Jugular Venous Blood Research Articles

Hydroperoxide in Internal Jugular Venous Blood Reflects Occurrence of Subarachnoid Hemorrhage-Induced Delayed Cerebral Vasospasm

To investigate the association between subarachnoid hemorrhage-induced delayed cerebral vasospasm (DCVS) and oxidative stress, an oxidation product, hydroperoxide, was measured in 3 specimens: peripheral arterial blood, cerebrospinal fluid (CSF), and internal jugular venous blood (IJVB). Hydroperoxide was measured using the diacron reactive oxygen metabolites (d-ROMs) test. The hydroperoxide levels were evaluated based on the rate of change in the d-ROMs test value on day 6 relative with that on day 3 (d-ROMs change rate). The subjects were 20 patients. The d-ROMs change rate in IJVB was significantly higher in patients with DCVS on day 6 than in those without it (P < .01). When the patients were classified into the following 3 groups: Group A (no DCVS occurred throughout the clinical course); Group B (DCVS occurred, but no cerebral infarction [CI] was induced); and Group C (DCVS occurred and caused CI), the d-ROMs change rate in IJVB was the highest in Group C, followed by Group B then A (P < .01). The d-ROMs change rates in peripheral arterial blood and CSF were not related to the development of DCVS. It was concluded that the more severe DCVS occurs and is more likely to progress to CI as the IJVB hydroperoxide level rises early after the development of subarachnoid hemorrhage.

Clinical utility of serum biochemical variables for predicting acid-base balance in critically ill horses.

Profiles from serum biochemical analyzers include the concentration of strong electrolytes (including l-lactate), total carbon dioxide (tCO2 ), and total protein. These variables are associated with changes in acid-base balance. Application of physicochemical principles may allow predicting acid-base balance from serum biochemistry without measuring whole blood pH and pCO2 . The purpose of the study was to determine if the acid-base status of critically ill horses could be accurately predicted using variables included in standard serum biochemical profiles. Two jugular venous blood samples were prospectively obtained from critically ill horses and foals. Samples were analyzed using a whole blood gas and pH analyzer (BG) and a serum biochemistry multi analyzer system (AMAS). Linear regression, Deming regression, and Bland-Altman plots were used for method comparison and P<.05 was considered significant. Values from 70 horses and foals for Na, K, Cl, and total protein concentrations, and consequently the calculated variables used for acid base interpretation, were different between the AMAS and BG analyzer. Using physicochemical principles, BG results accurately predicted pH, whereas the AMAS results did not when a fixed value for pCO2 was used. Measurement of pCO2 is required in critically ill horses for accurate prediction of whole blood pH. Differences in the measured values of Na and Cl concentration exist when measured in serum by the AMAS and in whole blood or plasma by BG, indicating that the accurate prediction of whole blood pH is analyzer-dependent. Application of physicochemical principles to plasma or serum provides a practical method to evaluate analyzer accuracy.

Evaluation of serial venous and arterial lactate concentrations in healthy anesthetized sheep undergoing ovariectomy

ObjectiveTo determine if lactate concentrations in jugular venous and auricular arterial blood differ in anesthetized sheep. Study designProspective, controlled experimental study. AnimalsTwelve healthy adult ewes, 4–7 years and weighing 62–77 kg. MethodsJugular venous blood was collected before anesthesia (PreOv) for measurement of lactate concentration, packed cell volume and total protein. Ewes were administered a standard anesthesia protocol. Jugular venous (IntraOv) and auricular arterial (IntraOa) blood samples were obtained 40 minutes after induction of anesthesia, and again in recovery (PostOv and PostOa). An additional blood sample was drawn 6 weeks post-operatively from non-fasted sheep (NF_Lact). Lactate concentrations were compared among PreOv, IntraOv and IntraOa, PostOv and PostOa, and between PreOv and NF_Lact with paired t-test and repeated measure analyses of variance (anova) with PreOv as a covariate (p = 0.05). ResultsIntraOv lactate concentration had decreased from PreOv There were significant differences between arterial and venous IntraO and PostO lactate concentrations. There was no significant difference between IntraO and PostO, or PreOv and NF_Lact. Conclusions and clinical relevanceLactate concentrations were significantly lower in anesthetized sheep compared to non-anesthetized sheep. Lactate concentrations in venous blood were higher than in arterial blood. Therefore, anesthetic status and sampling site should be considered when interpreting lactate concentrations, and the sampling site should be consistent for repeated measurements.

A comparison of traditional and quantitative analysis of acid-base imbalances in hypoalbuminemic dogs.

To compare the traditional (HH) and quantitative approaches used for the evaluation of the acid-base balance in hypoalbuminemic dogs. Prospective observational study. ICU of a veterinary teaching hospital. One hundred and five client-owned dogs. Jugular venous blood samples were collected from each patient on admission to determine: total plasma protein (TP), albumin (Alb), blood urea nitrogen (BUN), glucose (Glu), hematocrit (HCT), Na(+) , Cl(-) , K(+) , phosphate (Pi ), pH, PvCO2, bicarbonate (HCO3 (-) ), anion gap (AG), adjusted anion gap for albumin (AGalb ) or phosphate (AGalb-phos ), standardized base excess (SBE), strong ion difference (SID), concentration of nonvolatile weak buffers (Atot ), and strong ion gap (SIG). Patients were divided in 2 groups according to the severity of the hypoalbuminemia: mild (Alb = 21-25 g/L) and severe (Alb ≤20 g/L). All parameters were compared among groups. Patients with severe hypoalbuminemia showed significant decrease in TP (P = 0.011), Atot (P = 0.050), and a significant increase in adjusted AG (P = 0.048) and the magnitude of SIG (P = 0.011) compared to animals with mild hypoalbuminemia. According to the HH approach, the most frequent imbalances were simple disorders (51.4%), primarily metabolic acidosis (84.7%) associated with a high AG acidosis. However, when using the quantitative method, 58.1% of patients had complex disorders, with SIG acidosis (74.3%) and Atot alkalosis (33.3%) as the most frequent acid-base imbalances. Agreement between methods only matched in 32 cases (kappa < 0.20). The agreement between the HH and quantitative methods for interpretation of acid-base balance was poor and many imbalances detected using the quantitative approach were missed using the HH approach. Further studies are necessary to confirm the clinical utility of using the quantitative approach in the decision-making process of the severely ill hypoalbuminemic patients.

Effect of tulathromycin on abomasal emptying rate in healthy lactating goats

Tulathromycin is a long-acting semi-synthetic macrolide antibiotic that is synthesized from erythromycin. Macrolides have pharmacodynamic properties beyond their antimicrobial effects, including anti-inflammatory and immunomodulatory properties that are perceived to be clinically beneficial. An additional pharmacodynamic property of macrolides is a prokinetic effect, which is marked in adult cattle and calves administered erythromycin and less prominent in calves administered spiramycin, tilmicosin, and tylosin. Based on structural similarities to erythromycin, the hypothesis was that parenteral administration of tulathromycin would increase abomasal emptying rate in healthy adult goats. Accordingly, five adult lactating goats (30–36 months of age) received each of the following 3 treatments: IM injection of 2mL of 0.9% NaCl (control); IM injection of tulathromycin (2.5mg/kg body weight); IV injection of tulathromycin (2.5mg/kg body weight). Abomasal emptying rate was assessed by acetaminophen absorption, which was injected into the abomasum through a surgically placed abomasal cannula at 50mg/kg BW, 15min after each treatment. Jugular venous blood samples were obtained periodically after injection and plasma acetaminophen concentrations determined using a colorimetric nitration assay. The maximum observed plasma acetaminophen concentration (Actual Cmax) and time of actual Cmax (Actual Tmax) were determined, and pharmacokinetic modeling was used to calculate model Cmax and model Tmax and abomasal emptying half-time (T50). Results showed that tulathromycin (IM and IV) increased abomasal emptying rate, as indicated by a shorter time to actual Tmax and model Tmax, and shorter T50, than control. The clinical relevance of these findings remains to be determined.

Effects of ulinastatin on cerebral oxygen metabolism and CRP levels in patients with severe traumatic brain injury.

The aim of the present study was to investigate the effects of ulinastatin on cerebral oxygen metabolism and C-reactive protein (CRP) levels in patients with severe traumatic brain injury (sTBI). A total of 92 patients with sTBI, admitted to the First Affiliated Hospital of Xinxiang Medical University (Xinxiang, China), were randomly divided into control and observation groups. The control group received conventional therapy plus a placebo (0.9% sodium chloride), while the observation group were administered conventional therapy plus 200,000 units ulinastatin via intravenous injection twice a day for seven days. Arterial and jugular venous blood was collected for blood gas analysis. The jugular venous blood lactate (JVBL), jugular venous bulb oxygen saturation (SjvO2), arteriovenous oxygen content difference (AVDO2) and cerebral extraction of oxygen (CEO2) levels were measured on day 1, 3, 5 and 7, as well as the level of CRP in the peripheral blood. In the control group, the level of JVBL decreased as compared with the level at day 1, however, no statistically significant differences were observed (P>0.05). By contrast, the observation group exhibited a significant reduction in the level of JVBL (P<0.05), which was also significantly lower compared with the control group (P<0.05). Statistically significant differences were observed between the two groups with regard to SjvO2, AVDO2 and CEO2 on day 3, 5 and 7. The CRP levels in the two groups increased and peaked on day 3. However, the CRP level in the observation group significantly decreased on day 5 (35.27±15.18 mg/l) and day 7 (22.65±10.48 mg/l), which was lower compared with the control group (56.19±13.24 mg/l and 47.36±15.73 mg/l, respectively); statistically significant differences were observed (P<0.05). Therefore, ulinastatin effectively improved cerebral oxygen metabolism and reduced the CRP level in patients with sTBI.

Perirenal fat associated with microalbuminuria in obese rats

To determine whether perirenal fat is associated with increased urinary albumin excretion and whether perirenal fat affects renal vascular endothelial function in obese rats. Wistar rats were randomly divided into normal and obesity group, which were fed with normal and high-fat diet, respectively. Blood and urine samples were collected. Endothelial function of the aorta was determined by measuring endothelium-dependent vasodilatation. Renal tissues were collected for CD34 immunohistochemistry and free fatty acids (FFA) measurement. Levels of glomerular nitric oxide (NO) and reactive oxygen species (ROS) were measured. After 24 weeks, plasma FFA, high-sensitivity C-reactive protein, and malondialdehyde levels were elevated and were significantly higher in renal venous blood than in jugular venous blood in obese rats. Urinary albumin/creatinine ratio, glomerular CD34 expression, glomerular ROS level, and renal cortex FFA levels were higher in obese rats. Endothelial dysfunction was more severe in the infra-renal aorta than in the thoracic aorta in obese rats. Plasma adiponectin and glomerular NO levels were lower in obese rats. Perirenal fat is associated with increased urinary albumin excretion in obese rats. The mechanism may be renal vascular endothelial dysfunction caused by increased oxidative stress and activation of inflammatory molecular pathways due to elevated FFA and low adiponectin levels.

Influence of intranasal and carotid cooling on cerebral temperature balance and oxygenation

The present study evaluated the influence of intranasal cooling with balloon catheters, increased nasal ventilation, or percutaneous cooling of the carotid arteries on cerebral temperature balance and oxygenation in six healthy male subjects. Aortic arch and internal jugular venous blood temperatures were measured to assess the cerebral heat balance and corresponding paired blood samples were obtained to evaluate cerebral metabolism and oxygenation at rest, following 60 min of intranasal cooling, 5 min of nasal ventilation, and 15 min with carotid cooling. Intranasal cooling induced a parallel drop in jugular venous and arterial blood temperatures by 0.30 ± 0.08°C (mean ± SD), whereas nasal ventilation and carotid cooling failed to lower the jugular venous blood temperature. The magnitude of the arterio-venous temperature difference across the brain remained unchanged at −0.33 ± 0.05°C following intranasal and carotid cooling, but increased to −0.44 ± 0.11°C (P < 0.05) following nasal ventilation. Calculated cerebral capillary oxygen tension was 43 ± 3 mmHg at rest and remained unchanged during intranasal and carotid cooling, but decreased to 38 ± 2 mmHg (P < 0.05) following increased nasal ventilation. In conclusion, percutaneous cooling of the carotid arteries and intranasal cooling with balloon catheters are insufficient to influence cerebral oxygenation in normothermic subjects as the cooling rate is only 0.3°C per hour and neither intranasal nor carotid cooling is capable of inducing selective brain cooling.

Arterial-jugular bulb differences in pCO2, lactate, serum sodium and C-reactive protein in neurocritical patients

Several reports indicate the potential usefulness of monitoring brain metabolic parameters and their correlation with the system [1-4]. We want to establish differences and correlation in pCO2, lactate, serum sodium and C-reactive protein (CRP) between arterial and jugular venous bulb blood.

Jugular bulb oxygen saturation and the pyruvate lactate ratio are good signals for cerebral metabolism and oxygenation during hypothermia with altered target ventilation

Background The effect of deliberate hypothermia and hypocapnia on brain protection during neurosurgical procedures has been studied for many years, but in this study, the combination of deliberate hypothermia and hypocapnia was analyzed to detect their effects on cerebral oxygenation by the assessment of SjvO 2 and cerebral metabolism by the measurement of both jugular bulb lactate and pyruvate. Patients and methods Sixty patients scheduled for excision of supratentorial space-occupying lesions were randomly allocated into two groups. In group I, hypocapnia was induced combined with hypothermia, and in group II, normocapnia was maintained combined with hypothermia. Hypothermia was induced using a water blanket under the patient controlling the tympanic membrane temperature at 35°C. Jugular bulb venous and arterial blood gas analyses were performed before the induction of hypothermia ± hypocapnia (baseline), and then every 20 min till closure of the dura. The arterio-jugular venous oxygen content difference (AJDO 2 ) and the cerebral oxygen extraction ratio (COER) were calculated. Jugular bulb lactate and pyruvate levels were measured before the induction of hypothermia ± hypocapnia (baseline) and then every 30 min till closure of the dura. Results There was a significant increase in pjH and significant decreases in both PjCO 2 and SjvO 2 in the hypocapnic group after the induction of hypocapnia. SjvO 2 reached 80.32 ± 4.59% in the normocapnic group, whereas it reached 75.3 ± 4.02% in the hypocapnic group. AJDO 2 and COER started to decrease after induced hypothermia in both groups compared with readings before induced hypothermia, but the hypocapnic group had a significantly higher AJDO 2 and COER than the normocapnic group during the period of induced hypothermia (AJDO 2 reached 3.98 ± 0.47 ml/dl and COER reached 25.93 ± 4.13% in comparison with the hypocapnic group, where AJDO 2 reached 4.58 ± 0.51 ml/dl and COER reached 31.96 ± 4.01%).Jugular bulb lactate and pyruvate levels were significantly higher during hypocapnia than during normocapnia. Conclusion Cerebral oxygenation and metabolism were better during hypothermia combined with normocapnia as reflected by relative ͽͽSjvO 2 and ͿͿAJDO 2 and COER as well as ͿͿjugular bulb lactate and pyruvate.

Neurological outcome of normothermic versus hypothermic cardiopulmonary bypass in simple congenital heart diseases

Objective We hypothesized that normothermic cardiopulmonary bypass (CPB) may provide equivalent results to hypothermic CPB on neurological outcome. Patients and methods Forty patients were randomized to one of two groups: group 1 that underwent normothermic CPB (>35°C) and group 2 that underwent mild hypothermic CPB (32°C). Perfusion on bypass was performed by a nonpulsatile pump flow with an average flow rate around 2.4 l/m 2 /min. A pH-stat carbon dioxide management strategy was used. The arterial and jugular venous blood gases, mean cerebral blood flow velocity (CBFV), and pulsatile index were measured as basal, after induction of anesthesia, at the onset of CPB, 20-30-40 min after the CPB, at the cessation of CPB, and at the end of the operation. Neurological outcomes were assessed by computed tomography scanning and Wechsler Preschool and Primary Scale of Intelligence preoperatively, at the third postoperative day and 1 month after surgery. Postoperative ICU variables such as duration of mechanical ventilation, time to extubation, and ICU length of stay were recorded. Results There was a significant increase in SjvO 2 and decrease in CeO 2 in the hypothermia group of patients after establishment of hypothermia by 10 and 20 min when compared with the normothermic group ( P 2 was maximal during normothermic CPB and after rewarming phase of hypothermic CPB. There were no significant changes in computed tomography scanning and Wechsler Preschool and Primary Scale of Intelligence between the studied groups at any time period. There was significant prolongation in duration of postoperative mechanical ventilation, extubation time, and duration of ICU stay in the hypothermic group of patients compared with the normothermic group ( P Conclusion During CPB for correction of congenital heart defects, the normothermic and hypothermic CPB were comparable with respect to the neurological outcome. However, normothermia permits shorter time on mechanical ventilation, more rapid extubation, and shorter ICU stay time compared with hypothermia.

A note on arterial to venous oxygen saturation as reference for NIRS-determined frontal lobe oxygen saturation in healthy humans

A note on arterial to venous oxygen saturation as reference for NIRS-determined frontal lobe oxygen saturation in healthy humans

The effect of equine Chorionic Gonadotrophin (eCG) on luteal vascularity in the mare

Although progesterone is required to maintain the pregnant state, oestrogen is also a feature of early equine pregnancy. As early as day 40 a marked increase in serum oestrogen concentrations originates from the primary and any secondary corpora lutea (CL) in response to the gonadotrophic actions of eCG. Oestrogen is a known stimulator of the vascular endothelial growth factor (VEGF) which promotes vasculogenesis and angiogenesis. This study assessed changes in luteal vascularity between days 14 to 50 of gestation. Fifteen pregnant mares in a clinical setting were examined at three time points (days 14–16, 20–30 and 40–50 after ovulation). At each examination pregnancy was confirmed and jugular venous blood samples assayed for progestagen and eCG concentrations. Ultrasonographic and Doppler examinations were performed using a SonoSite Micromaxx (SonoSite Ltd, Hitchin, UK) with a linear probe (5.0 10.0 MHz). Images were obtained in colour flow mode with the medium flow sensitivity pre-set. All images had a standard depth of 7.7 cm with a frequency of 3.92 MHz and pulse repetition frequency of 2.1 MHz. The colour image was frozen at peak systolic flow and recorded; acquisition was repeated 3 to 5 times for each CL. Images were analysed using ImageJ software (National Institutes of Health, Bathesda, USA).

Efficacy of intramuscular meperidine hydrochloride versus placebo in experimental foot lameness in horses

There are no peer reviewed, blinded controlled studies regarding the skeletal analgesic efficacy of intramuscularly administered meperidine in horses. Using an adjustable heart bar shoe model of equine foot pain, the objective of this study was to test the hypothesis that meperidine (pethidine) administered intramuscularly would prove more efficacious in alleviating lameness than a saline placebo. Crossover pharmacodynamic experiment. Eight healthy adult Thoroughbred horses randomly underwent weekly i.m. treatments 1 h after lameness induction: saline placebo (1 ml/45 kg bwt) or meperidine hydrochloride (1 mg/kg bwt i.m.). Heart rate (HR) and lameness score (LS) responses were assessed by a blinded observer every 20 min for 5 h after lameness induction and then hourly through 12 h after treatment. Jugular venous blood samples were obtained at -1, 0, 0:05, 1, 2, 4, 6, 8, 10 and 12 h and were subsequently analysed for drug concentrations (lower limit of detection, 1 ng/ml). Repeated measures ANOVA and post hoc Tukey's test were used to identify analgesic effects at a significance level of P<0.05. Mean (± s.e.) HR were lower in meperidine trials at 2.3, 3.3 and 3.7 h post administration (P<0.05). Mean LS were lower in meperidine trials at 2.0, 2.3 and 3.3 h post administration (P<0.05). Mean plasma (meperidine) peaked at 227 ± 52 ng/ml at 1 h post administration and decreased to 2.7 ± 0.3 ng/ml at 12 h post administration. In 3 of 8 subjects, plasma (meperidine) was below the lower limit of detection at 12 h after administration. Intramuscular meperidine was more effective than the saline placebo but only for 2.0-3.7 h post administration compared with the 8-12 h durations of efficacy reported previously using this same model when horses were treated with nonsteroidal anti-inflammatory drugs (NSAIDs). Meperidine may be a suitable nonNSAID alternative analgesic for acute foot pain with efficacy lasting from 2-3 h after a single i.m. dose.

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Introduction: Recently, ILCOR and AHA have been recommended to treat patients, who returned spontaneous circulation (ROSC) from cardiac arrest, by therapeutic hypothermia. Recently, we have tried to examine predictors, such as internal jugular venous blood oxygen saturation (SjvO2), glucagon, glucose, glial fibrillary acidic protein, procalcitonin, interleukin-8, interleutin-6, S100B and high morbidity group box 1 in serum and/or cerebrospinal fluid (CSF) within 48 hours after ROSC. But those values could not be got within a few hours except for SjvO2. Therefore, we need a predictor to detect the outcome as soon as possible for farther treatments. Methods: This retrospective cohort study included patients with ROSC after CPR who were admitted to our university hospital between January 2000 and May 2011 or an affiliated hospital between January 2006 and May 2011. Clinical parameters recorded on arrival included age (A), arterial blood pH (B), time from CPR to ROSC (C), pupil diameter (D), and initial rhythm (E). Glasgow outcome scale (GOS) was recorded at 6 months and the patients were divided according to favorable or unfavorable neurological outcomes based on GOS score. Multiple logistic regression analysis was performed to derive a formula to predict neurological outcomes based on basic clinical parameters. Results: The regression equation was derived using a teaching dataset consisting of 389 records: EP = 1/(1 + e-x), where EP is the estimated probability of having a favorable outcome, and x = (-0.034 × A) + (4.669 × B) - (0.105 × C) - (0.976 × D) + (2.603 × E) - 28.279. The sensitivity, specificity, and accuracy were 86%, 91% and 91%, respectively, for the validation dataset (n = 100). Conclusions: The 6 month neurological outcomes can be predicted in patients resuscitated from OHCA using clinical parameters that can be easily recorded at the site of CPR.

Effect of large colon ischemia and reperfusion on concentrations of calprotectin and other clinicopathologic variables in jugular and colonic venous blood in horses

To determine the effect of large colon ischemia and reperfusion on concentrations of the inflammatory neutrophilic protein calprotectin and other clinicopathologic variables in jugular and colonic venous blood in horses. 6 healthy horses. Horses were anesthetized, and ischemia was induced for 1 hour followed by 4 hours of reperfusion in a segment of the pelvic flexure of the large colon. Blood samples were obtained before anesthesia, before induction of ischemia, 1 hour after the start of ischemia, and 1, 2, and 4 hours after the start of reperfusion from jugular veins and veins of the segment of the large colon that underwent ischemia and reperfusion. A sandwich ELISA was developed for detection of equine calprotectin. Serum calprotectin concentrations and values of blood gas, hematologic, and biochemical analysis variables were determined. Large colon ischemia caused metabolic acidosis, a significant increase in lactate and potassium concentrations and creatine kinase activities, and a nonsignificant decrease in glucose concentrations in colonic venous blood samples. Values of these variables after reperfusion were similar to values before ischemia. Ischemia and reperfusion induced activation of an inflammatory response characterized by an increase in neutrophil cell turnover rate in jugular and colonic venous blood samples and calprotectin concentrations in colonic venous blood samples. Results of this study suggested that large colon ischemia and reperfusion caused local and systemic inflammation in horses. Serum calprotectin concentration may be useful as a marker of this inflammatory response.

Is CGRP a marker for chronic migraine?

Calcitonin gene-related peptide (CGRP) research was initiated by Poyner et al.,1 who found that the calcitonin gene encodes the 37–amino acid neuropeptide CGRP in neuronal tissue. Within months, the Lund group produced antibodies toward α-CGRP and developed sensitive methods to study the role of this peptide in the cranial circulation. Intracranial vessels and the trigeminal ganglion harbor this potent vasodilator peptide.2 Functionally, CGRP has a substantial role in the trigeminovascular reflex.3 The calcitonin family is now well-characterized and contains 6 members: calcitonin, amylin, adenomedullin-2, adrenomedullin, and CGRP (2 isoforms: α-CGRP and β-CGRP).4 The α- and β-isoforms of CGRP are similar in their biological activities but show different tissue distributions. β-CGRP is mainly found in enteric nerves and in the pituitary gland, while α-CGRP is found predominantly in sensory neurons and in the CNS.5 CGRP causes cranial vasodilatation and facilitates nociception. During a migraine attack, trigeminal activation results in the release of CGRP from presynaptic nerve terminals and induces vasodilatation and neurogenic inflammation in leptomeningeal and extracranial vessels, which gives rise to the typical throbbing pain of migraine. Goadsby and Edvinsson6 showed that plasma concentrations of CGRP are elevated in the external jugular venous blood during migraine headaches and that sumatriptan can abort the rise in CGRP and the headache.4 CGRP given IV causes headache only in migraine patients and CGRP antagonists are effective for the acute treatment of migraine.7 Until now, CGRP elevation in the plasma has not been reproduced in all studies.8 However, technical problems have sometimes hampered the proper measurements of CGRP.9

Comparison of two analyzers for measurement of plasma total carbon dioxide concentration in horses

To determine the degree of agreement between 2 analyzers for measurement of total CO₂ concentration (ctCO₂) in equine plasma. 6 healthy untrained horses, 6 trained Standardbreds undergoing a simulated race protocol, and 135 trained Standardbreds at a racetrack. Jugular venous blood samples were obtained from all horses. Two analyzers (commonly used analyzer A and less expensive analyzer B) were used to measure plasma ctCO₂ in each sample. Validation of both analyzers was conducted in accordance with guidelines established by the Clinical and Laboratory Standards Institute and involved characterization of linearity, total analytic error, and bias estimation. Total analytic error (instrument SD) was 0.58 mmol/L (coefficient of variation, 1.6%) and 0.49 mmol/L (coefficient of variation, 1.4%) for analyzers A and B, respectively, when measuring an aqueous standard containing 36.0 mmol of CO₂/L. A 1 g/L decrease in plasma protein concentration corresponded to an increase in ctCO₂ measured with analyzer B of 0.065 mmol/L. A difference plot indicated that analyzer B produced values 2.7% higher than analyzer A for 103 samples from the 6 trained and exercised Standardbreds (mean plasma protein concentration, 67 g/L). Analyzer B provided adequate precision and linearity for measurement of ctCO₂ from 5 to 40 mmol/L and was therefore suitable for measuring ctCO₂ in equine plasma, provided allowances are made for changes in plasma protein concentration.

Impact of the blood sampling site on time-concentration drug profiles following intravenous or buccal drug administration.

The aim of this study was to examine the effect of the sampling site on the drug concentration-time profile, following intravenous or buccal (often called 'oral transmucosal') drug administration. Buprenorphine (20 μg/kg) was administered IV or buccally to six cats. Blood samples were collected from the carotid artery and the jugular and medial saphenous veins for 24 h following buprenorphine administration. Buprenorphine concentration-time data were examined using noncompartmental analysis. Pharmacokinetic parameters were compared using the Wilcoxon signed rank test, applying the Bonferroni correction. Significance was set at P < 0.05. Following IV administration, no difference among the sampling sites was found. Following buccal administration, maximum concentration [jugular: 6.3 (2.9-9.8), carotid: 3.4 (1.9-4.9), medial saphenous: 2.5 (1.7-4.1) ng/mL], area under the curve [jugular: 395 (335-747), carotid: 278 (214-693), medial saphenous: 255 (188-608) ng·min/mL], and bioavailability [jugular: 47 (34-67), carotid: 32 (20-52), medial saphenous: 23 (16-55)%] were higher in the jugular vein than in the carotid artery and medial saphenous vein. Jugular venous blood sampling is not an acceptable substitute for arterial blood sampling following buccal drug administration.

Prostaglandin E1 or E2 (PGE1, PGE2) prevents premature luteolysis induced by progesterone given early in the estrous cycle in ewes

The objective of this study was to determine whether prostaglandin E1 (PGE1) or prostaglandin E2 (PGE2) prevents premature luteolysis in ewes when progesterone is given during the first 6 days of the estrous cycle. Progesterone (3 mg in oil, im) given twice daily from Days 1 to 6 (estrus = Day 0) in ewes decreased (P < 0.05) luteal weights on Day 10 postestrus. Plasma progesterone concentrations differed (P < 0.05) among the treatment groups; toward the end of the experimental period, concentrations in jugular venous blood decreased (P < 0.05) compared with the other treatment groups. Plasma progesterone concentrations in ewes receiving PGE1 or PGE1 + progesterone were greater (P < 0.05) than in vehicle controls or in ewes receiving PGE2 or PGE2 or PGE2 + progesterone. Chronic intrauterine treatment with PGE1 or PGE2 prevented (P < 0.05) decreases in plasma progesterone concentrations, luteal weights, and the proportion of luteal unoccupied and occupied LH receptors on Day 10 postestrus in ewes given exogenous progesterone, but did not affect (P > 0.05) concentrations of PGF2α in inferior vena cava blood. Progesterone given on Days 1 to 6 in ewes advanced (P < 0.05) increases in PGF2α in inferior vena cava blood. We concluded that PGE1 or PGE2 prevented progesterone-induced premature luteolysis by suppressing loss of luteal LH receptors (both unoccupied and occupied).