bluuebunny/crossref_metadata_2025_split huggingface dataset:
Purine metabolite washout and platelet aggregation at reflow after tourniquet ischemia: effect of intravenous regional lidocaine
Authors: NAESH O. , HALJAMAE H. , SKIELBOE M. , ANDERSEN P. , SZTUK F. , IBSEN A. , HINDBERG I. 
Published: January 2009

Tourniquet ischemia will influence the biochemical milieu of tissue cells and affect the metabolism of purines in skeletal muscle distal to the occlusion. At reperfusion, generation of oxygen radicals by the hypoxanthine‐xanthine oxidase system may ensue, influencing white blood cell and thrombocyte aggregation, causing damage to the endothelial cell barrier and inducing non‐reflow type phenomena. Amide‐type local anaesthetics are known to affect local vasotone, leukocyte adherence and platelet function but the influence of lidocaine on purine metabolite washout and platelet aggregation following tourniquet ischemia for lower limb surgery is not known in detail. Therefore, the effects of regional intravenous lidocaine during tourniquet ischemia for knee surgery on purine catabolite washout and platelet function following reflow were assessed.Eight patients served as control (G‐group) and 8 (L‐group) received 100 ml of lidocaine (2.5 mg/ml) in the emptied venous bed of the leg to be operated. All patients had spinal anaesthesia (0.5% bupivacainc). Effluent venous blood from the leg and radial arterial blood was collected and analysed for xanthine (X), hypoxanthine (HX), base excess (BE), pH and potassium before and after reperfusion. Platelet ADP‐induced aggregation (ADP‐agg.) and secretion of beta‐thromboglobulin (β‐TG) were measured in the effluent blood as well as systemically. After tourniquet release (TR), X and HX were significantly increased in effluent venous blood but the washout was enhanced in the L‐group during the initial reperfusion phase. BE was significantly higher in the L‐group both before and after TR whereas pH and potassium washout was comparable between the groups. No systemic effects on platelets were detected after tourniquet release but ADP‐agg. in effluent venous blood was attenuated in 6 out of 8 patients in the L‐group (NS).It is concluded that HX and X are generated during leg ischemia. Regional intravenous lidocaine, most probablythrough a vasodilatory mechanism and inhibition of white blood cell activation, may attenuate non‐reflow phenomena and thereby exert beneficial effects on post‐ischemic recovery by enhancing post‐ischemic tissue reperfusion.
Autotransfusion after open heart surgery: quality of shed mediastinal blood compared to banked blood
Authors: SCHMIDT H. , KONGSGAARD U. E. , GEIRAN O. , BROSSTAD F. 
Published: January 2009

The need to conserve a patient's own blood and avoid homologous transfusion is now well recognized. Therefore, techniques designed to reduce requirements for homologous blood transfusions have been developed. One of the methods is autotransfusion of shed mediastinal blood after open‐heart surgery. The objectives of the present study were to investigate osmotic fragility and oxygen transport capacity of shed mediastinal blood compared to patient blood and stored packed red blood cells (SAGM).Shed mediastinal blood from ten consecutive patients undergoing elective cardiac surgery (coronary bypass grafting) was studied and compared to patient blood, 10 units of 3 weeks old and 10 units of 5 weeks old stored packed red blood cells (SAGM). Oxygen transport capacity was investigated by calculation of p50 for oxygen by use of the oxygen status algorithm (OSA 2.0) programme and measurement of 2,3‐diphosphoglycerate (2,3‐DPG) concentrations. The osmotic fragility was determined using increasing concentrations of saline.2,3‐DPG concentrations in shed mediastinal blood (5,3 mikromol/ml erythrocyte) were within the range measured in patient blood, but significantly higher than SAGM blood (P<0.001). P50 for oxygen (3.5 kPa) in shed mediastinal blood was not significantly different compared to patient blood, but significantly higher (P<0.01) compared with stored SAGM blood. The osmotic fragility in shed mediastinal blood was not significantly different compared to patient blood, but significantly lower (P<0.001) than the osmotic fragility in stored SAGM blood. This suggests that red cells saved from shed mediastinal blood have better oxygen transport capacity and may have longer survival compared to stored blood.
Direct cadiac electorphysiologic effects of sufentanil and vecuronium in isolated guinea‐pig hearts
Authors: Weber G. , Stark G. , Stark U. 
Published: January 2009

Sufentanil and vecuronium are commonly used simultaneously in anaesthesia. Bradycardia and asystole have been described immediately after the administration of these two compounds. Therefore, the purpose of the present study was to evaluate the direct cardiac effects of sufentanil and vecuronium in all parts of the cardiac pacemaker and conduction system.The electrophysiological effects of sufentanil and vecuronium were studied in isolated spontaneously beating guinea‐pig hearts perfused by the method of Langendorff. At a concentration of 0.1 μmol/1 sufentanil a significant reduction of the spontaneous sinus rate, prolongation of atrioventricular, intraventricular and His' bundle conduction could be observed. The highest concentration of 10 μmol/1 of sufentanil led to an overall slowing of conduction velocity and to an profound slowing of spontaneous sinus rate. AV nodal as well as atrial and ventricular refractoriness were markedly prolonged at this high concentration of sufentanil. In contrast, during perfusion with vecuronium at a concentration of 0.1 μmol/1 up to 10 μmol/1 no significant effects on cardiac conduction and pacemaker activity could be observed.In conclusion, the electrophysiological effects of sufentanil are comparable to that of unspecific calcium antagonists. Therefore, especially in patients with a preexisting damage of the cardiac conduction system, the indirect effect of the combination of sufentanil and vecuronium which is predominantly responsible for bradycardia and asystole may be worsened by the direct effects of sufentanil.
Do changes in carhiac output affect the inspiratory to end‐tidal oxygen dfference?
Authors: BENGTSSON J. , EDERBERG S. , STENQVIST O. , BENCTSO J. P. 
Published: January 2009

Background. The paramagnetic technique has made it possible to monitor the end‐tidal oxygen concentration and P(I‐ET)O2, i. e. inspiratory to end‐tidal oxygen difference, breath‐by‐breath. Little is known about the implications of a changing P(I‐ET)O2, but so far studies have shown it to be a quick and sensitive variable to detect hypoventilation. This study was designed to observe the circulatory effects on P(I‐ET)O2 in an experimental setting but monitored as in a clinical situation.Methods. We assessed the oxygen difference during changes in cardiac output induced by intravenous ephedrine‐hydrochloride in 12 healthy male volunteers. P(I‐ET)O2 was measured with a fast‐response paramagnetic differential oxygen sensor. Cardiac output was measured with non‐invasive transthoracie electrical bioimpedance. As stimultaneous changes in metabolism and ventilation will also influence P(I‐ET)O2, oxygen uptake and expired minute volume were monitored. After a rest period, the subjects had an intravenous injection of ephedrine‐hydrochloride 0.1 mg·kg‐1 followed by a 30‐min observation period.Results. Cardiac output increased significantly as did the oxygen uptake and the ventilation. We found no biologically significant correlation between cardiac output and P(I‐ET)O2. The P(I‐ET)O2 was influenced by ventilation and metabolism.
Effects of halothane and isoflurane on antigen‐ and leukotriene‐D4‐induced constriction of guinea pig trachea
Authors: TUDORIC N. , COON R. L. , KAMPINE J. P. , BOSNJAK Z. J. 
Published: January 2009

We investigated the mechanism of the action of volatile anesthetics on the airway smooth muscle constricted by an antigen and leukotriene‐D4(LTD4).Excised tracheal rings from ovalbumin‐sensitized guinea pigs were suspended in eight tissue baths. Halothane or isoflurane was aerated into four tissue baths, while the remaining four served as time controls. To assess the antispasmogenic activity of halothane and isoflurane, concentration‐response curves for antigen and LTD4were constructed exposed to anesthetics and compared to controls. The spasmolytic activity of halothane and isoflurane was measured in the tracheal rings constricted by a single antigen challenge or by EC50of LTD4.Both halothane and isoflurane produced significant rightward shifts of ovalbumin and LTD4concentrationresponse curve with corresponding increases in the EC50values. Halothane increased the EC50value for LTD1from 5.38±0.43×10‐9M to 1.2±0.18×10‐8M, and for ovalbumin from 1.2±0.06×10‐4mg/ml to 3.03±0.28×10‐4mg/ml. Isoflurane increased the EC50value for LTD4from 5.17±0.64×10‐9M to 8.98±1.01×10‐9M, and for ovalbumin from 1.21±0.09×10‐4mg/ml to 2.61±0.19×10‐4mg/ml. Furthermore, halothane and isoflurane significantly reduced the magnitude of antigen‐and LTD4‐induced constriction. In 30 min intervals, 1% and 2% halothane reduced the magnitude of the ovalbumin‐induced constriction by 32% and 50%, respectively, while isoflurane (2% and 4%) caused relaxation of 16% and 35%, respectively. The magnitude of LTD4‐induced constriction was reduced by 17% and 24%, with 1% and 2% halothane, respectively. Isoflurane (2% and 4%) reduced this constriction by 25% and 25%, respectively.In conclusion, halothane and isoflurane attenuate and prevent the constrictive response of airway smooth muscle to allergen and LTD4. A direct, nonspecific dilating effect is suggested as the mechanism responsible for the observed effects.
Hyperkalaemia associated with haemorrhagic shock in rabbits: mochfication by succinylcholine, vecuroniurn and blood transfusion
Authors: ANTOCNINI J. F. , MARK K. 
Published: January 2009

In haemorrhagic patients, hyperkalaemia may occur after succinylcholine administration. We investigated in haemorrhagic rabbits whether vecuronium caused hyperkaelemia and if blood transfusion prevented succinylcholine‐induced hyperkalaemia.Rabbits were lightly anaesthetized with halothane/N2O and 30‐35 ml/kg blood were withdrawn to cause arterial pH to decrease to ∼ 7.0‐7.1. Group C (n = 12) received 3 ml saline, Group S (n = 13) received succinylcholine lmg/kg. Group V (n = 7) received vecuronium 0.25 mg/kg and Group T (n = 9) was transfused with 10 ml/kg blood 10 min prior to receiving succinylcholine 1 mg/kg. K+ analysis was repeated at 5 min, and at 10 min in most animals.Haemorrhage increased K+ (mmol·1‐1, mean ± SD): Group C, 3.4±0.3 to 6.8±1.8; Group S, 3.8±0.5 to 6.9±2.3; Group V, 3.8±0.3 to 7.1±1.9; Group T, 3.6±0.5 to 7.6±2.9. K+ decreased in Group T (to 5.4±1.8) after blood transfusion. K+ increased at 5 min in Group S (to 8.7±2.6) and at 10 min for Group C (to 8.4±1.7) and Group T (to 7.2±2.3). The K+ increase at 5 min for Group S (1.8±0.8) was significantly higher than those for Group C (1.0±0.6) or Group V (0.9±0.4), but was not different from that of Group T (1.5±0.7).We conclude that haemorrhage and succinylcholine cause hyperkalaemia in rabbits. Muscle relaxation itself does not appear to be a factor, but transfusion may lessen the hyperkalaemia.
Bio‐/haemocompatibility: implications and outcomes for sensors?
Authors: KYROLAINEN M. , RIGSBY P. , EDDY S. , VADGAMA P. 
Published: January 2009

Sensors are a sample contacting technology, and when exposed to biological matrices tend to suffer from the problem of poor biocompatibility and surface fouling. The effects are evidenced by time dependant signal drift (particularly for those devices which are implanted intravascularly). Practical methods to reduce such effects require an understanding of the interface between the electrode and its environment prior to assessment of the potential areas for improvement. Current procedures employed to overcome the observed losses in electrode sensitivity (following exposure to whole blood) include surface modification of the outer diffusion limiting membrane (via variation in film porosity) or even biomimicry of the fluid cell membrane. At amperometric electrodes incorporation of additional inner perm‐selective membranes has achieved a reduction in electrode passivation from undesirable surface active compounds as has the use of low polarisation potentials. Other studies have attempted to induce an aqueous barrier between the matrix and the electrode tip which physically prevents passage of cellular components from the sensor surface.Careful choice of the system and materials will ultimately lead to biocompatible non‐fouling devices capable of functioning in an array of bio‐environments suitable for clinical monitoring of the critically ill patient.
Central venous versus mixed venous oxygen content
Authors: FABER T. 
Published: January 2009

Mixed venous oxygen content (commonly measured as oxygen saturation) is a highly relevant parameter in the monitoring of critically ill patients; unfortunately, its measurement requires catheterization of the pulmonary artery. Though less invasive, the central venous oxygen saturation is an unsatisfactory substitute, due to fluctuations in perfusion distribution and regional oxygen extraction in the course of illness.The present study examined the relation of oxygen contents in simultaneously withdrawn central venous and mixed venous blood samples from critically ill patients, in order to validate a hypothetical algorithm for the estimation of mixed venous oxygen content from a central venous sample: Although the proposed algorithm had a fairly high power of prediction, its merits in comparison to assuming simple proportionality between central venous and mixed venous oxygen content seemed marginal.However, as it is likely that the results so far are mathematically coupled, further prospective studies are necessary.
Indicators of histohypoxia
Authors: WILLIS N. , MOGRIDGE J. 
Published: January 2009

Cellular tissue damage due to inadequate oxygen supply is frequently encountered in the critically ill patient and can be the end result of a number of conditions. The eventual disruption to the normal processes required for the cell to survive can be due either to the hypoxic state per se or by damage caused during reperfusion of the tissue.Blood gas analysis is commonly used as a macro indicator of oxygen supply, state of art blood gas analysers provide information for oxygen tension (pO2), haemoglobin oxygen saturation (SO2) and concentration (THb), ideally, in arterial and mixed venous blood.The concurrent measurement of carbon dioxide tension (pCO2) and pH will allow the calculation of variables which assist in differentiating between respiratory and non‐respiratory conditions.Measurement of cardiac output and clinical assessment of the patients' oxygen requirements will complete the macro picture of supply and demand and although computed indicators of hypoxia have been improved in recent years (1, 2) the definitive diagnosis of histohypoxia requires the measurement of the cellular and subcellular products of metabolic processes that are present when an inappropriate concentration of oxygen has been experienced.However, increases, for example, in blood lactate concentration can occur when an ischaemic area is reperfused and it is argued conversely, that the absence of hyperlactataemia in conditions such as acute respiratory distress syndrome does not necessarily preclude delivery dependence of oxygen consumption with the attendant potential for tissue hypoxia (3). Nevertheless there is general agreement that blood lactate levels can serve as a reliable clinical guide to therapy (4).The laboratory measurement of the metabolic products that accumulate when cellular oxygen supply is limited has become far less labour intensive and with the development of increasingly sophisticated instrumentation, these analytes can be available in small to medium hospital laboratories as well as the larger units.The relatively rapid and accurate analysis of metabolites that accumulate in hypoxic states has allowed us to measure concentrations of blood lactate, pyruvate, β‐hydroxybutyrate and acetoacetate and calculate the lactate/pyruvate ratio and β‐hydroxybutyrate/acetoacetate ratio.These measurements and ratios can then be compared with the non invasive macro blood gas indicators in order to determine their effectiveness as additional “routine” investigations and to indicate how each of the variables contributes to the eventual diagnosis.The parameters used in this study are as follows:Oxygen tension ‐ pO2,Haemoglobin oxygen saturation ‐ SaO2Haemoglobin concentration ‐ THbHydrogen ion concentration as ‐ pHConcentration of extractable oxygen ‐ CxOxygen extraction tension ‐ pxConditional extraction at an assumed pvO2 = 30 mmHg ‐ C(a‐30)O2Lactate and pyruvateβ‐hydroxybutyrate and acetoacetate
Notes on the apparent discordance of pulse oximetry and multi‐wavelength haemoglobin photometry
Authors: NIJLAND R. , JONGSMA H. W. , NlJHUIS J. G. , OESEBURG B. , ZlJLSTRA W. G. 
Published: January 2009

Multi‐wavelength photometers, blood gas analysers and pulse oximeters are widely used to measure various oxygen‐related quantities. The definitions of these quantities are not always correct. This paper gives insight in the various definitions for oxygen quantities. Furthermore, the possible influences of dyshaemoglobins and fetal haemoglobin on the accuracy of pulse oximetry are discussed.As pulse oximeters are constructed for the determination of arterial oxygen saturation, they should be validated with sample oxygen saturation values and not with the oxyhaemoglobin fraction. The influence of carboxy‐haemoglobin is insubstantial over an oxygen saturation range of 0% to 100%. Through the presence of methaemoglobin, pulse oximetry will give an underestimation above 70% and an overestimation below 70% oxygen saturation. The influence of fetal haemoglobin is insignificant in the neonatal use of pulse oximetry, in the range of 75% to 100% arterial oxygen saturation. However, a pulse oximeter underestimates the arterial oxygen saturation at the 25% level with 5%, if the pulse oximeter has been calibrated in human adults. Such a low level of arterial oxygen saturation can be present in the fetus during labor.
Preliminary evaluation of a new continuous intra‐arterial blood gas monitoring device
Authors: PAPPERT D. , ROSSAINT R. , LEWANDOWSKI K. , KUHLEN R. , GERLACH H. , FALKE K. J. 
Published: January 2009

Continuous intra‐arterial blood gas monitoring is a new technique, possibly offering therapeutic advantages through improved monitoring in patients prone to hypoxaemia, hypercapnia and/or respiratory acidosis. Therefore, we studied the clinical applicability, reliability, precision and side effect of long‐term continuous intraarterial blood gas monitoring in patients suffering from severe acute respiratory distress syndrome.In 10 patients continuous intra‐arterial blood gas monitoring based on fluorescent optodes technique was performed. At 4 h intervals, arterial blood samples for in vitro blood gas analyses were drawn, stored in ice, and analysed within 3 min. Evaluation of data retrieved from the continuous intra‐arterial blood gas monitoring and in vitro blood gas analysis was based on 596 data points using 10 catheters. Average length of insertion was 281±215 h, max. lengths of stay was 750 h. Arterial blood gas data obtained in vivo were compared to the mean of in vivo and in vitro arterial blood gases.Inter‐catheter bias, expressed as percent difference between continuous intra‐arterial blood gas and mean in vitro blood gas analysis was 0. 19±0. 23% for pH, 1. 1 ±5. 2% for PaCO2 and 1. 6±5. 7% for PaO2. No significant gas partial pressure dependent change in precision was demonstrable. There was no significant time dependent drift in sensor precision over the study period. No negative side‐effects related to IABG monitoring were observed.We conclude that long‐term use of this new device is possible in patients and represents a reliable alternative to conventional in vitro arterial blood gas analysis, when continuous monitoring of blood gases and/or acid‐base balance is critical.
Base excess or buffer base (strong ion difference) as measure of a non‐respiratory acid‐base disturbance
Authors: SIGGAARD‐ANDERSEN O. , FOGH‐ANDERSEN N. 
Published: January 2009

Stewart in 1983 (Can J Physiol Pharmacol 1983: 61: 1444) reintroduced plasma buffer base under the name “strong ion difference” (SIDl. Buffer base was originally introduced by Singer and Hastings in 1948 (Medicine (Baltimore) 1948: 27: 223). Plasma buffer base, which is practically equal to the sum of bicarbonate and albuminate anions, may be increased due to an excess of base or due to an increased albumin concentration. Singer and Hastings did not consider changes in albumin as acid‐base disorders and therefore used the base excess, i. e., the actual buffer base minus the buffer base at normal pH and pCO2, as measure of a non‐respiratory acid‐base disturbance. Stewart and followers, however, consider changes in albumin concentration to be acid‐base disturbances: a patient with normal pH, pCO2, and base excess but with increased plasma buffer base due to increased plasma albumin concentration get the diagnoses metabolic (strong ion) alkalosis (because plasma buffer base is increased) combined with metabolic hyperalbuminaemic acidosis. Extrapolating to whole blood, anaemia and polycytaemia should represent types of metabolic alkalosis and acidosis, respectively. This reveals that the Stewart approach is absurd and anachronistic in the sense that an increase or decrease in any anion is interpreted as indicating an excess or deficit of a specific acid. In other words, a return to the archaic definitions of acids and bases as being the same as anions and cations.We conclude that the acid‐base status (the hydrogen ion status) of blood and extracellular fluid is described in terms of the arterial pH, the arterial pCO2, and the extracellular base excess. It is measured with a modern pH‐blood gas analyser. The electrolyte status of the plasma is a description of the most important electrolytes, usually measured in venous blood with a dedicated electrolyte analyser, i. e., Na+ Cl‐, HCO3“, and K+. Albumin anions contribute significantly to the anions, but calculation requires measurement of pH in addition to albumin and is usually irrelevant. The bicarbonate concentration may be used as a screening parameter of a nonrespiratory acid‐base disturbance when respiratory disturbances are taken into account. A disturbance in the hydrogen ion status automatically involves a disturbance in the electrolyte status, whereas the opposite need not be the case.
The oxygen status of fetal blood
Authors: SIGGAARD‐ANDERSEN O. , HUCH R. 
Published: January 2009

Objective: To estimate the acid‐base and oxygen status of fetal blood and compare with maternal placental venous blood.Data sources and calculations: We selected pH and blood gas data from the literature pertaining to umbilical vein and artery blood obtained by cordocentesis and estimated values for the 30th and 40th gestational week.Average values for maternal venous blood leaving the placenta were estimated on the assumption of equal maternal arterio‐venous and umbilical veno‐arterial total oxygen concentration differences.Results: pH and pCO2 of maternal blood leaving the placenta and umbilical vein blood are almost identical at week 30. A small pCO2 and pH difference may exist at week 40. The pO2 of the maternal placental venous blood and umbilical vein blood are almost identical at week 30, but at week 40 a pO2 difference indicates an umbilical arterio‐venous shunting of as much as 30%. The fetal mixed venous pO2 falls from 2. 6 kPa to 2. 2 kPa from the 30th to the 40th gestational week.Conclusion: More accurate measurements are needed to confirm our results. Future measurements should be performed with a combined pH‐blood gas analyser and haemoximeter to allow determination of the complete oxygen status of the blood.