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Arterial Blood Samples (arterial + blood_sample)
Selected AbstractsTreatment of Premature Calves with Clinically Diagnosed Respiratory Distress SyndromeJOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 2 2008T. Karapinar Background: Respiratory distress syndrome (RDS) has been reported previously in premature calves. However, there have been no published data on the effect of surfactant replacement therapy in the treatment of premature calves with RDS. Hypothesis: Surfactant replacement therapy added to the standard treatment for premature calves clinically diagnosed with RDS would increase the viability of the calves. Animals: Twenty-seven premature calves with clinically diagnosed RDS. Methods: Twenty calves were instilled intratracheally with bovine lung surfactant extract and provided with standard treatment for RDS (surfactant group). Seven calves were given only standard care for RDS without surfactant therapy and placed in the control group. Standard treatment for newborn calves with RDS includes warming, administration of intranasal oxygen, fluid replacement, administration of antibiotics, and immunoglobulin solution. Arterial blood samples were collected from the calves at 3 observation points, the first just before treatment (hour 0) and at 2 hours (hour 2) and 24 hours (hour 24) after treatment was started to determine if ventilation was adequate, improving, or deteriorating. Blood gases, pH, bicarbonate, and lactate concentrations were measured. Results: In the surfactant group, mean partial pressure of oxygen significantly increased at hours 2 and 24. Mean partial pressure of carbon dioxide decreased and mean arterial blood pH increased at hour 24 in the surfactant group compared with the control group (P < .05). Of the 20 calves in the surfactant group, 12 survived and 8 died. All 7 calves in the control group died. Conclusions and Clinical Importance: The results of this study suggest that surfactant replacement therapy may reduce neonatal deaths in premature calves with clinically diagnosed RDS. [source] The use of propofol and remifentanil for the anaesthetic management of a super-obese patientANAESTHESIA, Issue 8 2007L. La Colla Summary Morbid obesity is defined as body mass index (BMI) >,35 kg.m,2, and super-obesity as BMI >,55 kg.m,2. We report the case of a 290-kg super-obese patient scheduled for open bariatric surgery. A propofol-remifentanil TCI (target controlled infusion) was chosen as the anaesthetic technique both for sedation during awake fibreoptic nasotracheal intubation and for maintenance of anaesthesia during surgery. Servin's weight correction formula was used for propofol. Arterial blood samples were taken at fixed time points to assess the predictive performance of the TCI system. A significant difference between measured and predicted plasma propofol concentrations was found. After performing a computer simulation, we found that predictive performance would have improved significantly if we had used an unadjusted pharmacokinetic set. However, in conclusion (despite the differences between measured and predicted plasma propofol concentrations), the use of a propofol-remifentanil TCI technique both for sedation during awake fibreoptic intubation and for Bispectral Index-guided propofol-remifentanil anaesthesia resulted in a rapid and effective induction, and operative stability and a rapid emergence, allowing rapid extubation in the operating room and an uneventful recovery. [source] Arterial concentration of 99mTc-sestamibi at rest, during peak exercise and after dipyridamole infusionCLINICAL PHYSIOLOGY AND FUNCTIONAL IMAGING, Issue 6 2004Niels Peter Rønnow Sand Summary Tracers for myocardial perfusion imaging during stress should not only have high cardiac uptake but they should also have a fast blood clearance to prevent myocardial tracer uptake after the ischaemic stimulus. The present study characterize the early phase of the arterial 99mTc-sestamibi (MIBI) time-activity curve after venous bolus injection at rest, during peak exercise and after dipyridamole infusion. We included 11 patients undergoing angioplasty for one-vessel disease (rest study) and 20 patients evaluated for the detection of haemodynamic significant coronary stenoses by 99mTc-sestamibi single photon emission computed tomography (SPECT) using either bicycle exercise testing (10 patients) or standard dipyridamole testing (10 patients). Arterial blood samples of 1 ml were taken from the left femoral artery (rest study) or the right radial artery (exercise and dipyridamole studies) every 5 s during the first 5 min postinjection. In the exercise and the dipyridamole studies blood sampling were extended to include blood samples every 5 min 5,30 min postinjection. Peak MIBI concentration was lower and decrease in concentration slower after tracer injection during exercise than during dipyridamole stress testing. This may cause an underestimation of perfusion defects during exercise because of MIBI uptake after the ischaemic stimulus. The implications of the study not only refer to the choice of stress modality when using MIBI. This study also underlines the importance of considering early blood clearance in addition to regional myocardial tracerkinetic aspects such as myocardial extraction fraction when new tracers are introduced. [source] The Effect of Glutathione Modulation on the Concentration of Homocysteine in Plasma of RatsBASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 3 2000Kjell K. Øvrebø Elevated plasma homocysteine concentration in humans is associated with increased risk of arteriosclerosis and ischaemic heart disease. We studied whether the plasma homocysteine concentration could be changed by administration of drugs that modulate the concentration of glutathione in both plasma and tissue. Male wistar rats received reduced glutathione (0.5 mmol/kg), N -acetylcysteine (0.5 mmol/kg), L-buthionine-[S,R]-sulfoximine (2 mmol/kg) or Ringer acetate intravenously. Twenty min. later an arterial blood sample was drawn for the measurement of homocysteine and other thiols in the plasma. The thiols were quantified by reversed-phase ion-pair liquid chromatography and fluorescence detection. The total homocysteine concentration in plasma of fasted rats was 6.1±0.5 ,M. Intravenous administration of reduced glutathione or N -acetylcysteine reduced the homocysteine concentration in plasma significantly by 51% to 3.0±0.3 ,M and 63% to 2.2±0.2 ,M, respectively (P<0.05). In contrast, L-buthionine-[S,R]-sulfoximine increased the concentration of homocysteine by 41% to 8.6±0.6 ,M (P<0.05). The glutathione concentration in plasma was 19.5±1.9 ,M in controls and was unchanged by N -acetylcysteine administration. Reduced glutathione increased plasma glutathione to 379.7±22.9 ,M (P<0.05), whereas L-buthionine-[S R]-sulfoximine lowered the plasma glutathione concentration to 5.3±0.4 ,M. Homocysteine was negatively correlated to the glutathione (r=,0.399, P<0.01) and the cysteine (r=,0.52, P<0.01) concentrations in plasma. Our conclusion is that modulation of the glutathione levels influences the concentration of homocysteine in plasma of rats. [source] The effects of obstructive jaundice on the pharmacodynamics of propofol: does the sensitivity of intravenous anesthetics change among icteric patients?ACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 10 2009J. C. SONG Background Some studies suggest that certain clinical symptoms of cholestasis, such as fatigue and pruritus, result from altered neurotransmission. Patients with obstructive jaundice also have labile blood pressure and heart rate. In the present study, the authors investigated whether obstructive jaundice affects a patient's sensitivity to hypnotics and the haemodynamic profile of propofol. Methods Thirty-six ASA physical status I/II/III patients with serum total bilirubin (TBL) from 7.8 to 362.7 ,mol/l scheduled for bile duct surgery were recruited. A computer-controlled propofol infusion programmed for effect site target was used to rapidly attain and maintain sequential increase of the compartment concentration (from 1 to 3 ,g/ml). Each target-controlled concentration was maintained for about 12 min, and arterial blood samples were drawn for propofol concentration determination. The bispectral index (BIS) and mean arterial pressures (MAP) were used as indices of the propofol effect. The relation between the concentration and the effects was described by the Hill equation. The pharmacodynamic parameters were optimized using a nonlinear mixed-effect model. Results TBL was not a significant covariate of EC50 for the pharmacodynamic model. For BIS and MAP, the parameters of the pharmacodynamic model were Emax=75.77%, EC50=2.34 ,g/ml, and ,=1.82, and Emax=47.83%, EC50=1.49 ,g/ml, and ,=1.88, respectively. Conclusions We demonstrated that obstructive jaundice with serum TBL from 7.8 to 362.7 ,mol/l had no effect on propofol pharmacodynamics observed by BIS and MAP. [source] In Vivo Time-Course Changes in Ethanol Levels Sampled With Subcutaneous MicrodialysisALCOHOLISM, Issue 3 2008Eric A. Engleman Background:, The objective of this study was to determine time-course changes in in vivo ethanol (EtOH) concentrations using a novel subcutaneous (s.c.) microdialysis sampling technique. The hypothesis to be tested was that EtOH concentrations in the s.c. fluid would reflect blood EtOH concentrations. If this is the case, then s.c. microdialysis could allow a more detailed analysis of changes in in vivo levels of EtOH under different drinking paradigms. Methods:, Adult male and female Wistar rats and male alcohol-preferring (P) rats were used in this study. A loop-style microdialysis probe was designed for s.c. applications. After initial in vitro characterization, probes were implanted under the skin between the shoulder blades. Animals were allowed to recover 4 to 24 hours prior to microdialysis collection (2.0 ,l/min flow rate with isotonic saline). In vivo microdialysis experiments were then conducted to determine (i) the extraction fraction (or clearance) using EtOH no-net-flux (NNF) coupled with the alcohol clamp method, (ii) the dose,response and time-course effects after systemic EtOH administration and to compare with blood EtOH levels, and (iii) the time-course changes in EtOH levels during and after an EtOH drinking episode. Results:, In vivo probe recovery (extraction fraction) obtained using the alcohol clamp method was 69 ± 3%, and was comparable to the in vitro recovery of 73 ± 2%. For the EtOH dose,response experiment, rats injected i.p. with 0.5, 1.0, or 2.0 g/kg EtOH showed a clear dose,response effect in the s.c. dialysate samples. Peak concentrations (70, 123, and 203 mg%, respectively) were reached by 15 minutes after injection. In an experiment comparing levels of EtOH in s.c. dialysis and arterial blood samples in rats administered 1.0 g/kg EtOH, similar time-course changes in in vivo EtOH concentrations were observed with both i.g. and i.p. EtOH administration. In P rats drinking 15% EtOH during a 1-hour scheduled access period, EtOH levels in s.c. microdialysates rose rapidly over the session and peaked at approximately 50 mg% at 60 to 80 minutes. Conclusions:, Overall, these experiments indicate that s.c. EtOH and blood EtOH concentrations follow a similar time course. Moreover, s.c. microdialysis can be useful as an experimental approach for determining detailed time-course changes in in vivo EtOH concentrations associated with alcohol drinking episodes. [source] Effects of low dose dexamethasone treatment on basal cardiovascular and endocrine function in fetal sheep during late gestationTHE JOURNAL OF PHYSIOLOGY, Issue 2 2002Andrew J. W. Fletcher This study investigated the effects on ovine fetal basal cardiovascular and endocrine functions of fetal intravenous dexamethasone treatment, resulting in circulating concentrations that were one-fifth of the values measured clinically in human infants following maternal antenatal glucocorticoid therapy. Between 117-120 days gestation (dGA; term: ca 145 dGA), 26 Welsh Mountain sheep fetuses were surgically prepared under general anaesthesia with vascular catheters and a Transonic flow probe positioned around a femoral artery. At 125 ± 1 dGA, fetuses were infused with dexamethasone (2.06 ± 0.13 ,g kg,1 h,1i.v.; n= 13) or saline (n= 13) for 48 h. Daily fetal arterial blood samples were taken and cardiovascular data were recorded continuously (data acquisition system). Pressor, vasoconstrictor and chronotropic responses to exogenously administered doses of phenylephrine, angiotensin II and arginine vasopressin (AVP) were determined at 124 ± 1 (pre-infusion), 126 ± 1 (during infusion) and 128 ± 1 (post-infusion) dGA. Fetal cardiac baroreflex curves were constructed using peak pressor and heart rate responses to phenylephrine. Dexamethasone treatment elevated fetal mean arterial blood pressure by 8.1 ± 1.0 mmHg (P < 0.05), increased femoral vascular resistance by 0.65 ± 0.12 mmHg (ml min,1),1 (P < 0.05), depressed plasma noradrenaline concentrations and produced a shift in set-point, but not sensitivity, of the cardiac baroreflex (P < 0.05). Elevations in fetal arterial blood pressure, but not femoral vascular resistance and the shift in baroreflex set-point, persisted at 48 h following dexamethasone treatment. By 48 h following dexamethasone infusion, basal plasma noradrenaline concentration was restored, whilst plasma adrenaline and neuropeptide Y (NPY) concentrations were enhanced, compared with controls (P < 0.05). Fetal dexamethasone treatment did not alter the fetal pressor or femoral vasoconstrictor responses to adrenergic, vasopressinergic or angiotensinergic agonists. These data show that fetal treatment with low concentrations of dexamethasone modifies fetal basal cardiovascular and endocrine functions. Depending on the variable measured, these changes may reverse, persist or become enhanced by 48 h following the cessation of treatment. [source] Effect of perinatal asphyxia on thyroid-stimulating hormone and thyroid hormone levelsACTA PAEDIATRICA, Issue 3 2003DN Pereira Aim: To compare serum concentrations of thyroid hormones,T4, T3, free T4 (FT4) and reverse T3 (rT3),and thyroid-stimulating hormone (TSH) found in the umbilical cord blood of term newborns with and without asphyxia and those found in their arterial blood collected between 18 and 24 h after birth. A further aim of the study was to assess the association between severity of hypoxic-ischemic encephalopathy and altered thyroid hormone and TSH levels, and between mortality and FT4 levels in the arterial blood of newborns between 18 and 24 h of life. Methods: A case-control study was carried out. The case group comprised 17 term newborns (Apgar score ,3 and ,5 at the first and fifth minutes; umbilical cord blood pH ,7.15) who required bag and mask ventilation for at least one minute immediately after birth. The control group consisted of 17 normal, term newborns (Apgar score ,8 and ,9 at the first and fifth minutes; umbilical cord blood pH ,7.2). Cord blood and arterial blood samples were collected immediately after birth and 18 to 24 h after birth, respectively, and were used in the blood gas analysis and to determine serum concentrations of T4, T3, FT4, rT3 and TSH by radioimmunoassay. All newborns were followed-up until hospital discharge or death. Results: Gestational age, birthweight, sex, size for gestational age, mode of delivery and skin color (white and non-white) were similar for both groups. No differences were found in mean levels of cord blood TSH, T4, T3 and FT4 between the groups. In the samples collected 18 to 24 h after birth, mean levels of TSH, T4, T3 and FT4 were significantly lower in the asphyxiated group than in the control group. Mean concentrations of arterial TSH, T4 and T3 between 18 and 24 h of life were lower than concentrations found in the cord blood analysis in asphyxiated newborns, but not in controls. In addition, asphyxiated newborns with moderate/severe hypoxic-ischemic encephalopathy presented significantly lower mean levels of TSH, T4, T3 and FT4 than those of controls. None of the asphyxiated newborns with FT4 ,2.0 ng/dl died; 6 out of the 11 asphyxiated newborns with FT4 < 2.0 ng/dl died. Conclusions: Serum concentrations of TSH, T4, T3 and FT4 are lower in asphyxiated newborns than in normal newborns between 18 and 24 h of life; this suggests central hypothyroidism secondary to asphyxia. Asphyxiated newborns with moderate/severe hypoxic-ischemic encephalopathy present a greater involvement of the thyroid function and consequently a greater risk of death. [source] | ||||||||||