken hourly over 3 h for the final 3 d of each 2-wk period. Portal blood flow was determined by primed continuous infusion of para-aminohippurate. No changes were seen in dry matter intake, portal blood flow, or net portal flux of any of the volatile fatty acids with the exception of butyrate flux, which decreased with monensin addition. Addition of monensin decreased net portal flux of ammonia, decreased recycling of urea, and tended to increase the net portal flux of glucose. Addition of sodium propionate increased the net portal flux of glucose and decreased the net portal flux of alpha-amino-N. These results are interpreted to suggest that changes in the products of ruminal fermentation may not be exactly translated into the products appearing in the portal circulation, and more information is needed to describe these relationships.     

Response of nitrogen metabolism in preparturient dairy cows to methionine supplementation

Three multiparous Holstein cows (607 kg of BW) were surgically prepared with an elevated carotid artery and indwelling catheters in the hepatic, portal, and two mesenteric veins to study the effects of methionine supplementation on amino acid metabolism during the last 2 wk of pregnancy. The study began 15 d before the expected calving date. Dietary treatments were Control (1.53 Mcal NE(l)/kg, 15.6% CP, and 40% ruminally undegradable protein) and Control supplemented with 60 g/d of ruminally protected methionine (MET, supplying 39 g/d of DL-methionine and approximately 18 g/d of methionine available for intestinal absorption). Each cow received both dietary treatments in a crossover design. Cows were fed once daily. After 5 d on treatment, a blood flow marker (para-aminohippurate) was infused into a mesenteric vein, and arterial, portal, and hepatic blood samples were obtained at 0, 2, 6, 12, and 18 h after feeding. Net flux of methionine was calculated as the plasma arteriovenous difference multiplied by plasma flow. Dry matter intake (10.8 kg/d) and portal (824 L/h) and hepatic (995 L/h) plasma flows were not affected (P > .10) by treatment. Arterial plasma concentration of methionine was greater (P = .10) with MET (27.67 microM) than with Control (16.42 microM). Net portal absorption of methionine increased (P = .10) with MET (26.2 g/d) compared with Control (9.5 g/d). The net portal methionine flux was negatively correlated (r = -.59; P < .001) with arterial urea concentrations. Net flux of methionine across splanchnic tissues shifted (P = .06) from a net uptake with Control (4 g/d) to a net output with MET (11 g/d). Therefore, MET increased by 15 g/d the methionine supply to the rest of the body. The net uptake of methionine by splanchnic tissues observed with Control indicated a net mobilization of methionine by peripheral tissues. Results indicate that methionine was the limiting amino acid with Control and that MET was beneficial because it increased methionine supply to peripheral tissues and reduced arterial urea concentrations.     

克伦特罗对绵羊肝脏挥发性脂肪酸和糖代谢的影响

在 4头门静脉、肝静脉、颈静脉、肠系膜静脉和股动脉上安装血管导管的绵羊中研究了克伦特罗 (CL ,0 8mg/kgBW ,肠系膜静脉给药每天 2次 ,连续 5d)对其肝脏物质代谢的影响。结果表明 :CL可增加绵羊肝脏中的VFA流量 ,其中门静脉处乙酸、丙酸和丁酸的流量分别较对照期增加 19 4 9% (P <0 .0 1)、2 0 2 % (P >0 .0 5 )和4 5 5 % (P >0 .0 5 ) ,而肝静脉处VFA流量两期水平接近。CL也提高肝脏中葡萄糖的异生作用 ,在肝静脉处血中葡萄糖流量上升了 2 5 96 % (P <0 .0 1)。门静脉处血中葡萄糖循环水平也相应提高。此外在CL作用下肝静脉处胰岛素水平也较对照期有所下降。提示CL可增加进入绵羊肝脏中VFA的流量并促进肝脏对VFA的吸收和利用。通过降低胰岛素水平或对肝脏的直接作用CL还可增加绵羊血中葡萄糖的水平     

TRANSSPLENIC PORTAL SCINTIGRAPHY USING 99MTC-MEBROFENIN IN NORMAL DOGS

Transsplenic portal scintigraphy using sodium pertechnetate is superior to per-rectal portal scintigraphy due to improved visualization of the portal vasculature with decreased patient and personnel exposure. The purpose of this study was to describe the use of 99mTc-mebrofenin, the radiopharmaceutical of choice for the evaluation of hepatic function, in place of pertechnetate for transsplenic portal scintigraphy in normal dogs. Sixteen juvenile dogs underwent transsplenic portal scintigraphy using 37-130 MBq 99mTc-mebrofenin in a 0.2-0.5 ml volume. After the initial dynamic acquisition obtained at 4 frames/s in right lateral recumbency, static right lateral, and ventral views were obtained at 5, 10, 15, 20, 25, 30, 40, 50, and 60 min. A nuclear angiogram of the splenic and portal veins was visible in all dogs, followed by rapid distribution of the radiopharmaceutical in the liver. Hepatic morphology was more easily defined than with pertechnetate. Transit time could not be calculated due to the high hepatic extraction of 99mTc-mebrofenin. Mean +/- SD shunt fraction was 0.8 +/- 0.8%. Time to peak liver activity was 3.1 +/- 1.1 min, and hepatic excretion T1/2 was 19.4 +/- 6.3 min. No visible blood pool and cardiac activity was seen after 5 min. The mean +/- SD time to visualization of defined biliary activity was 8.8 +/- 2.9 min. Absorption from the spleen was significantly higher than that reported for pertechnetate (87.9 +/- 8.2%, vs. 52.5 +/- 19.1%). 99mTc-mebrofenin can be used in place of pertechnetate for transsplenic portal scintigraphy, with the advantage of combining quantitative parameters of liver function with the already known advantage of transsplenic portal scintigraphy.     

Effect of increasing ruminal butyrate absorption on splanchnic metabolism of volatile fatty acids absorbed from the washed reticulorumen of steers

Four steers fitted with a ruminal cannula and chronic indwelling catheters in the mesenteric artery, mesenteric vein, hepatic portal vein, hepatic vein, and the right ruminal vein were used to study the absorption and metabolism of VFA from bicarbonate buffers incubated in the temporarily emptied and washed reticulorumen. Portal and hepatic vein blood flows were determined by infusion of p-aminohippurate into the mesenteric vein, and portal VFA fluxes were calibrated by infusion of isovalerate into the ruminal vein. The steers were subjected to four experimental treatments in a Latin square design with four periods within 1 d. The treatments were Control (bicarbonate buffer) and VFA buffers containing 4, 12, or 36 mmol butyrate/kg of buffer, respectively. The acetate content of the buffers was decreased with increasing butyrate to balance the acidity. The butyrate absorption from the rumen was 39, 111, and 300 +/- 4 mmol/h for the three VFA buffers, respectively. The ruminal absorption rates of propionate (260 +/- 12 mmol/h), isobutyrate (11.4 +/- 0.7 mmol/h), and valerate (17.3 +/- 0.7 mmol/h) were not affected by VFA buffers. The portal recovery of butyrate and valerate absorbed from the rumen increased (P < 0.01) with increasing butyrate absorption and reached 52 to 54 +/- 4% with the greatest butyrate absorption. The liver responded to the increased butyrate absorption with a decreasing fractional extraction of propionate and butyrate, and with the greatest butyrate absorption, the splanchnic flux was 22 +/- 1% and 18 +/- 1% of the absorbed propionate and butyrate, respectively. The increased propionate and butyrate release to peripheral tissues was followed by increased (P < 0.05) arterial concentrations of propionate (0.08 +/- 0.01 mmol/kg) and butyrate (0.07 +/- 0.01 mmol/kg). Arterial insulin concentration increased (P = 0.01) with incubation of VFA buffers compared with Control and was numerically greatest with the greatest level of butyrate absorption. We conclude that the capacity to metabolize butyrate by the ruminal epithelium and liver is limited. If butyrate absorption exceeds the metabolic capacity, it affects rumen epithelial and hepatic nutrient metabolism and affects the nutrient supply of peripheral tissues.     

Effects of glucagon and insulin on lipolysis and ketogenesis in sheep.

The hepatic and portal productions of acetoacetate and beta-hydroxybutyrate and lipolysis were studied in normal and insulin-controlled alloxan-diabetic sheep. Since hyperinsulinemia is associated with glucagon administration, the latter group of sheep were used to maintain constant plasma insulin levels. After control values were obtained glucagon was infused intraportally at 90 mug/hr for two hours. The ketone body production by portal drained viscera was not significantly affected by glucagon. In alloxanized sheep, glucagon significantly (P less than 0.01) increased net hepatic production of acetoacetate (from -0.54 +/- 0.08 to 0.46 +/- 0.07 g/hr). Lipolysis also increased. However, in the normal sheep, hyperinsulinemia prevented any stimulatory effect of glucagon on hepatic ketogenesis and lipolysis. Therefore, while glucagon appears capable of stimulating ketogenesis andlipolysis, these effects are readily suppressed by insulin.     

Minimally-invasive catheterization of the portal, hepatic and cranial mesenteric veins and the abdominal aorta for quantitative determination of hepatic metabolism in dairy cows

The objective of this study was to establish a minimally-invasive, ultrasound (US)-guided technique for the placement of indwelling catheters into the portal, hepatic, and cranial mesenteric veins as well as the abdominal aorta. Catheters were placed in eight healthy dairy cows on day 1. The patency of catheters was tested daily until day 14 when a necropsy was carried out. On day 6, energy intake and hepatic net output of glucose, removal of lactate, and oxygen were determined in seven cows. Post mortem examination revealed that all implanted catheters were in the intended locations. Loss of patency in one portal vein catheter on day 9 was attributable to a fibrin clot. Significant correlations were found between mean energy intake and mean hepatic plasma flow (r=0.91; P=0.004), hepatic glucose output (r=0.81; P=0.027) and hepatic removal of lactate (r=-0.70; P=0.08) and oxygen (r=-0.77; P=0.039), as well as between hepatic glucose net output and removal of lactate (r=-0.92; P=0.004). Minimally-invasive, US-guided transcutaneous catheter placement into the cranial mesenteric, portal and hepatic veins as well as the technique for catheterization of the abdominal aorta appear to be safe, and suitable for studies of quantitative hepatic metabolism in cattle.     

Portal blood flow in beef steers: comparison of techniques and relation to hepatic blood flow, cardiac output and oxygen uptake

We compared two techniques for measuring blood flow through portal-drained viscera (PDV) of beef steers and measured portions of cardiac output and total oxygen uptake attributable to PDV and hepatic tissues. Four steers (198 +/- 2 kg), equipped with chronic catheters in appropriate vessels, a transit-time ultrasound probe around the hepatic portal vein and a temporary cardiac output thermodilution catheter, were fed a 60:40 hay: concentrate diet. Treatments, designed to alter blood flow, were: 12 equal meals every 2 h (CNTL); CNTL plus 2 mg clenbuterol in one meal (CLEN); and a 65-h fast (FAST). Blood flow through PDV was measured by dilution of p-aminohippurate (PAH) and transit-time ultrasound. Hepatic blood flow was measured by PAH dilution and cardiac output was measured by thermodilution. Blood flow measured by transit-time ultrasound was consistently slower (45%, P less than .01) than blood flow measured by PAH dilution. Necropsy revealed anatomical constraints that precluded proper placement and function of the flow probes. Cardiac output (liters/h) was greater (P less than .05) for CLEN (3,082) than for CNTL (1,655) or FAST (1,047). Percentage of cardiac output flowing through PDV and hepatic tissues was less (P less than .05) for CLEN (23 and 24%) than for CNTL (31 and 38%) or FAST (32 and 38%). Whole body oxygen uptake (mmol/h) was greatest (P less than .05) for CLEN (4,220), intermediate for CNTL (2,999) and least for FAST (1,965). Percentage of oxygen uptake attributable to hepatic tissues was greater (P less than .05) for FAST (31%) than for CLEN (18%), with CNTL intermediate (24%). Percentage of oxygen uptake attributable to PDV (22%) was not affected (P greater than .05) by treatments.     

Dynamic computed tomographic quantitation of hepatic perfusion in dogs with and without portal vascular anomalies

OBJECTIVE: To compare hepatic, pancreatic, and gastric perfusion on dynamic computed tomography (CT) scans of clinically normal dogs with those of dogs with portal vascular anomalies. SAMPLE POPULATION: Dynamic computed tomography (CT) scans of 10 clinically normal dogs and 21 dogs with portal vascular anomalies. PROCEDURES: Retrospective analysis of dynamic CT scans. Hepatic arterial perfusion, hepatic portal perfusion, total hepatic perfusion, hepatic perfusion index, gastric perfusion, and pancreatic perfusion were calculated from time attenuation curves. RESULTS: Mean +/- hepatic arterial perfusion was significantly higher in affected dogs (0.57 +/- 0.27 mL/min x mL(-1)) than in clinically normal dogs (0.23 +/- 0.11 mL/min x mL(-1)), and hepatic portal perfusion was significantly lower in affected dogs (0.52 +/- 0.47 mL/min x mL(-1)) than in clinically normal dogs (1.08 +/- 0.45 mL/min x mL(-1)). This was reflected in the hepatic perfusion index, which was significantly higher in affected dogs (0.59 +/- 0.34), compared with clinically normal dogs (0.19 +/- 0.07). Gastric perfusion was significantly higher in dogs with portal vascular anomalies (0.72 +/- 0.44 mL/min x mL(-1)) than in clinically normal dogs (0.41 +/- 0.21 mL/min x mL(-1)), but total hepatic perfusion and pancreatic perfusion were not significantly different. Among subgroups, dogs with congenital intrahepatic portosystemic shunts and dogs with arterioportal fistulae had higher hepatic arterial perfusion than did clinically normal dogs. Dogs with congenital intrahepatic portosystemic shunts also had an increase in gastric perfusion and hepatic perfusion index. CONCLUSIONS AND CLINICAL RELEVANCE: Hepatic perfusion variables measured on CT scans revealed differences in hemodynamics between clinically normal dogs and those with portal vascular anomalies.     

Secretion of dopamine and norepinephrine in hypophyseal portal blood and prolactin in peripheral blood of Holstein cattle

The objective was to test the hypothesis that dopamine regulates prolactin (PRL) secretion by determining acute changes in catecholamine concentrations in hypophyseal portal blood of cattle, and their relation to peripheral blood concentration of PRL in hypophyseal stalk-transected (HST) and sham-operated controls (SOC). Holstein heifers (606 +/- 21 kg BW; mean +/- SE) were subjected to neurosurgery for 8 h to collect hypophyseal portal blood with a stainless steel cannula designed with a cuff placed under the pituitary stalk and peripheral blood via a jugular vein catheter. PRL plasma concentration was measured by radioimmunoassay, and dopamine and norepinephrine in portal plasma by radioenzymatic assay. During anesthesia before HST or SOC, PRL plasma concentration ranged from 20-40 ng/ml throughout 255 min. PRL abruptly increased and remained above 90 ng/ml after HST compared with a steady decrease to <20 ng/ml in SOC heifers throughout 440 min. Within 5 min after severing the hypophyseal stalk, dopamine in portal blood (>8 ng/ml) was significantly increased (P < 0.05) compared with peripheral blood (<2 ng/ml). Norepinephrine concentration in portal blood was significantly greater (P < 0.05) than in peripheral blood during the first 60 min. The sustained high PRL level in peripheral plasma after severing the hypophyseal stalk stimulated hypothalamic dopamine secretion from hypophyseal portal vessels during the prolonged period of blood collection. Norepinephrine concentration in these cattle was greater in hypophyseal portal than in peripheral blood, implicating both an important hypothalamic source of the catecholamine as well as an adrenal gland contribution during anesthesia.     

Effects of head-down positioning on regional central nervous system perfusion in isoflurane-anesthetized horses

OBJECTIVE: To test the hypothesis that head-down positioning in anesthetized horses increases intracranial pressure (ICP) and decreases cerebral and spinal cord blood flows. ANIMALS: 6 adult horses. PROCEDURES: For each horse, anesthesia was induced with ketamine hydrochloride and xylazine hydrochloride and maintained with 1.57% isoflurane in oxygen. Once in right lateral recumbency, horses were ventilated to maintain normocapnia. An ICP transducer was placed in the subarachnoid space, and catheters were placed in the left cardiac ventricle and in multiple vessels. Blood flow measurements were made by use of a fluorescent microsphere technique while each horse was in horizontal and head-down positions. Inferential statistical analyses were performed via repeated-measures ANOVA and Dunn-Sidak comparisons. RESULTS: Because 1 horse developed extreme hypotension, data from 5 horses were analyzed. During head-down positioning, mean +/- SEM ICP increased to 55+/-2 mm Hg, compared with 31+/-2 mm Hg during horizontal positioning; cerebral perfusion pressure was unchanged. Compared with findings during horizontal positioning, blood flow to the cerebrum, cerebellum, and cranial portion of the brainstem decreased significantly by approximately 20% during head-down positioning; blood flows within the pons and medulla were mildly but not significantly decreased. Spinal cord blood flow was low (9 mL/min/100 g of tissue) and unaffected by position. CONCLUSIONS AND CLINICAL RELEVANCE: Head-down positioning increased heart-brain hydrostatic gradients in isoflurane-anesthetized horses, thereby decreasing cerebral blood flow and, to a greater extent, increasing ICP. During anesthesia, CNS regions with low blood flows in horses may be predisposed to ischemic injury induced by high ICP.     

Assessment of acid-base status and plasma lactate concentrations in arterial,mixed venous,and portal blood from dogs during experimental hepatic blood inflow occlusion

OBJECTIVE: To determine the effects of extended experimental hepatic blood flow occlusion (ie, portal triad clamping [PTC]) in dogs by measuring acid-base status and plasma lactate concentrations in arterial, mixed venous, and portal blood and evaluating the relationship between metabolic and concurrent hemodynamic changes. ANIMALS: 6 healthy Beagles. PROCEDURE: During anesthesia with isoflurane, cardiac output and arterial blood pressure were measured. Arterial, mixed venous, and portal blood samples were collected simultaneously for blood gas analyses and plasma lactate measurements before PTC and at 8-minute intervals thereafter. RESULTS: PTC resulted in severe hemodynamic and metabolic alterations. Eight minutes after PTC, significant decreases in cardiac index from a baseline value of 3.40 +/- 0.27 to 1.54 +/- 0.26 L/min/m2 and in mean arterial blood pressure from a baseline value of 74 +/- 6 to 43 +/- 6 mm Hg were recorded. After PTC, results indicative of lactic acidosis were found in portal blood at 16 minutes, in mixed venous at 32 minutes, and in arterial blood at 48 minutes. Significant differences in measured variables were also found between arterial and portal blood samples, between mixed venous and portal blood samples, and between arterial and mixed venous blood samples after PTC, compared with differences at baseline. CONCLUSIONS AND CLINICAL RELEVANCE: Analysis of mixed venous blood is preferable to analysis of arterial blood in the assessment of metabolic derangement. In a clinical setting, occluded portal blood is released to the systemic circulation, and the degree of reperfusion injury may depend on the metabolic status of pooled portal blood.     

Relationship between level of forage intake,blood flow and oxygen consumption by splanchnic tissues of sheep fed a tropical grass forage

Four Polwarth castrated male sheep (42 ± 4.4 kg live weight (LW) surgically implanted with chronic indwelling catheters into the mesenteric, portal and hepatic veins, housed in metabolism cages and offered Cynodon sp. hay at rates (g of dry matter (DM)/kg LW) of 7, 14, 21 or ad libitum, were used in a 4 × 4 Latin square experiment to evaluate the effect of the level of forage intake on blood flow and oxygen consumption by the portal‐drained viscera (PDV), liver and total splanchnic tissues (ST). The portal blood flow and the oxygen consumption by PDV linearly increased at increased organic matter (OM) intake. No effect of level of OM intake was obtained for the hepatic artery blood flow and oxygen consumption by liver. As a consequence, the level of OM intake only tended to directly affect hepatic blood flow and oxygen consumption by total ST. Oxygen consumption was linearly and positively related to blood flow across PDV, liver and total ST. The heat production by PDV and total ST, as proportion of metabolizable energy (ME) intake, decreased curvilinearly at increased ME intake. In conclusion, the oxygen consumption by PDV, but not by liver, was directly related to the level of forage intake by sheep. Moreover, when ingested at levels below maintenance, most of ME was spent as heat produced by ST.     

Effects of propionate infusion and dietary energy on dry matter intake in sheep

Four nonlactating, nonpregnant, mature ewes equipped with multiple venous and arterial catheters were used to evaluate the influence of propionate as a satiety signal in ruminants. Our experiment was a 4 x 4 Latin square with portal infusion (physiological saline [Sa] or sodium propionate [Pr]) and DE intake (Lo, 63% of maintenance requirement, or Hi, 200% of maintenance requirement) as factors. One 240-min infusion of Pr (1 mmol/min) or Sa into the portal vein began at approximately 0800 on d 8 of each 8-d period. Feed intake was measured and hepatic blood was sampled every 30 min during infusion. Intake of DM and digestible energy (DEI) during infusion were not affected by infusion or diet and were most rapid at 30 min postfeeding. Average 30-min DMI and DEI were 539 g and 1,484 kcal, respectively, at 240 min. Cumulative DMI and DEI were unaffected by infusion but tended to be greater with Lo. After 30 min, animals tended to consume Lo at a greater rate than Hi, suggesting that satiety was delayed. Insulin concentration was increased (P less than .02) when animals consumed Hi (36.1 mU/liter) vs Lo (16.8 mU/liter) and was elevated (P less than .01) at 30 and 60 min postfeeding when animals were infused with Pr. Plasma acetate tended to be reduced with Pr infusion. Plasma Pr tended to increase with Pr infusion, especially when sheep were fed Lo. Satiety, DMI, and DEI were not affected by Pr infusion in this study.     

Nitric oxide generation in a rat model of acute portal hypertension

OBJECTIVE: To document blood nitric oxide concentrations in the portal vein and systemic circulation in a rat model of acute portal hypertension and compare values with a control group and a sham surgical group. ANIMALS: 30 rats; 10 controls (group 1), 10 sham surgical (group 2), and 10 rats with surgically induced acute portal hypertension (group 3). PROCEDURE: Following induction of anesthesia, catheters were placed surgically in the carotid artery, jugular, and portal veins of group 2 and 3 rats and in the carotid artery and jugular vein of group 1 rats. Baseline heart and respiratory rates, rectal temperature, and vascular pressure measurements were obtained, and blood was drawn from all catheters for baseline nitric oxide (NO) concentrations. Acute portal hypertension was induced in the group 3 rats by tying a partially occluding suture around the portal vein and a 22-gauge catheter. The catheter was then removed, resulting in a repeatable degree of portal vein impingement. After catheter placement, all variables were remeasured at 15-minute intervals for 3 hours. RESULTS: Blood nitric oxide concentrations were greater in all vessels tested in group 3 than in group 2 rats. CONCLUSIONS AND CLINICAL RELEVANCE: Acute portal hypertension in this experimental model results in increased concentrations of NO in the systemic and portal circulation. On the basis of information in the rat, it is possible that increased NO concentrations may develop in dogs following surgical treatment of congenital portosystemic shunts if acute life-threatening portal hypertension develops. Increased NO concentrations may contribute to the shock syndrome that develops in these dogs.     

Concentrations of free steroids in the jugular and hepatic portal veins of pigs after ingestion of testosterone, estrogen, or progesterone or transplantation of ovaries to the intestine.

Estrogen, progesterone or testosterone were administered orally to ovariectomized gilts fitted with indwelling catheters. Blood samples were taken from the jugular and hepatic portal veins at intervals varying from a few minutes to daily over periods that varied from 1 d to several months. Concentrations of free steroids rose dramatically in the hepatic portal vein within a few min of feeding steroids and remained high for 3-8 hr before declining to base levels. Concentrations in the jugular vein sometimes rose very slightly for the same period. At 48 hr after administration the concentrations remained at baseline in the hepatic portal vein, but rose several-fold in the jugular and remained elevated for several days. Autotransplantation of the ovaries to the intestine resulted in very large ovaries consisting of many large, heavily luteinized cystic follicles. Concentrations of progesterone and estrogen in the hepatic portal vein were very high, but were low in the jugular vein. The gut wall allows for passage of some orally administered free steroids to the liver via the hepatic portal vein. The free steroids are essentially metabolized before they reach the jugular vein, but can be recirculated via the enterohepatic route.     

Net absorption of amino acids by portal-drained viscera and hind half of beef cattle fed a high concentrate diet

Two experiments were conducted to measure the effect of level of feed intake on net amino acid absorption by portal-drained viscera of six beef heifers with catheters in a mesenteric vein, portal vein and iliac artery (Exp. 1) and to evaluate intrajugular infusion of insulin or glucose on amino acid uptake by hind half of four beef steers with catheters in posterior aorta and vena cava (Exp. 2). Experiment 1 was a replicated 3 X 3 Latin square design. Treatments were calculated intakes of 84, 157 or 225 kcal metabolizable energy (ME)/kg.75 live weight. Treatments in Exp. 2 were control (no infusion), insulin infusion (1.4 IU/min for 90 min) and glucose infusion (2.5 mmol/min for 90 min) in that order. Mean live weight of animals +/- SE was 295 +/- 4 kg (Exp. 1) and 345 +/- 15 kg (Exp. 2). The diet used in both experiments was pelleted, 85% concentrate (2.9 Mcal ME/kg dry matter). Blood flow (BF) was measured by dilution of a primed, continuous infusion of para-aminohippuric acid into the mesenteric vein (Exp. 1) or the posterior aorta (Exp. 2). Net uptake or absorption was the product of BF times portal-arterial (Exp. 1) or arteriovenous (Exp. 2) differences in amino acid concentrations in blood. Increased feed intake caused linear (P less than .05) increases in net absorption of several amino acids, including lysine, methionine, leucine and valine (Exp. 1). Feed intake did not affect (P greater than .05) net absorption of glutamate or glutamine.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of increasing ruminal butyrate on portal and hepatic nutrient flux in steers.

Six Holstein steers (mean +/- SE BW = 344 +/- 10 kg) fitted with hepatic, portal, and mesenteric vein and mesenteric artery catheters and a ruminal cannula were used in a 6 x 6 Latin square design to evaluate the effects of increasing ruminal butyrate on net portal-drained visceral and hepatic nutrient flux. Steers were fed a 40% brome hay, 60% concentrate diet in 12 portions daily at 1.25 x NEm. Water (control) or butyrate at 50, 100, 150, 200, or 250 mmol/h was supplied continuously via the ruminal cannula. Simultaneous arterial, portal, and hepatic blood samples were taken at hourly intervals from 15 to 20 h of ruminal infusion. Portal and hepatic blood flow was determined by continuous infusion of P-aminohippurate, and net nutrient flux was calculated as the difference between venous and arterial concentrations times blood flow. Ruminal and arterial concentrations and total splanchnic flux of butyrate increased (P less than .01) with increased butyrate infusion. Arterial concentrations of acetate (P less than .10), alpha-amino-N (P less than .05), and glucose (P less than .01) decreased with increased butyrate, whereas arterial beta-hydroxybutyrate (P less than .01) and acetoacetate (P less than .05) increased. Increased butyrate produced an increased portal-drained visceral flux of acetoacetate and an increased net hepatic flux of beta-hydroxybutyrate. Urea N and glucose net portal and hepatic fluxes were not affected by ruminal butyrate. Alpha-amino-N uptake by the liver decreased with increased butyrate (P less than .10). Simple linear regression (r2 = .985) indicated that 25.8% of ruminally infused butyrate appeared in portal blood as butyrate. Only 14% could be accounted for as net portal-drained visceral flux of acetoacetate plus beta-hydroxybutyrate.