Permanent Indwelling Catheters Research Articles

Resolution of urethral obstruction using temporary urethral stents in two female cats.

The management of urethral obstructions is well documented in male cats but is less established for females. These cases describe two female cats that presented with non-dissolvable urocystoliths. Urocystoliths were removed by laser lithotripsy and basket retrieval. Following urolith removal, urethral obstruction occurred in both cats. Both cats were successfully managed using temporary urethral stents in lieu of indwelling urethral catheters permitting outpatient, spontaneous recovery of the urethra. Use of temporary urethral stents has not been described in cats. These novel stents are constructed from materials available in most veterinary facilities, placed without advanced imaging and reside entirely within the urethra and vestibule. Temporary stents are used to bypass urethral disease, facilitating outpatient recovery, and are easily removed when no longer needed. For these reasons, temporary stents are a cost-efficient alternative to permanent stents or indwelling urinary catheters attached to closed urine-collection systems.

Current treatment options of refractory ascites in liver cirrhosis - A systematic review and meta-analysis.

Refractory ascites is a severe complication of liver cirrhosis and treatment options consist in large volume paracentesis, transjugular intrahepatic portosystemic shunt, alfapump®, peritoneovenous shunt and permanent indwelling peritoneal catheter. Our aim was to assess the efficacy, mortality and complications of each treatment. We performed a systematic review using Pubmed and Embase. Frequencies were summarized with Comprehensive Meta-Analysis Software. Seventy-seven studies were included. In patients with transjugular intrahepatic portosystemic shunt, 1-year mortality was 33% (95% CI 0.29-0.39, I2=82.1; τ2=0.37; p<0.001) with lower mortality in newer studies (26% vs. 44%). At 6 months, mortality in patients with alfapump® was 24% (95% CI 0.16-0.33, I2=0.00; τ2=0.00; p=0.83), 31% developed acute kidney injury (95% CI 0.18-0.48, I2=44.0; τ2=0.22; p=0.15). Mortality at 12 months was 44% (95% CI 32%-58%, I2=76.7, τ2=0.44, p<0.001) in peritoneovenous shunts and 45% (95% CI 38%-53%, I2=61.4, τ2=0.18, p=0.003) in large volume paracentesis, respectively. Overall mortality in patients with permanent indwelling catheters was 66% (95% CI 33%-89%, I2=82.5, τ2=1.57, p=0.001). Mortality in patients with transjugular intrahepatic portosystemic shunt was lower in newer studies, probably due to a better patient selection. Acute kidney injury was frequent in patients with alfapump®. Permanent indwelling catheters seemed to be a good option in a palliative setting.

Sodium butyrate improves antioxidant stability in sub-acute ruminal acidosis in dairy goats

BackgroundCurrently, little is known about the effect of sodium butyrate (NaB) on oxidative stress following grain-induced sub-acute ruminal acidosis in dairy goats. In the present study, 18 lactating dairy goats implanted with a ruminal cannula and permanent indwelling catheters in the portal and hepatic veins were randomly allocated into 3 treatment groups over 20 weeks: low grain (LG, 40% grain; n = 6), high grain (HG, 60% grain; n = 6) and high grain with sodium butyrate (HG + NaB, 60% grain + NaB; n = 6).ResultsWhen added to the HG diet, NaB increased the mean ruminal pH and reduced the levels of ruminal, portal and hepatic LPS; Additionally, we observed an increase in SOD1, SOD2, SOD3, GPX1 and CAT mRNA expression, increased levels of TSOD and CAT enzyme activity as well as increased total antioxidant capacity (T-AOC) and decreased malondialdehyde (MDA) in both the liver and plasma, while GPx activity increased in the liver of goats fed the HG + NaB diet. The mRNA expression of UGT1A1, NQO1, MGST3, and Nrf2, as well as total Nrf2 protein levels were increased in goats fed the HG + NaB diet.ConclusionsOur study indicates that sodium butyrate could improve the oxidative status in sub-acute ruminal acidosis through the partial activation of Nrf2-dependent genes.

Risk factors of postoperative urinary retention after hip surgery for femoral neck fracture in elderly women

The aim of the present study was to evaluate risk factors for postoperative urinary retention (POUR) in female patients with femoral neck fractures. We recruited 72 female patients (age 86.5 ± 6.7 years) from among 90 cases of hip surgery carried out between January and December 2011 at Goto Chuo Hospital. We evaluated the risk factors for POUR, including the administration of anticholinergic drugs, diabetes mellitus, preoperative dementia and/or delirium, neurological disorders, age, hypertension, overactive bladder, and the postoperative duration of the use of an indwelling urethral catheter using a multiple logistic regression analysis. In the present study, POUR occurred in eight out of 72 cases (11.1%). The multivariate analysis showed that the indwelling period of the urethral catheter (per 1-day increase; P = 0.04, OR 0.33 95% CI 0.11-0.96), and preoperative dementia and/or delirium (P = 0.03, OR10.4, 95%CI 1.21-89.2) correlated with the occurrence of POUR. Diabetes mellitus (P = 0.78), anticholinergic agents (P = 0.23), neurological disorders (P = 0.83), age (P = 0.86), hypertension (P = 0.76) and overactive bladder (P = 0.34) did not significantly correlate with the occurrence of POUR. The present study showed that the early removal of the urethral catheter, and preoperative dementia and/or delirium had significant correlations with POUR. The femoral neck fractures and the surgical procedure used for the hip surgery do not induce damage to the bladder and nerve system related to the voiding function, and the voiding function in all of the patients recovered after short-term intermittent catheterization. Physicians should not place permanent indwelling urethral catheters without carrying out urological assessments.

Effects of β-hydroxy β-methyl butyrate supplementation to sows in late gestation on absorption and hepatic metabolism of glucose and amino acids during transition

A multicatheter sow model was established to study the effects of dietary β-hydroxy β-methyl butyrate (HMB) supplementation on net portal flux (NPF) and net hepatic flux (NHF) of HMB, glucose, and the AA Ala, Gly, Ile, Leu, Phe, Tyr, and Val. Eight second parity sows were fitted with permanent indwelling catheters in an artery and in the portal, hepatic, and mesenteric veins. Eight hourly sets of blood samples were taken starting 30 min before the morning meal on day -3 and day 3 relative to parturition. Four control (CON) sows were fed a standard lactation diet from day -15 and throughout the experiment, and 4 HMB sows were fed the control diet supplemented with 15 mg Ca(HMB)(2)/kg BW mixed in one third of the morning meal from day -10 until parturition. Net portal flux of HMB was affected by treatment (Trt; P < 0.01) and peaked in the HMB sows at 6.9 mmol/h 30 min after the morning meal and then decreased towards preprandial level (0.0 mmol/h) 3.5 h after the meal, revealing that dietary HMB was rapidly absorbed from the intestine. The NHF of HMB tended to be affected by Trt (P = 0.06) showing a small hepatic uptake of HMB (1.1 mmol/h) in HMB sows. Net portal flux of glucose and all measured AA, except for Gly and Tyr, were affected the Trt × time interaction (P < 0.01). The NPF was positive for all nutrients, indicating absorption from the intestine to the portal blood. Absorption rates appeared to be more stable for HMB than for CON sows. Net hepatic flux of glucose was not affected by Trt. It was negative from 1.5 to 2.5 h after the meal, indicating hepatic uptake, but positive before and after, indicating net hepatic release of glucose. Net hepatic fluxes of AA were negative and were not affected by Trt (P > 0.10), except for Phe (P < 0.05). In conclusion, HMB reduced the variation in net portal flux of glucose and AA during 8 h of blood sampling and suggest that the improved sow productivity observed by others may be due to a more uniform nutrient absorption pattern into portal blood.

Effect of abomasal infusion of oligofructose on portal-drained visceral ammonia and urea-nitrogen fluxes in lactating Holstein cows

The effects of abomasal infusion of oligofructose in lactating dairy cows on the relationship between hindgut fermentation and N metabolism, and its effects on NH3 absorption and transfer of blood urea-N across the portal-drained viscera versus ruminal epithelia were investigated. Nine lactating Holstein cows fitted with ruminal cannulas and permanent indwelling catheters in major splanchnic blood vessels were used in an unbalanced crossover design with 14-d periods. Treatments were continuous abomasal infusion of water or 1,500g/d of oligofructose. The same basal diet was fed with both treatments. Eight sample sets of arterial, portal, hepatic, and ruminal vein blood, ruminal fluid, and urine were obtained at 0.5h before the morning feeding and at 0.5, 1.5, 2.5, 3.5, 4.5, 5.5, and 6.5h after feeding. It was hypothesized that an increased supply of fermentable substrate to the hindgut would increase the uptake of urea-N from blood to the hindgut at the expense of urea-N uptake to the forestomach. The study showed that abomasal oligofructose infusion decreased the total amount of urea-N transferred from the blood to the gut, NH3 absorption, and arterial blood urea-N concentration. Subsequently, hepatic NH3 uptake and urea-N production also decreased with oligofructose infusion. Additionally, urea-N concentration in milk and urinary N excretion decreased with oligofructose treatment. The oligofructose infusion did not affect ruminal NH3 concentrations or any other ruminal variables, nor did it affect ruminal venous − arterial concentration differences for urea-N and NH3. The oligofructose treatment did not affect milk yield, but did decrease apparent digestibility of OM, N, and starch. Nitrogen excreted in the feces was greater with the oligofructose infusion. In conclusion, the present data suggest that increased hindgut fermentation did not upregulate urea-N transfer to the hindgut at the expense of urea-N uptake by the rumen, and the observed reduction in arterial blood urea-N concentration appeared not to be due to increased urea-N transport, but rather could be explained by reduced NH3 input to hepatic urea-N synthesis caused by increased sequestration of NH3 in the hindgut and excretion in feces. Increasing the hindgut fermentation in lactating dairy cows by abomasal infusion of 1,500g/d of oligofructose shifted some N excretion from the urine to feces and possibly reduced manure NH3 volatilization without impairing rumen fermentation.

The management of malignant ascites in Palliative care: An audit of clinical practice and development of standards and guidelines

BackgroundMalignancy is the underlying cause in approximately 10% of all cases of ascites. About 15–50% of patients with malignancy will develop ascites. Cancers commonly associated with the development of ascites...

Effect of time duration of ruminal urea infusions on ruminal ammonia concentrations and portal-drained visceral extraction of arterial urea-N in lactating Holstein cows

The effects of a 6 versus 24h ruminal urea infusion in lactating dairy cows fed a basal diet deficient in N on ruminal ammonia concentration, arterial urea-N concentration, net portal-drained viscera (PDV) urea-N flux, arterial urea-N extraction across the PDV, and renal urea-N kinetics were investigated. Three Danish Holstein cows fitted with ruminal cannulas and permanent indwelling catheters in major splanchnic blood vessels were randomly allocated to a 3 × 3 Latin square design with 21-d periods. Treatments were ventral ruminal infusion of water for 24h (water INF), 24-h infusion of 15g of urea/kg of dry matter intake (DMI; 24-h INF), and 6-h infusion of 15g of urea/kg of DMI (6-h INF). The 6-h INF was initiated 0.5h after the afternoon feeding, and ran until 2230h. Eight sample sets of arterial, portal, and hepatic blood, ruminal fluid, and urine were obtained at 0.5h before the morning feeding and 0.5, 1.5, 2.5, 3.5, 4.5, 5.5, and 6.5h after feeding (i.e., 9 to 15.5h after the 6h infusion was terminated). A substantial decrease in DMI for 6-h INF compared with 24-h INF and water INF was observed, and it has to be recognized that DMI may have confounding effects. However, the experimental setting plan was met (i.e., to cause changes in the daily pattern of ruminal ammonia and blood urea-N concentrations). The arterial urea-N concentration for 24-h INF and 6-h INF were greater than the arterial urea-N concentration with water INF throughout the sampling window. However, the arterial urea-N concentration for 6-h INF decreased steadily with sampling time reflecting a carryover effect from the ruminal urea infusion. The ruminal ammonia concentration and net portal flux of ammonia for 6-h INF were not different from water INF; hence, no carryover effect on ruminal ammonia concentration was observed. The portal flux of urea-N was not affected by treatment (i.e., even the combination of low ruminal ammonia and high arterial urea-N concentration with 6-h INF was not used by the cow to increase the uptake of urea-N across the PDV). Arterial urea-N extraction across the PDV was increased with water INF especially from 0.5 to 3.5h postprandial relative to the urea infusion treatments, reflecting increased epithelial permeability for urea-N. This indicates that daily ruminal peak of ammonia or blood urea-N concentrations overruled potential signals from low ruminal ammonia concentration observed during the sampling window. In conclusion, dairy cows appear unable to increase transport of urea-N from blood to gut in periods with low ruminal ammonia concentrations, even in a situation with infrequent N supply and apparent carryover effects on blood urea-N. It is speculated that mechanisms responsible for downregulation of epithelial urea-N transport based on daily maximum concentrations of ammonia in the rumen or urea-N in the blood suppresses any short-term signal from low ruminal ammonia during periods with low ruminal N supply.

Metabolic effects of feeding high doses of propanol and propylacetate to lactating Holstein cows

Three lactating Holstein cows implanted with ruminal cannulas and permanent indwelling catheters in major splanchnic blood vessels were used to investigate alcohol metabolism and metabolic effects of feeding high doses of propanol and propylacetate. Cows were fed three diets control (basal ration; C), propanol (C plus 50g propanol/kg DM; P), and propylacetate (C plus 50g propanol/kg DM and 15g propylacetate/kg DM; PPA) in a 3×3 Latin square design with 14d period. Daily rations were fed in three equally sized portions at 8 hour intervals and 8 hourly sets of ruminal fluid, arterial, hepatic portal vein, and hepatic vein samples were collected at day 14 of each period. Milk fat yield decreased for P and PPA compared with C, however, dry matter intake and milk yield were not affected by treatment. Portal uptake of propanol accounted for 48 to 61% of ingested propanol and differed among all 3 treatments C≪PPA<P. A number of metabolic variables responded to P and PPA treatments including decreased proportion of ruminal acetate to total VFA; increased proportions of ruminal propionate, isovalerate, valerate, and caproate; increased arterial glucose concentration; decreased arterial BHBA and acetate concentrations; increased net portal flux of propanol; increased net hepatic flux of glucose; and increased propanol, isopropanol, and caproate uptake by the liver. Contrary to our hypothesis that propylacetate supplementation would exacerbate the metabolic effects of propanol, we observed for a number of variables that treatment differences between C and P were partly reversed in PPA. This applied to ruminal propanol and propylacetate; arterial concentrations of ethanol, propanol, isopropanol, and isobutyrate; net portal flux of ethanol, propanol, and isopropanol; net hepatic flux of BHBA, propanol, isopropanol, and isobutyrate; net splanchnic flux of propionate; hepatic extraction of ethanol and portal recovery of dietary ethanol. The overall metabolic effect of feeding large doses of propanol was a glucogenic response presumably driven by hepatic metabolism of propanol to propionate and the increased glucogenic status was followed by a decreased milk fat yield. Inclusion of propylacetate in the diet apparently activated increased metabolism of propanol in either the rumen or ruminal epithelium and reduced the metabolic impact of the combined presence of propanol and propylacetate.

Effect of amino acid or casein supply on whole-body, splanchnic, and mammary glucose kinetics in lactating dairy cows

This study was conducted to establish how AA supplied in a free form or as protein (casein, CN) affect the whole-body rate of appearance (WB Ra) of glucose, splanchnic and mammary glucose kinetics, and milk lactose secretion in lactating dairy cows. Five Holstein cows fitted with a rumen cannula and permanent indwelling catheters in the abomasum, portal, hepatic, and mesenteric veins, and one mesenteric artery, were used in a Youden square with 4 periods of 14 d each. Cows were fed a hay-based diet providing 100 and 70% of their net energy and metabolizable protein (MP) requirements, respectively. Treatments consisted of abomasal infusions of water (70% of MP requirements: control, Con), free AA (95% of MP requirements: AA1; and 120% of MP requirements: AA2), or CN (95% of MP requirements: CN1). The free AA mixture had the same profile as CN. On d 14 of each period, [6,6-2H2]glucose (25.8 mmol/h) was infused into a jugular vein, and blood samples (n=8) were taken over 4h from arterial, portal, hepatic, and mammary sources to measure glucose enrichment and concentration. Splanchnic and mammary plasma flows were determined by downstream dilution of para-aminohippurate and with the Fick principle, respectively. The last 6 milkings of each period were weighed and sampled to measure the yields of milk and components. The AA1 and CN1 treatments were not different for any of the measured parameters. Supplying AA linearly increased glucose WB Ra (AA2 vs. Con: +151 mmol/h) and liver net flux (+149 mmol/h). Utilization of glucose from the plasma compartment by the portal-drained viscera and liver and true portal absorption were not affected by AA supply. From these observations, we suggest that the increased WB Ra was due to increased net hepatic production. The AA from the infusion, in excess of that used to cover the increase in milk protein, were converted to glucose with an apparent efficiency close to 100% of maximum theoretical efficiency. Milk and lactose yields increased linearly with infusions of AA, by 14 and 16% with AA2 treatment, respectively. However, mammary glucose uptake was not significantly altered by AA infusions; this suggests that the mammary gland exerts active control on the uptake and utilization of glucose. For all treatments, the sum of true portal glucose absorption and true hepatic glucose production contributed more than 99% of WB Ra in the lactating cow; this would suggest that renal glucose synthesis makes only a small contribution to WB Ra under these conditions.

Validation of 99m-Technetium Labelled Mebrofenin Hepatic Extraction Method to Quantify Meal Induced Splanchnic Blood Flow Responses Using a Porcine Model

Purpose: The objective of this study was to evaluate a clinical diagnostic method to measure the total splanchnic blood flow (SBF) using the Fick principle and a tracer (99m-Technetium labelled mebrofenin) (Tc99-M) extracted by the liver(1; 2). The method was tested against an indicator dilution method independent of liver extraction using paraaminohippuric acid (PAH) as the indicator in a multi-catheterized porcine model. We also wanted to investigate whether Tc99-M was metabolized in any way in the intestines. Methods: Five permanent indwelling catheters were placed in the abdominal aorta, the inferior vena cava, the portal vein, the hepatic vein, and the superior mesenteric vein in 15 pigs (average weight 60 kg). Two weeks after surgery the SBF was measured by both methods and the portal blood flow, intestinal, and hepatic oxygen uptake, and net intestinal and hepatic fluxes of lactate, and glucose, were measured before and for 70 minutes after ingestion of a standard meal. The concentration of Tc99-M was measured in plasma from the hepatic vein, the portal vein, and the abdominal aorta for each sampling time. The placement of catheters was confirmed at autopsy. Results: The mean baseline SBF was 2961 and 2762 mL/min measured by PAH and Tc99-M, respectively, with a non-significant difference (p = 0.12) between the two methods. The SBF increased significantly after the meal to 3977 measured by Tc99-M and 3981 mL/min measured by PAH, respectively, with no significant difference (p = 0.98) between the two methods. Total splanchnic O2-flux was at baseline 7.19 ± 0.20 mmol/min and 9.81 ± 0.30 after feeding (p < 0.001), the intestinal O2-flux 3.75 ± 0.16mmol/min vs. 4.92 ± 0.13 mmol/min postprandial (p < 0.001). The arterial-portal difference in Tc99-M concentration was 0.21% of the arterial concentration (p = 0.48), indicating no net intestinal extraction or metabolism. Conclusion: The Fick principle is a robust technique for measuring the total SBF when compared to the indicator dilution method. Because there was no difference in the content of Tc99-M between the arterial and portal vein plasma, the SBF can be determined from an arterial and a hepatic vein sample. Tc99-M may potentially detect splanchnic ischemia and other perfusion disturbances in man.

Effects of supplementation with 2-hydroxy-4-(methylthio)-butanoic acid isopropyl ester on splanchnic amino acid metabolism and essential amino acid mobilization in postpartum transition Holstein cows

The present study aimed to investigate the effects of 2-hydroxy-4-(methylthio)-butanoic acid isopropyl ester (HMBi) supplementation on splanchnic AA metabolism, essential AA (EAA) mobilization, and plasma AA status in postpartum transition dairy cows. The EAA mobilization was calculated by difference: EAA excretion in milk protein − net portal absorption of EAA or net splanchnic release of EAA. Eight Holstein cows fitted with permanent indwelling catheters in the hepatic portal vein, hepatic vein, mesenteric vein, and an artery in the dry period preceding second parturition were used in the study. Cows were randomly allocated to 1 of 4 treatments in a 2×2 factorial arrangement with factor 1: control (calcium carbonate) versus HMBi [1.5g of HMBi/kg of dry matter (DM)] and factor 2: high dietary ethanol (19g/kg of DM) versus high dietary propanol (16g/kg of DM). Only factor 1 data are presented. Treatments were administered in 4 total mixed rations and initiated on the day of parturition. Cows were sampled 14 d before expected parturition and 4, 15, and 29 d after parturition. Supplementation with HMBi tended to increase milk fat content but not fat yield, tended to impose a slower rate of decrease in milk casein content with increasing days in milk (DIM), prevented the decrease in plasma Met associated with parturition for control, reduced plasma concentration of Ser, tended to reduce plasma concentrations of Gly and His, and tended to increase hepatic uptake of Met postpartum. Cows excreted 248±18g more EAA in the milk at 4 DIM than was released from splanchnic tissues. The EAA deficiency decreased as lactation progressed and was not affected by HMBi supplementation. It was estimated that 4,700±600g of EAA from extra-splanchnic tissues were secreted in milk protein during the first 29 DIM. Extra-splanchnic EAA mobilization can be crucial to sustain milk protein yield in the postpartum transition period and HMBi is a fast-working Met source that can improve Met status of postpartum transition cows.

Metabolic effects of feeding ethanol or propanol to postpartum transition Holstein cows

Eight lactating Holstein cows implanted with a ruminal cannula and permanent indwelling catheters in major splanchnic blood vessels were used to investigate metabolism of propanol and ethanol in the postpartum transition period. Cows were randomly allocated to 1 of 4 treatments in a randomized design with a 2 by 2 factorial arrangement of treatments. Factor 1 was 2.6g of calcium carbonate/kg of dry matter (DM) versus 1.5g of 2-hydroxy-4-(methylthio)-butanoic acid isopropyl ester/kg of DM. Factor 2 was supplementation with 14g of propanol/kg of DM (propanol treatment; PT) versus 14g of ethanol/kg of DM (ethanol treatment; ET). Only factor 2 data are presented in the present paper. Treatments were administered in silage-based total mixed rations and cows were fed the experimental total mixed ration from the day of parturition. Daily rations were fed in 3 equally sized portions at 8-h intervals. Eight hourly sets of ruminal fluid, arterial, and hepatic portal and hepatic vein samples were collected at day −15±5, 4, 15, and 29 relative to parturition. Dry matter intake and milk yield increased with days in milk (DIM), but were not affected by treatment. From prepartum to 4 DIM ruminal concentrations of propanol and ethanol increased with PT and ET, respectively. Postpartum, alcohol intake increased 49% in PT and 34% in ET from 4 to 29 d in milk, respectively. Ruminal concentrations of the alcohols remained unaffected by DIM. Treatments did not affect total ruminal volatile fatty acid concentrations, but the molar proportion of acetate increased in ET and the molar proportion of propionate increased in PT compared with the contrasting treatment. Propanol treatment decreased milk fat content at 15 to 29 DIM compared with ET. The net portal release of propanol and ethanol increased with increasing ruminal concentration of the respective alcohol. The portal release of alcohol accounted for 43 to 85% of ingested propanol and 36 to 57% of ingested ethanol. Hepatic uptake of propanol and ethanol equaled the net portal flux and no effect of treatment was detected for net splanchnic release of propanol and ethanol. In conclusion, ruminal metabolism is a major component of alcohol metabolism in dairy cows. The postpartum transition dairy cow has sufficient metabolic capacity to cope with high dietary concentrations of primary alcohols even when alcohol intake is abruptly increased at the day of calving. Alcohol intake affects milk fat content and alcohol composition of silage might be important to improve predictions of milk composition.

Effects of nitrogen supply on inter-organ fluxes of urea-N and renal urea-N kinetics in lactating Holstein cows

The effects of decreasing ruminal urea infusion in lactating dairy cows fed a basal diet deficient in rumen degradable protein on inter-organ urea-N fluxes, epithelial urea-N extraction, and renal urea-N kinetics were investigated. Eight Danish Holstein cows fitted with a ruminal cannula and permanent indwelling catheters in the major splanchnic blood vessels and the gastrosplenic vein were used. The cows were randomly allocated to a triplicate incomplete 3×3 Latin square design with 14-d periods. Treatments were continuous ventral ruminal infusion of water, 4.1g of feed urea/kg of dry matter intake, and 8.5g of feed urea/kg of dry matter intake. Dry matter intake and milk yield decreased linearly with decreasing urea infusion. Arterial blood urea-N and ruminal ammonia concentrations decreased linearly with decreasing urea infusion. In absolute amounts, the urea-N recycling did not increase when urea infusion was decreased. Arterial urea-N extraction across the portal-drained viscera and rumen wall increased linearly with decreasing urea infusion (2.46, 3.65, and 4.32±0.31% and 7.5, 11.5, and 16.9±0.9%, respectively), indicating that cows responded to the changes in N supply. The relative urea-N extraction across the ruminal wall increased compared with the total portal-drained viscera extraction. We observed a postprandial decrease in ruminal extraction of arterial urea-N that might reflect that the activity of the protein, presumably facilitating urea-N transport, is regulated by ruminal ammonia. The urea-N clearance by the kidneys decreased (35, 30, and 25±2L/h) and the urea-N reabsorbed by the kidney increased (42, 51 and 56±3%) with decreasing urea infusion, indicating that the kidneys salvaged urea-N with low-N supply. The urea transporter B mRNA abundance in rumen papillae (papillae harvested at sampling days) was not affected by dietary N supply. The study showed, that rumen wall extraction of arterial urea-N is subjected to both long- and short-term regulation. Extraction increases with decreasing N supply long-term; however, a short-term postprandial decrease in extraction was observed. No association between long-term adaptation of urea-N extraction across the rumen wall and urea transporter B mRNA abundance could be demonstrated.

Effect of decreasing dietary phosphorus supply on net recycling of inorganic phosphate in lactating dairy cows

Five ruminally cannulated lactating Holstein cows, fitted with permanent indwelling catheters in the mesenteric vein, hepatic vein, portal vein, and an artery were used to study intestinal absorption and net recycling of inorganic phosphate (Pi) to the gastrointestinal tract. Treatments were low P (LP; 2.4g of P/kg of DM) and high P (HP; 3.4g of P/kg of DM). The dietary total P (tP) concentrations were obtained by replacing 0.50% calcium carbonate in the LP diet with 0.50% monocalcium phosphate in the HP diet. Diets were fed for 14 d and cows were sampled on d 14 in each period. Cows were fed restrictively, resulting in equal dry matter intakes as well as milk, fat, and protein yields between treatments. Net Pi recycling (primarily salivary) was estimated as the difference between net portal plasma flux (net absorption of Pi) and apparently digested tP (feed – fecal tP difference). Phosphorus intake, apparently digested tP, and fecal tP excretion decreased with LP. An effect of decreased tP intake on net portal plasma flux of Pi could not be detected. However, despite numerically minute net fluxes across the liver, the net splanchnic flux of Pi was less in LP compared with that in HP. Though arterial plasma Pi concentration decreased, net Pi recycling was not decreased when tP intake was decreased, and recycling of Pi was maintained at the expense of deposition of Pi in bones. Data are not consistent with salivary Pi secretion being the primary regulator of Pi homeostasis at low tP intakes. On the contrary, maintaining salivary Pi recycling at low tP intakes indicates that rumen function was prioritized at the expense of bone P reserves.

Effect of abomasal glucose infusion on plasma concentrations of gut peptides in periparturient dairy cows

Six Holstein cows fitted with ruminal cannulas and permanent indwelling catheters in the portal vein, hepatic vein, mesenteric vein, and an artery were used to study the effects of abomasal glucose infusion on splanchnic plasma concentrations of gut peptides. The experimental design was a randomized block design with repeated measurements. Cows were assigned to one of 2 treatments: control or infusion of 1,500g of glucose/d into the abomasum from the day of parturition to 29 d in milk. Cows were sampled 12±6 d prepartum and at 4, 15, and 29 d in milk. Concentrations of glucose-dependent insulinotropic polypeptide, glucagon-like peptide 1(7–36) amide, and oxyntomodulin were measured in pooled samples within cow and sampling day, whereas active ghrelin was measured in samples obtained 30min before and after feeding at 0800h. Postpartum, dry matter intake increased at a lower rate with infusion compared with the control. Arterial, portal venous, and hepatic venous plasma concentrations of the measured gut peptides were unaffected by abomasal glucose infusion. The arterial, portal venous, and hepatic venous plasma concentrations of glucose-dependent insulinotropic polypeptide and glucagon-like peptide 1(7–36) amide increased linearly from 12 d prepartum to 29 d postpartum. Plasma concentrations of oxyntomodulin were unaffected by day relative to parturition. Arterial and portal venous plasma concentrations of ghrelin were lower postfeeding compared with prefeeding concentrations. Arterial plasma concentrations of ghrelin were greatest prepartum and lowest at 4 d postpartum, giving a quadratic pattern of change over the transition period. Positive portal venous-arterial and hepatic venous–arterial concentration differences were observed for glucagon-like peptide 1(7–36) amide. A negative portal venous–arterial concentration difference was observed for ghrelin pre-feeding. The remaining portal venous–arterial and hepatic venous–arterial concentration differences of gut peptides did not differ from zero. In conclusion, increased postruminal glucose supply to postpartum transition dairy cows reduced feed intake relative to control cows, but did not affect arterial, portal venous, or hepatic venous plasma concentrations of gut peptide hormones. Instead, gut peptide plasma concentrations increased as lactation progressed. Thus, the lower feed intake of postpartum dairy cows receiving abomasal glucose infusion was not attributable to changes in gut peptide concentrations.

Effects of particle size and dry matter content of a total mixed ration on intraruminal equilibration and net portal flux of volatile fatty acids in lactating dairy cows

Effects of physical changes in consistency of ruminal contents on intraruminal equilibration and net portal fluxes of volatile fatty acids (VFA) in dairy cows were studied. Four Danish Holstein cows (121±17 d in milk, 591±24kg of body weight, mean ± SD) surgically fitted with a ruminal cannula and permanent indwelling catheters in the major splanchnic blood vessels were used. The experimental design was a 4 × 4 Latin square with a 2 × 2 factorial design of treatments. Treatments differed in forage (grass hay) particle size (FPS; 3.0 and 30mm) and feed dry matter (DM) content of the total mixed ration (44.3 and 53.8%). The feed DM did not affect chewing time, ruminal variables, or net portal flux of VFA. However, decreasing the FPS decreased the overall chewing and rumination times by 151±55 and 135±29 min/d, respectively. No effect of the reduced chewing time was observed on ruminal pH or milk fat percentage. Cows maintained average ventral ruminal pH of 6.65±0.02, medial ruminal pH of 5.95±0.04, and milk fat of 4.42±0.12% with chewing time of 28.0±2.1 min/kg of DM when fed short particles. The medial ruminal pool of wet particulate matter was decreased by 10.53±2.29kg with decreasing FPS, thereby decreasing the medial pool of total VFA, acetate, propionate, butyrate, isobutyrate, and isovalerate by 1,143±333, 720±205, 228±69, 140±51, 8.0±2.3, and 25.2±5.6 mmol, respectively. Ventral pool variables were not affected by treatments. Relatively large intraruminal differences of VFA concentrations and pH between the ventral and medial pools were observed, VFA concentrations being largest and pH being the lowest medially. This indicates that the ruminal mat acts as a barrier retaining VFA. The effects of reduced FPS were limited to the VFA pool sizes of the mat, leaving ruminal pH, ruminal VFA concentrations, and net portal flux of VFA unaffected. Consequently reduced FPS affected the intraruminal equilibration of VFA between mat and ventral rumen with an estimated turnover rate of isobutyrate increasing from 50±3%/h with long particles to 61±3%/h with short particles. The estimated ruminal fluid flow and therefore intraruminal VFA transport between medial and ventral phase was not affected by the FPS. In conclusion, the ruminal mat pool of VFA was proportional to the size of the mat and the only detected effects of decreasing FPS were decreasing the mat size and an increasing turnover of the mat pool of VFA.

The Stimulatory Effect of Corticotrophin on Testicular Testosterone Release in Male Rabbits

Intravenous injection of 1-24 ACTH synthetic analogue (10 micrograms/kg body weight 1-24 ACTH) via permanent indwelling jugular catheters to intact male rabbits, resulted in a rapid rise of plasma corticosteroid (C) and plasma testosterone (T) levels. Mean C levels were significantly elevated during the period between 10 and 100 min after ACTH administration whereas mean T concentrations showed a significant rise at 20 min after the 1-24 ACTH administration. On the other hand a significant suppression of plasma T levels was observed 120 min p.i., indicating a biphasic effect of 1-24 ACTH on plasma T levels. Castrated animals reacted to 1-24 ACTH with mean C levels, comparable to concentrations in intact rabbits, whereas their lowered plasma T concentrations showed no changes. When 1-24 ACTH was administered to intact animals 96 h after pretreatment with HCG, plasma T levels were significantly elevated at 20 min after 1-24 ACTH injection whereas a second HCG injection was ineffective in modifying T concentrations. From these results we concluded, that exogenously applied 1-24 ACTH can effectively stimulate the testicular T release in adult male rabbits and that such release is independent of the LH receptors in Leydig cells.

Effect of abomasal glucose infusion on splanchnic amino acid metabolism in periparturient dairy cows

Six Holstein cows fitted with ruminal cannulas and permanent indwelling catheters in the portal vein, hepatic vein, mesenteric vein, and an artery were used to study the effects of abomasal glucose infusion on splanchnic AA metabolism. The experimental design was a split plot, with cow as the whole plot, treatment as the whole-plot factor and days in milk (DIM) as the subplot factor. Cows were assigned to 1 of 2 treatments: control or infusion of 1,500 g/d of glucose into the abomasum from the day of calving to 29 DIM. Cows were sampled prepartum and at 4, 15, and 29 DIM. Postpartum dry matter intake increased at a lower rate with infusion compared with the control. Arterial concentrations of all essential AA (EAA) were lower with infusion compared with the control. Net portal fluxes of His, Ile, Leu, Lys, Met, Phe, Thr, Val, Ala, Pro, Ser, and Tyr were lower with infusion compared with the control and the net portal fluxes of these AA showed positive correlations with dry matter intake, whereas the net portal fluxes of Asp, Glu, and Gln were unaffected by treatment. Net hepatic fluxes of EAA were not affected by treatment but increased as lactation progressed with both treatments. On a net basis, all EAA were removed by the liver prepartum and at 4 DIM, whereas Met, Phe, and Thr were the only EAA being removed at 29 DIM. Except for Ala, AA removed by the liver might be used primarily for noncatabolic processes, as exemplified by the 16% of hepatic Gly uptake accounted for as urinary hippurate. The measured hepatic uptake of glucogenic precursors (glucogenic AA, volatile fatty acids, lactate, and glycerol) accounted for 50 to 90% of the hepatic release of glucose. The hepatic urea output accounted for more than 100% of the hepatic ureagenic precursor uptake, indicating that the glucogenic precursors unaccounted for are nonnitrogen-containing compounds. In conclusion, an increased exogenous glucose supply to the small intestine did not seem to affect the amount of EAA and non-EAA available for peripheral tissues in early lactation, and the study did not indicate an AA-sparing effect of small intestinal glucose absorption. In periparturient dairy cows, hepatic catabolism of AA was not driven by the increased whole-body demand for glucose, and Ala was the only AA that contributed substantially to hepatic gluconeogenesis. In very early lactation, the supply of EAA might be of greater concern than the supply of glucogenic substrates.

Absorption and metabolism of benzoic acid in growing pigs1

Dietary benzoic acid (BA) supplementation causes a pronounced reduction in urinary pH but only small changes in blood pH. The present study aimed to investigate the portal absorption profile, hepatic metabolism of BA, and renal excretion of hippuric acid (HA) underlying the relatively small impact of BA on systemic acid-base status. Eight growing pigs (BW = 63 +/- 1 kg at sampling) fitted with permanent indwelling catheters in the abdominal aorta, hepatic portal vein, hepatic vein, and mesenteric vein were allocated to 4 sampling blocks and randomly assigned to control (CON; nonsupplemented diet) or BA supplementation (B; control diet + 1% BA top-dressed). Feed intake was restricted to 3.6% of BW and the ration divided into 3 equally sized meals offered at 8-h intervals. Blood pH (7.465 and 7.486 +/- 0.004) and urinary pH (4.99 and 7.01 +/- 0.09) were less (P = 0.03 and P < 0.01) in B compared with CON. The arterial concentration, net portal flux, and net hepatic uptake of BA increased (P < 0.01) in B compared with CON. The net portal flux of BA increased (P < 0.01) after feeding with B, but remained positive (P < 0.01) at all sampling times (n = 8). Recovery of dietary BA as increased net portal flux and hepatic uptake of BA was 87 +/- 5% and 89 +/- 15%, respectively. The recovery of dietary BA as urinary excretion of BA and HA was 0.08 +/- 0.02% and 85 +/- 7%, respectively. It is concluded that the small impact of BA supplementation on systemic acid-base status was caused by a protracted BA absorption and efficient hepatic extraction and glycine conjugation in combination with efficient renal clearance of HA. Together, these physiological mechanisms prevented major BA and HA accumulation in body fluids.