Jugular Venous Blood Samples Research Articles

Elevated Brain Serotonin Turnover in Patients With Depression

The biological basis for the development of major depressive disorder (MDD) remains incompletely understood. To quantify brain serotonin (5-hydroxytryptamine [5-HT]) turnover in patients with MDD. Patients with depression were studied both untreated and during administration of a selective serotonin reuptake inhibitor (SSRI) in an unblinded study of sequential design. Healthy volunteers were examined on only 1 occasion. Direct internal jugular venous blood sampling was used to directly quantify brain serotonin turnover. The effect of serotonin transporter (5-HTT) genotype on brain serotonin turnover was evaluated and the influence of SSRI therapy on serotonin turnover was investigated. Participants were recruited from the general community following media advertisement. Experimental procedures were performed in the research catheterization laboratory of a major training hospital and medical research institute. Studies were performed in 21 patients fulfilling the DSM-IV and International Statistical Classification of Diseases, 10th Revision diagnostic criteria for MDD and in 40 healthy volunteers. Treatment for patients consisted of SSRI administration for approximately 12 weeks. Brain serotonin turnover before and after SSRI therapy. Brain serotonin turnover was significantly elevated in unmedicated patients with MDD compared with healthy subjects (mean [SD] internal jugular venoarterial 5-hydroxyindoleacetic acid plasma concentration difference, 4.4 [4.3] vs 1.6 [2.4] nmol/L, respectively; P = .003). Analysis of the influence of the 5-HTT genotype in MDD indicated that carriage of the s allele compared with the l allele was associated with greater than a 2-fold increase in brain serotonin turnover (mean [SD] internal jugular venoarterial 5-hydroxyindoleacetic acid plasma concentration difference, 6.5 [4.7] vs 2.7 [2.9] nmol/L, respectively; P = .04). Following SSRI therapy, brain serotonin turnover was substantially reduced (mean [SD] internal jugular venoarterial 5-hydroxyindoleacetic acid plasma concentration difference, 6.0 [4.0] nmol/L prior to treatment vs 2.0 [3.3] nmol/L following therapy; P = .008). Brain serotonin turnover is elevated in unmedicated patients with MDD and is influenced by the 5-HTT genotype. The marked reduction in serotonin turnover following SSRI treatment and the accompanying improvement in symptoms suggest that high brain serotonin turnover may be a biological substrate of MDD.

Effect of parenteral administration of erythromycin, tilmicosin, and tylosin on abomasal emptying rate in suckling calves

To determine the effect of parenteral administration of erythromycin, tilmicosin, and tylosin on abomasal emptying rate in suckling calves. 8 male Holstein-Friesian calves < 35 days old. Calves received each of 4 treatments in random order (2 mL of saline [0.9% NaCl] solution, IM [control treatment]; erythromycin, 8.8 mg/kg, IM; tilmicosin, 10 mg/kg, SC; and tylosin, 17.6 mg/kg, IM). Calves were fed 2 L of milk replacer containing acetaminophen (50 mg/kg) 30 minutes later. Jugular venous blood samples and transabdominal ultrasonographic abomasal dimensions were obtained periodically after suckling. Abomasal emptying rate was assessed on the basis of the time to maximal plasma acetaminophen concentration and ultrasonographic determination of the halftime of abomasal emptying. One-tailed Dunnett post tests were conducted whenever the F value for group was significant. Emptying rate was faster for erythromycin, tilimicosin, and tylosin than for the control treatment, as determined on the basis of time to maximal plasma acetaminophen concentration. Ultrasonography indicated that the half-time of abomasal emptying was significantly shorter for erythromycin than for the control treatment. Tylosin and tilmicosin accelerated the abomasal emptying rate, but not significantly, relative to the emptying rate for the control treatment. Administration of erythromycin, tilmicosin, and tylosin at the label dosage increased abomasal emptying rate in calves. The clinical importance of an increase in abomasal emptying rate in cattle remains to be determined.

Evaluation of the Accutrend for lactate measurement in dogs

Lactate concentrations are increasingly quantified in dogs using point-of-care instruments, but often without canine-specific method evaluation and instrument-specific reference intervals. The objectives of this study were to 1) determine the precision of the Accutrend (Roche Diagnostics) for lactate determination in dogs, 2) determine the accuracy of the Accutrend using the Rapidlab 865 (Bayer Diagnostics) as the reference method, and 3) establish and compare reference intervals for lactate concentration in clinically healthy dogs for both instruments. Precision was evaluated using low and high control materials, and variable (1 drop) and fixed (25 microL) sample volumes. Accuracy was determined by comparing lactate concentrations obtained with the Accutrend with those from the Rapidlab 865 in 273 heparinized canine jugular venous blood samples from 100 clinically healthy dogs and 107 systemically ill dogs (173 samples). Lactate reference intervals were established for both analyzers using data from the 100 clinically healthy dogs. The precision of the Accutrend was good (coefficients of variation, < or = 5.3%) for 25-microL samples but not when a drop was used. Lactate concentrations obtained on the Accutrend correlated poorly with those from the Rapidlab 865 (r = 0.864, mean bias = 0.66 mmol/L, 95% confidence interval [CI] = 0.57-0.76 with 95% limits of agreement = -0.87 (lower limit, 95% CI = -1.03 to -0.71) and 2.20 (upper limit, 95% CI = 2.04 to 2.36). The reference interval for canine lactate concentration on the Accutrend was 1.2-3.1 mmol/L compared with 0.46-2.31 mmol/L on the Rapidlab. Although precision was good with fixed sample volumes, blood lactate concentrations obtained on the Accutrend were significantly different than those on the Rapidlab 865, with systematic and random errors resulting in a positive bias. Further evaluation of the Accutrend is required before its use in dogs can be recommended.

Hyponatremia and Comparison of NT-pro-BNP Concentrations in Blood Samples from Jugular Bulb and Arterial Sites after Traumatic Brain Injury in Adults: A Pilot Study

Hyponatremia after traumatic brain injury (TBI) may influence neurological function and treatment. A causal relationship between elevated serum concentrations of Type B natriuretic peptide (BNP) and hyponatremia has been implied after subarachnoid hemorrhage and other neurosurgical disorders, although the source of BNP has not been identified. We evaluated if hyponatremia and increased BNP occur after TBI and if BNP is produced/released by the brain within 24 h after injury. NT-proBNP was measured in concomitant jugular venous and arterial blood samples within 24 h after TBI. NT-proBNP was elevated in both samples in six patients (24%). One patient (4%) showed an increased jugular NT-proBNP concentration above a normal arterial concentration, suggesting a brain source. In the other 24 patients the difference between jugular and arterial NT-proBNP was not statistically significant. Hyponatremia (< or =136 mEq/l) also occurred in six patients (24%), but only two (8%) had both increased arterial NT-proBNP and hyponatremia. In both the urine sodium was slightly elevated above normal, but not statistically different from other patients. The difference in serum sodium between hypo- and normo-natremic groups was significant, but mean NT-proBNP and jugular:arterial NT-proBNP differences were not. In this pilot study BNP is elevated within 24 h after TBI in some patients. However, it does not originate from the brain and increased NT-proBNP concentrations are not consistently associated with hyponatremia or increased urinary sodium loss.

The effect of colic on oxygen extraction in horses

Blood oxygen transport and oxygen extraction were assessed in horses with colic. A gravity score (GS) ranging from 1 to 3 was attributed to each colic case with healthy horses used as controls. Jugular venous and carotid arterial blood samples were collected and concentrations of 2,3-diphosphoglycerate, adenosine triphosphate, inorganic phosphate and chloride were determined. pH and partial pressures of carbon dioxide (PCO 2), and oxygen (PO 2) were also measured. Oxygen equilibrium curves (OEC) were constructed under standard conditions and oxygen extraction ratios calculated. Haemoglobin oxygen affinity measured under standard conditions (P50 std) was unchanged in colic horses compared with healthy controls. Horses with the highest GS, i.e. 3 had lower blood pH values than healthy animals. Arterial and venous partial pressures of oxygen at 50% haemoglobin saturation (P50 a and P50 v) were significantly higher in horses suffering from colic (GS = 3) than in healthy horses. The oxygen extraction ratio was also significantly increased in colic horses with a GS of 3. A rise in the oxygen extraction ratio detected in the most severely affected animals seemed to reflect the compensatory properties of the oxygen transport system where extraction of oxygen from the blood increases when systemic oxygen delivery decreases, as might be anticipated in horses with colic.

Serial alterations in digital hemodynamics and endothelin-1 immunoreactivity, platelet-neutrophil aggregation, and concentrations of nitric oxide, insulin, and glucose in blood obtained from horses following carbohydrate overload

To quantify changes in endothelium-derived factors and relate those changes to various aspects of digital hemodynamics during the prodromal stages of carbohydrate overload (CHO)-induced laminitis in horses. 20 adult horses without abnormalities of the digit. Digital and jugular venous blood samples were collected at 1-hour intervals (for assessment of endothelin-1 [ET-1] immunoreactivity and measurement of glucose, insulin, and nitric oxide [NO] concentrations) or 4-hour intervals (CBC and platelet-neutrophil aggregate assessment) for 8 hours or 16 hours after induction of CHO-associated laminitis in horses treated with an ET-1 antagonist. Effects of treatment, collection site, and time and the random effects of horse on each variable were analyzed by use of a repeated-measures model. Where treatment and collection site had no significant effect, data were combined. Compared with baseline values, CHO resulted in changes in several variables, including a significant increase from baseline in digital blood ET-like immunoreactivity at 11 hours; digital blood ET-like immunoreactivity was significantly greater than that in jugular venous blood at 8, 9, 11, and 12 hours. Digital and jugular venous blood concentrations of glucose increased from baseline significantly at 3, 4, and 5 hours; insulin concentration increased significantly at 5 hours; and the number of platelet-neutrophil aggregates increased significantly at 12 hours. In horses, concurrent increases in venous blood ET-1 immunoreactivity, insulin and glucose concentrations, and platelet-neutrophil aggregates support a role of endothelial dysfunction in the pathogenesis of CHO-induced laminitis.

NF-κB Activity and iNOS Expression in Monocytes from Internal Jugular Blood of Migraine Without Aura Patients During Attacks

This study investigated nuclear factor-kappa B (NF-kappaB) activity by electrophoresis mobility gel shift assay and IkappaBalpha expression by Western blot analysis in monocytes obtained from serial samples of internal jugular venous blood taken from seven migraine patients without aura during attacks. Inducible nitric oxide synthase (iNOS) expression was also assessed by reverse transcription-polymerase chain reaction. An increase in NF-kappaB activity peaked 2 h after attack onset. This was accompanied by a transient reduction in IkappaBalpha expression. Up-regulation of iNOS was evident at 4 h, maintained at 6 h and reduced at the end of the attack. These findings substantiate the hypothesis of transitory delayed inflammation, as suggested by the animal model, and suggest the possibility of using therapeutic approaches to target NF-kappaB transcription in the treatment of migraine.

Increased vascular endothelial growth factor and pregnancy-associated glycoproteins, but not insulin-like growth factor-I, in maternal blood of cows gestating twin fetuses1,2

Differences in placental mass and vascularity exist between cows gestating single vs. multiple fetuses. Therefore, the association between fetal number and placental development or function was assessed by comparing concentrations of vascular endothelial growth factor (VEGF), pregnancy-associated glycoproteins (PAG), IGF-I, and progesterone in the maternal blood of cattle selected for twin births and gestating 1 (n = 23) vs. 2 (n = 17) fetuses. Samples of jugular venous blood were collected serially at a mean of 57, 121, 192, and 234 d (range within groups was 20 d) after AI. Plasma concentrations of VEGF, IGF-I, and progesterone were measured by double-antibody RIA, and of PAG by an indirect sandwich ELISA. Concentrations of VEGF and progesterone were greater (P < 0.05) in dams with twin vs. single fetuses. Maternal VEGF concentrations did not differ among collection times, but progesterone concentrations increased (P < 0.01) between d 192 and 234. Conversely, PAG concentrations were low at d 57 and 121 and did not differ between dams carrying singles or twins. However, the subsequent increase (P < 0.01) in PAG was greater in dams with twins, resulting in greater (P < 0.01) PAG concentrations for dams with twins at d 192 and 234 (type of birth x time; P < 0.01). Maternal IGF-I concentrations were unaffected by fetal number. Because corpora lutea persisted for the duration of the evaluation period, maternal progesterone concentrations were likely related to the number of corpora lutea rather than the number of fetuses. It is postulated that the greater PAG and VEGF concentrations in the blood of dams gestating twins are the result of a larger uteroplacental mass, including increased numbers of binucleate cells and increased angiogenesis and vasculogenesis associated with a twin pregnancy. Although PAG and VEGF were elevated in dams gestating twins, variability within and among birth groups limits the use of PAG or VEGF measurements for the diagnosis of twins.

Effect of selenium supplementation and source on the selenium status of horses1

This study was conducted to determine the effect of Se supplementation and source on the Se status of horses. Eighteen 18-mo-old nonexercised horses were randomly assigned within sex to 1 of 3 treatments: 1) control (CTRL, no supplemental Se, 0.15 mg of Se/kg of total diet DM); 2) inorganic Se (INORG, CTRL + 0.45 mg of Se/kg of total diet DM from NaSeO3); or organic Se [ORG, CTRL + 0.45 mg of Se/kg of total diet DM from zinc-L-selenomethionine (Availa Se, Zinpro, Corp., Eden Prairie, MN)]. Horses were acclimated to the CTRL diet (7.1 kg of DM alfalfa hay and 1.2 kg of DM concentrate per horse daily) for 28 d. After the acclimation period, the appropriate treatment was top-dressed on the individually fed concentrate for 56 d. Jugular venous blood samples were collected on d 0, 28, and 56. Middle gluteal muscle biopsies were collected on d 0 and 56. Muscle and plasma were analyzed for Se concentrations. Glutathione peroxidase activity was measured in muscle (M GPx-1), plasma (P GPx-3), and red blood cells (RBC GPx-1). Data were analyzed as a repeated measures design. Mean plasma Se concentration on d 28 and 56 was greater (P < 0.05) for Se-supplemented horses compared with CTRL horses, and tended (P < 0.1) to be greater in ORG vs. INORG on d 28. Mean muscle Se concentration and P GPx-3 activities increased (P < 0.05) from d 0 to 56 but were not affected by treatment. Mean RBC GPx-1 activity tended to be greater (P < 0.1) in ORG than INORG or CTRL horses on d 28, and tended to be greater (P < 0.1) for INORG compared with ORG horses on d 56. Mean RBC GPx-1 activity of INORG and ORG horses was not different from that of CTRL on d 56. Mean M GPx-1 activity decreased (P < 0.01) from d 0 to 56. In conclusion, zinc-L-selenomethionine was more effective than NaSeO3 at increasing plasma Se concentration from d 0 to 28; however, both supplemental Se sources had a similar effect by d 56. No difference in Se status due to Se supplementation or source could be detected over a 56-d supplementation period by monitoring middle gluteal muscle Se, M GPx-1, or P GPx-3. Results for RBC GPx-1 also were inconclusive relative to the effect of Se supplementation and source.

Transcerebral Platelet Activation After Aortic Cross-Clamp Release is Linked to Neurocognitive Decline

Neurocognitive decline after cardiac surgery requiring cardiopulmonary bypass (CPB) may be caused in part by highly prothrombotic atheroemboli to the brain; the source of these emboli is likely the ascending aorta and aortic arch. We examined transcerebral platelet activation gradients using simultaneous measurements in arterial and jugular venous blood and then compared gradients with post-CPB-associated neurocognitive injury. Eighty-one patients undergoing elective coronary artery bypass graft surgery requiring CPB were studied. Neurocognitive function was measured preoperatively and again at 6 weeks postoperatively. Paired arterial and jugular venous blood samples were drawn before surgery, immediately before and after aortic cross-clamp removal (an event previously linked to embolic showers), and at the end of the operation. Transcerebral platelet activation gradients (venous minus arterial values) were compared in patients with and without cognitive deficit. Immediately after aortic cross-clamp removal, there was a significant increase in the transcerebral platelet activation gradient (increased % P-selectin-positive platelets during transcerebral passage) in the subset of patients who subsequently developed post-CPB cognitive deficit; this platelet activation gradient did not occur in patients without cognitive injury. In contrast, there was no transcerebral gradient of platelet activation in CPB patients as an entirety, nor was there a gradient at all other time points in the patient subset who went on to have cognitive deficit develop. This fleeting gradient of transcerebral platelet activation after cross-clamp removal was also significantly correlated with the overall change in cognitive injury score. Transient intracerebral platelet activation after removal of the aortic cross-clamp is associated with post-CPB neurocognitive injury.

Proinflammatory Cytokines, Adhesion Molecules, and Lymphocyte Integrin Expression in the Internal Jugular Blood of Migraine Patients Without Aura Assessed Ictally

The aim of the present research was to verify the levels of the soluble adhesion molecules sL- and sE-selectins, intercellular adhesion molecule (sICAM)-1, and vascular cell adhesion molecule-1 in serial samples of internal jugular venous blood taken from migraine patients without aura (MWoA) during attacks. The expression of leukocyte function antigen (LFA)-1 and very late activation antigen (VLA)-4 was also assessed on lymphocytes obtained from jugular venous blood. Levels of certain proinflammatory cytokines (tumor necrosis factor-alpha[TNF-alpha], interleukin-1beta[IL-1beta], IL-4, and IL-6) were also determined and correlated with those of adhesion molecules. Seven MWoA patients were admitted in the hospital during attacks and blood samples were taken immediately after catheter insertion, at 1, 2, and 4 hours after attack onset, and within 2 hours after its termination. The levels of adhesion molecules and cytokines were measured with ELISA method. The expression of LFA-1 and VLA-4 was assessed by flow cytometry. A parallel transient increase of sICAM-1, TNF-alpha, and IL-6 was observed in the first 2 hours after attack onset compared with the time of catheter insertion (P < .0001, <.001, and <.003, respectively). The proportion of CD4+ and CD8+ T-cells expressing high levels of LFA-1 showed instead a progressive down-regulation with significantly lower percentages at 2 and 4 hours after attack onset (P < .01 and <.022, respectively). No variation in the percentage of VLA-4 expressing cells was observed at any time of the study. The transient increase in sICAM-1 and TNF-alpha found in the internal jugular blood of MWoA patients assessed ictally can be induced by sensory neuropeptides released from activated trigeminal endings. The progressive decrease in sICAM-1 levels during attacks and the down-regulation of LFA-1 expression by lymphocytes could antagonize their transvascular migration, supporting the hypothesis of sterile inflammation in the dura mater during migraine attacks.

Comparison of ventral coccygeal arterial and jugular venous blood samples for pH, pCO 2, HCO 3, Be ecf and ctCO 2 values in calves with pulmonary diseases

The aim of this study was to determine whether venous blood samples can be used as an alternative to arterial samples in calves with respiratory problems and healthy calves. Jugular vein and ventral coccygeal artery were used to compare blood gas values. Sampling of the jugular vein followed soon after sampling of the ventral coccygeal artery in healthy calves (group I) and calves with respiratory problems (group II). Mean values of arterial blood for pH, pCO 2, HCO 3act in healthy calves were 7.475 ± 0.004, 4.84 ± 0.2 kPa, 28.45 ± 1.30 mmol/L compared with venous samples, 7.442 ± 0.006, 6 ± 0.3 kPa, 30.93 ± 1.36 mmol/L, respectively. In group II, these parameters were 7.414 ± 0.01, 5.93 ± 0.3, 27.73 ± 1.96 mmol/L for arterial blood and 7.398 ± 0.008, 6.85 ± 0.2 kPa, 29.77 ± 1.91 mmol/L for venous blood, respectively. There were no statistically significant differences between arterial and venous pH, HCO 3act, Be ecf, ctCO 2 values with the exception of pCO 2 ( P = 0.001) in group II. In group I, correlation ( r 2) between arterial and venous blood pH, pCO 2, HCO 3act were 84.5%, 87.5%, 95.7%, respectively compared with the same parameters in group II, 80.8%, 77.1%, 70.3%. In conclusion, venous blood gas values can predict arterial blood gas values of pH, pCO 2 and HCO 3ecf, Be ecf and ctCO 2 - for healthy calves but only pH values in calves with acute respiratory problems ( r 2 value > 80%).

Effects of intravenous sodium bicarbonate and sodium acetate on equine acid-base status

Changes in blood gases, pH, and plasma electrolyte concentrations in response to intravenously infused sodium bicarbonate (NaHCO3) and sodium acetate (NaCH3CO2) solutions (1.34 mEq/mL) in 5 light breed mares were investigated. Jugular venous blood samples were collected before and after completion of the infusions in 20-minute intervals for 200 minutes. Infusion of sodium bicarbonate and sodium acetate caused significant (P .05) thereafter. There were significant reductions (P < .01) in plasma-ionized calcium and potassium after infusion of both sodium bicarbonate and sodium acetate. This study found that significant metabolic alkalosis in horses and corresponding shifts in electrolyte concentrations can be induced by intravenous infusion of solutions of either sodium bicarbonate or sodium acetate, and they persist for at least 3 hours. These data show that the short-term elevation in pH and bicarbonate ion concentration is momentarily higher after infusion of sodium bicarbonate. This is likely due to the direct infusion of bicarbonate ions in the sodium bicarbonate treatment, such that further metabolism is not required to be effective. However, the longer-term alkalosis did not differ between isomolar solutions of sodium bicarbonate and sodium acetate.

Cerebral ammonia uptake and accumulation during prolonged exercise in humans

We evaluated whether peripheral ammonia production during prolonged exercise enhances the uptake and subsequent accumulation of ammonia within the brain. Two studies determined the cerebral uptake of ammonia (arterial and jugular venous blood sampling combined with Kety-Schmidt-determined cerebral blood flow; n = 5) and the ammonia concentration in the cerebrospinal fluid (CSF; n = 8) at rest and immediately following prolonged exercise either with or without glucose supplementation. There was a net balance of ammonia across the brain at rest and at 30 min of exercise, whereas 3 h of exercise elicited an uptake of 3.7 +/- 1.3 micromol min(-1) (mean +/-s.e.m.) in the placebo trial and 2.5 +/- 1.0 micromol min(-1) in the glucose trial (P < 0.05 compared to rest, not different across trials). At rest, CSF ammonia was below the detection limit of 2 microm in all subjects, but it increased to 5.3 +/- 1.1 microm following exercise with glucose, and further to 16.1 +/- 3.3 microm after the placebo trial (P < 0.05). Correlations were established between both the cerebral uptake (r2 = 0.87; P < 0.05) and the CSF concentration (r2 = 0.72; P < 0.05) and the arterial ammonia level and, in addition, a weaker correlation (r2 = 0.37; P < 0.05) was established between perceived exertion and CSF ammonia at the end of exercise. The results let us suggest that during prolonged exercise the cerebral uptake and accumulation of ammonia may provoke fatigue, e.g. by affecting neurotransmitter metabolism.

Pharmacokinetics of sevoflurane uptake into the brain

Two recent studies have examined the pharmacokinetics of sevoflurane in adults. Lu et al.(Pharmacokinetics of sevoflurane uptake into the brain and body, Anaesthesia 2003; 58: 951-6) observed that jugular bulb sevoflurane concentration initially rose unexpectedly rapidly and then approached arterial concentrations unexpectedly slowly, suggesting that a blood-brain diffusion barrier exists. They also observed a large alveolar-arterial sevoflurane gradient, suggesting that an alveolar-arterial diffusion barrier exists. Nakamura et al. (Predicted sevoflurane partial pressure in the brain with an uptake and distribution model: Comparison with the measured value in internal jugular vein blood. Journal of Clinical Monitoring and Computing 1999; 15: 299-305) found no diffusion barriers. We used a computer model to analyse both data sets and show that the observations of Lu et al. can be explained by contamination of jugular samples with extracerebral blood. It is possible that the alveolar-arterial gradients observed by Lu et al. are due to discrepancies in conversions between blood concentrations and gas partial pressures. Our study suggests that there is no blood-brain diffusion barrier for sevoflurane and that the data of Lu et al. must be interpreted with caution.

Chemokine Levels in the Jugular Venous Blood of Migraine Without Aura Patients During Attacks

To investigate changes in the levels of calcitonin gene-related peptide and its intracellular messenger cyclic adenosine monophosphate in serial samples of internal jugular blood taken from migraine patients without aura assessed during attacks, and to assess their relationship with the levels of IL-8, MCP-1, and RANTES in the same samples. Calcitonin gene-related peptide, the marker of trigeminovascular activation, is released in both the internal and external jugular venous blood of migraine patients during attacks. Experimental evidence demonstrated that when released from C-type sensory neurons in inflammatory pain models, it differentially induced expression of neutrophil chemotactic chemokine IL-8, but not monocyte chemotactic chemokine MCP-1 or lymphocyte chemotactic chemokine RANTES. These chemokines were never investigated in migraine. Eight migraine without aura patients were admitted to the hospital during the attacks. Internal jugular venous blood samples were taken immediately after catheter insertion, at the 1st, 2nd, and 4th hours after attack onset, and within 2 hours from its cessation. The levels of the sensory neuropeptide calcitonin gene-related peptide and the messenger cyclic adenosine monophosphate were measured by RIA method, and those of IL-8, MCP-1, and RANTES were measured by ELISA method. Higher calcitonin gene-related peptide levels were found in the internal jugular venous blood of migraine without aura patients compared with the time of catheter insertion (ANOVA: P<.0001) with a peak at the first hour (52.6+/-9.2 ng/mL). A transient increase in IL-8 was observed at the 2nd and 4th hours (P<.01 and P<.002, respectively), whereas no changes in the levels of MCP-1 and RANTES were found at any time of the study. The increase in IL-8 was accompanied by a parallel increase in cyclic adenosine monophosphate. The present study confirms previous findings of an increase in calcitonin gene-related peptide in internal jugular venous blood of migraine without aura patients during attacks. The transient increase in the levels of IL-8 concurs with the results of recent experimental research showing a calcitonin gene-related peptide-induced activation of IL-8 gene expression, but not RANTES and MCP-1, via the transcriptional factor AP-2, which mediates transduction in response to cyclic adenosine monophosphate. Although IL-8 is transiently increased during migraine attacks, an accumulation of leukocytes secondary to neurogenic inflammation is unlikely, as it is for other inflammatory events, because they are self limiting. Other events, including nitric oxide production, may contribute to counteract meningeal transvascular leukocyte migration during migraine attacks, as suggested by the model of sterile inflammation.

Endocrine secretion of prostaglandin F 2α in cyclic gilts is decreased by intrauterine administration of exogenous oxytocin

When administered systemically, oxytocin (OT) stimulates secretion of uterine prostaglandin F 2α (PGF 2α) in swine, but the role of endometrially-derived OT in control of PGF 2α release is not clear. This study determined the effect of exogenous OT, administered into the uterine lumen of intact cyclic gilts, on PGF 2α secretion during late diestrus. Intrauterine infusion of 40 USP units OT (in 30 ml 0.9% saline) was performed for 30 min (1 ml/min) into each uterine horn between 7:00 and 9:00 h on days 10, 12, 14 and 16 after estrus. Beginning 20 min before infusion, samples of jugular venous blood were drawn at 5–10-min intervals for 140 min for quantification of 13,14-dihydro-15-keto-PGF 2α (PGFM), the major stable metabolite of PGF 2α. Progesterone was analyzed in samples collected 0, 60 and 120 min after initiation of OT infusion. Treatment with OT did not alter plasma concentrations of PGFM on days 10 or 12 but decreased ( P<0.001) PGFM concentrations for 40 min after onset of infusion on day 16. Concentrations of PGFM also were reduced in the pre-treatment samples on day 14 ( P=0.05) and day 16 ( P<0.001) in OT-infused gilts. Plasma progesterone declined ( P<0.01) between days 10 and 16 in control-infused gilts but did not decline until after day 14 ( P<0.001) in gilts infused with OT. These results indicate that when OT is administered into the uterine lumen of pigs during late diestrus, it has an anti-luteolytic effect to reduce endocrine secretion of PGF 2α and delay the decline in progesterone that occurs during luteolysis.

Dietary Arginine Supplementation Enhances the Growth of Milk-Fed Young Pigs

This study was conducted to determine the effect of dietary arginine supplementation on the growth of artificially reared piglets. The pigs (n = 24; 7 d old) were removed from sows to a nursery facility and assigned randomly to 1 of the 3 treatments representing diets supplemented with 0, 0.2, or 0.4% L-arginine (on the basis of milk replacer powder). Each milk feeder was assigned to 1 dietary treatment. Fresh liquid milk replacer (18.6% dry matter) was provided daily ( approximately 0800 h) to piglets. Body weights of piglets were measured and jugular venous blood samples were obtained for metabolite analysis at d 7, 14, and 21 of age. Food intake did not differ between control and arginine-supplemented piglets [66.7 vs. 69.5 g dry matter/(kg body wt. d)]. Compared with control piglets, dietary supplementation with 0.2 and 0.4% L-arginine dose dependently increased (P < 0.05) plasma concentrations of arginine by 30 and 61%, and decreased (P < 0.05) plasma concentrations of ammonia by 20 and 35%, and those of urea by 19 and 33%, respectively. Dietary supplementation with 0.4% L-arginine also increased (P < 0.05) plasma concentrations of insulin and growth hormone by 24-27% in piglets, compared with controls. Between 7 and 21 d of age, the supplementation of 0.2 and 0.4% L-arginine to piglets enhanced (P < 0.05) average daily weight gain by 28 and 66%, and body weight by 15 and 32%, respectively, compared with control piglets. Collectively, both the metabolic and growth data demonstrate unequivocally that arginine is deficient in milk-fed young pigs and that this arginine deficiency represents a major obstacle to maximal growth in piglets.

Systemic and intraovarian effects of dominant follicles on ovine follicular growth

The objective was to study the endocrine activity in sheep with large ovarian follicles and the effects of dominant follicles on other follicles, looking for possible intraovarian differences. Induction of dominant follicles was achieved using controlled exogenous LH pulses every 90 min over 14 days in eight Scottish Blackface ewes. During this period, follicular development was assessed by daily transrectal ultrasonography and jugular venous blood samples were collected every 12 h for FSH, LH inhibin and oestradiol assay. The exogenous LH pulses caused the appearance of large follicles in all the ewes, which reached a maximum mean diameter of 7.2±0.5 mm on Day 5.5±2.6 after first detection. In the presence of a dominant follicle, no other follicle grew to a diameter larger than 4 mm and there was a decrease in the number of new growing follicles ( P<0.05) and in the number of smaller follicles ( P<0.01). This effect of dominance was mediated by changes in FSH concentration, since FSH level decreased ( P<0.05) as dominant follicles grew and the decrease in FSH levels was related to a decline in the number of remaining follicles ( P<0.05). However, the greatest decrease in the number of small follicles growing to larger sizes was observed in the ovary ipsilateral to the dominant follicle ( P<0.05). These data confirm that the presence of a large follicle depresses the recruitment and growth of other follicles by systemic factors and provide some evidence of local inhibitors blocking the final development of other putative large follicles.

Ultrasonographic evaluation of uterine involution and postpartum follicular dynamics in French Jennies ( Equus asinus)

Uterine involution and follicular dynamics during postpartum period were studied ultrasonographically in French jennies. For the study of uterine involution in postpartum jennies ( n=6, Group S), sonographic measurements of different parts of the uterus and endometrium were made at three-day interval, starting from the day of foaling and continued up to 33 days postpartum. Uterine dimensions were also recorded in non-pregnant jennies ( n=3, Group C) throughout a cycle and compared with the dimensions of Group S jennies observed on the day of complete involution. Follicular dynamics of first and second postpartum ovulatory cycles were studied and compared with that of the single estrous cycle of Group C jennies. Jugular venous blood samples of Group S jennies were collected at weekly intervals for 49 days, commencing at the appearance of first preovulatory follicle, to support the sonographic findings. The average involution period was 22.5±1.7 days. However, it was significantly delayed ( P<0.05) in jennies which came into first postpartum ovulatory heat within Day 9 than those who came later (25.0±1.0 versus 20.0±1.0). The endometrial layer was not discernible beyond Day 15 postpartum and thus was found to be unreliable index of uterine involution. The follicular growth rate (mm per day) and diameter (mm) of preovulatory follicle in postpartum jennies were similar to that in normal cycling jennies ( P>0.05). The first and second ovulations occurred at 14.6±0.8 and 39.0±0.8 days postpartum in Group S jennies. All the corpora lutea, either echogenic or centrally non-echogenic were functionally similar and had similar life span ( P>0.05). In conclusion, the postpartum reproductive events related to uterine involution and ovarian cyclicity apparently resemble that of mares.