bluuebunny/crossref_metadata_2025_split huggingface dataset:
Propofol and gastric effects of morphine
Authors: Hammas B. , Thörn S.‐E. , Wattwil M. 
Published: March 2003

Objective: The purpose of this study was to evaluate whether propofol abolishes morphine‐induced effects on gastric emptying and gastric tone.Method: The study was carried out before anesthesia in 40 patients (ASA I–II). Gastric tone was measured in 20 patients by an electronic barostat. Volume changes were thereby registered continuously in an intragastric flaccid bag with a constant preset pressure. All patients received i.v. morphine 0.1 mg · kg−1 before the measurements and, in a randomized order, 10 of the patients also received a bolus dose of propofol 1 mg · kg−1 before morphine. Gastric emptying was studied with the paracetamol method in 20 patients. All patients received morphine 0.1 mg · kg−1 i.v. 10 min before oral ingestion of 1.5 g paracetamol in 200 ml water and, in a randomized order, 10 of the patients also received propofol, a bolus dose of 0.3 mg · kg−1 before morphine, followed by an infusion of 1 mg · kg−1 · h−1 during the whole study (2 h).Results: The volume in the intragastric bag increased in all patients receiving morphine without propofol. In the group that received propofol before morphine, the volume in the intragastric bag decreased in all patients. The volume differences between the groups were statistically significant (P<0.01). There were no statistically significant differences of the AUC60, Cmax and Tmax of serum paracetamol concentrations between the morphine and propofol‐morphine groups.Conclusion: Propofol did not abolish morphine‐induced delay of gastric emptying even if propofol abolished the decrease of gastric tone induced by morphine.
Opioids in cancer and chronic non‐cancer pain therapy – indications and controversies
Authors: Breivik H. 
Published: March 2003

Indications for strong opioids for cancer‐related pain as well as for chronic non‐cancer pain are that non‐opioid drugs, and other less risky therapies, fail and that the pain is opioid‐sensitive. The WHO analgesic ladder principle continues to serve as an excellent educational tool in the efforts by WHO in collaboration with the World Federation of Societies of Anaesthesiologists (WFSA) and The International Association for the Study of Pain (IASP) to increase knowledge of pharmacological pain therapy and increase availability of essential opioid analgesics world‐wide. Opioids differ in pharmacodynamics and pharmacokinetics, and patients have different pharmacogenetics and pain mechanisms. Sequential trials of the increasing numbers of available opioid drugs are therefore appropriate when oral morphine fails.Controversies continue concerning diagnosis and handling of opioid‐insensitive pain in cancer and chronic non‐cancer pain, opioid‐induced neurotoxicities, risks of tolerance, addiction, pseudo‐addiction, and methods for improving effectiveness and decreasing adverse effects of long‐term opioid therapy, treating breakthrough pain with immediate release oral and transmucosal opioids.Consensus guidelines have recently been developed in the Nordic countries concerning the ethical practice of palliative sedation when opioids and other pain‐relieving therapies fail in patients soon to die. Guidelines for long‐term treatment with strong opioids of chronic non‐cancer‐related pain are also being developed in the Nordic countries, where very diverging traditions for the usage of such therapy still exist.
Intraoperative epidural blockade prevents the increase in protein breakdown after abdominal surgery
Authors: Lattermann R. , Schricker T. , Wachter U. , Goertz A. , Georgieff M. 
Published: March 2003

Background: The aim of this study was to investigate the effect of epidural blockade with bupivacaine, restricted to the intraoperative period, on protein catabolism after major abdominal surgery.Methods: Fourteen patients undergoing cystoprostatectomy were randomly assigned to receive either general anaesthesia with isoflurane (control group, n=7) or a combination of general anaesthesia and epidural blockade with bupivacaine from segment T4 to S5 (epidural group, n=7). Rates of urea (Ra urea) and glucose production (Ra glucose) were measured three days before and three days after the operation using stable isotope tracers ([15N2]urea, [6,6‐2H2]glucose). Protein breakdown was calculated from the urea production rate. Plasma concentrations of metabolic substrates (urea, glucose, lactate, glycerol, amino acids) and hormones (insulin, glucagon, cortisol, adrenaline, noradrenaline) were also determined.Results: Protein breakdown significantly increased after surgery in the control group (P<0.05), while it remained unaltered in the epidural group (control; 66 (54–76), epidural; 43 (29–58) mg · kg−1 · h−1, P<0.05, median (range)). Glucose plasma concentration and Ra glucose increased in both groups to a similar extent (P<0.05). Plasma concentration of branched chain amino acids decreased after epidural analgesia to a value significantly lower than in the control group (P<0.05). Glutamine plasma concentration decreased in the control group (P<0.05), but did not change in the epidural group. There were no differences in plasma concentrations of insulin, cortisol and catecholamines between the two groups. Glucagon plasma concentration in the epidural group was significantly lower than in the control group (P<0.05).Conclusion: Intraoperative epidural blockade inhibits the increase in protein breakdown after abdominal surgery.
Acute effects of angiotensin II on myocardial performance
Authors: Broomé M. , Haney M. , Häggmark S. , Johansson G. , Åneman A. , Biber B. 
Published: March 2003

Background: Specific angiotensin II (Ang II) receptors exist in many organs including peripheral blood vessels, cardiac myocytes and the central nervous system. This suggests multiple sites of actions for Ang II throughout the cardiovascular system. Cardiac effects of Ang II are not completely understood, though its prominent vasoconstrictor actions are well described. This study was designed to assess left ventricular function during administration of Ang II using relatively load‐independent methods in a whole‐animal model.Methods: Ang II was infused in incremental doses (0–200 μg  ·  h−1) in anaesthetised instrumented pigs (n=10). Cardiac systolic and diastolic function were evaluated by analysis of the left ventricular pressure–volume relationship.Results: Heart rate (HR), mean arterial pressure (MAP) and systemic vascular resistance (SVR) increased dose‐dependently with Ang II, while cardiac output (CO) remained unchanged. Systolic function indices, end‐systolic elastance (Ees) and preload recruitable stroke work (PRSW), demonstrated dose‐dependent increases. The diastolic function parameter tau (τ) did not change with increasing Ang II dose.Conclusion: Ang II infusion caused increases in contractility indices in anaesthetised pigs in the doses used in this study. The mechanisms for these systolic function effects may be a direct myocardial effect or modulated through changes in autonomic nervous system activity.
Procalcitonin following elective partial liver resection – origin from the liver?*
Authors: Kretzschmar M. , Krüger A. , Schirrmeister W. 
Published: March 2003

Background: The origin of the inflammatory peptide procalcitonin (PCT) is still unknown. In the present study PCT concentrations in arterial and hepatic‐venous blood were examined in patients undergoing elective partial liver resection (LR) using a fiberoptic pulmonary arterial catheter placed in a liver vein to obtain further information on the origin of PCT.Methods: In 28 patients (21 male/7 female; average age of 58.8±8.8 years) undergoing LR, arterial and hepatic venous PCT concentrations were measured during 24 h perioperatively. The parallel blood withdrawals occurred immediately before the Pringle maneuver (Hx), 2 min, 1, 2, 6, 12, and 24 h after Hx. Over the whole period, the oxygen saturation in hepatic venous blood (ShvO2) was monitored. PCT concentrations were assayed by immunoluminometry.Results: We observed a significant increase in PCT concentration already 6 h after Hx compared to the values before Hx. Twenty‐four hours after Hx we found the highest plasma concentrations. It was conspicuous that hepatic venous PCT concentrations were always higher than the arterial ones (significantly from the 6th hour after Hx). There was no correlation between the courses of ShvO2 and PCT rise. A significant correlation was verified between Hx duration and PCT concentration measured 24 h after Hx both in the hepatic venous and arterial blood.Conclusions: The results of our investigation can be interpreted as evidence that liver (or the hepatosplanchnicus?) is a source of PCT. The mechanism of PCT induction cannot be clarified by our study: whether the induction of PCT was caused by an endotoxin translocation during the impeded splanchnic outflow or by the direct surgery‐induced lesion (hypoxia) of the liver remains unclear. However, the latter appears more probable because of the observed correlation between Hx duration and PCT concentration rise.
Losartan increases renal blood flow during isoflurane anesthesia in sheep
Authors: Ullman J. , Eriksson S. , Rundgren M. 
Published: March 2003

Background: Inhaled anesthetics cause a transient reversible depression of renal function by direct renal effects or indirectly by changes in neurohumoral systems or cardiovascular performance. When the sympathetic nervous activity is decreased during anesthesia, other vasoactive systems like vasopressin (AVP) and particularly the renin angiotensin system (RAS) are of importance for blood pressure maintenance. Little is known about how the renal circulation is affected by angiotensin receptor blockade during isoflurane anesthesia.Methods: The study was performed on isoflurane anesthetized sheep equipped with flow probes (placed around a femoral and a renal artery) and a pulmonary artery catheter. During stable conditions the sheep were given one or more of the following substances: isotonic saline (NaCl); losartan (LOS) 10 mg ·  kg−1; prazosin (PRAZ) 0.2 mg · kg−1 and a vasopressin V1‐receptor antagonist (AVP‐a) 10 μg · kg−1.Results: LOS and AVP‐a did not affect mean arterial pressure (MAP), whereas PRAZ lowered MAP significantly (from 98±12 to 65±7 mmHg). Renal blood flow (RBF) increased after LOS treatment (148±34 to 222±33 ml · min−1). The other substances were without effect on RBF. Femoral blood flow remained unchanged after all treatments.Conclusion: We conclude that the sympathoadrenal system is still the major determinant for blood pressure maintenance during isoflurane anesthesia in sheep. The apparently increased activity of the renin angiotensin system in this situation causes a reduction in renal blood flow, which is counteracted by angiotensin II AT1‐receptor blockade.
Low‐dose dobutamine stress and left ventricular wall motion monitored with transesophageal echocardiography versus hemodynamic data derived from pulmonary artery catheterization in patients scheduled for CABG
Authors: Palmgren I. , Hultman J. 
Published: March 2003

Background: The clinical acceptance of transesophageal echocardiography (TEE) as a monitoring technique for left ventricular function in open‐heart surgery is now widely recognized. This technique’s accurate imaging capabilities have been found to improve the information obtained by the pulmonary catheter (PAC) and thermodilution. TEE is also a less invasive technique than PAC. However, because it is costly, further comparisons between the techniques are worthwhile. This study compares hemodynamic data obtained with PAC and how these correspond to echocardiography data using TEE.Methods: Twenty‐four anesthetized patients undergoing elective coronary artery bypass grafting (CABG) were studied. They were monitored with PAC and TEE. A low‐dose dobutamine protocol for viability was used with doses of 5 and 10 μg  ·  kg−1  ·  min−1. Endpoints for this stimulation included on‐line visual change in left ventricle wall motion (LVWM), increased arterial blood pressure more than 40 mmHg, a heart rate (HR) increase of more than 20%, or ST depression on ECG exceeding 0.2 mV. Visual assessment of LVWM using the transgastric short‐axis view was made off line by a blinded observer. Six segments were used and a wall motion score was made at each level of dobutamine stimulation.Results & Conclusion:Two patients reached the endpoint for elevated blood pressure with a dobutamine dose of 5 μg  ·  kg−1  ·  min−1, and twenty‐two patients were stimulated to 10 μg  ·  kg−1  ·  min−1. There were significant increases in cardiac output (CO), stroke volume (SV), systolic arterial pressure (SAP), mean arterial pressure (MAP), diastolic arterial pressure (DAP), pulmonary capillary wedge pressure (PCWP) and left ventricle stroke work index (LVSWI), but not in HR and systemic vascular resistance (SVR). Moreover, the LVWM increased significantly, but not fractional area change (FAC). The main finding, however, was the increase in SV with an accompanying improvement in LVWM, suggesting that visual assessment of improved wall motion could substitute PAC and thermodilution monitoring in clinical settings which demand a quick estimate of left ventricular performance.
Preconditioning − endogenous defence mechanisms of the heart
Authors: Sommerschild Hilchen T. , Kirkebøen Knut Arvid 
Published: March 2003

The term ‘preconditioning’ refers to the paradoxical phenomenon that pretreatment with a potential noxious stress‐stimulus can increase cellular tolerance to subsequent noxious stress‐stimuli. This was first described in an experimental model in dogs in which short‐lasting periods of myocardial ischemia resulted in reduced infarction during a subsequent long‐lasting coronary artery occlusion. Similar observations have also been made in other species and in other organs. During the last few years, the term preconditioning has been expanded to include pretreatment with other physical stress‐stimuli or pharmacological agents that can increase cellular resistance to injury. The phenomenon probably represents a general adaptive response to cellular stress, but mechanisms involved are not fully clarified.This review focuses on preconditioning in the heart. Firstly, we want to address the observation that activation of endogenous defence mechanisms can increase cellular tolerance to several potentially noxious stimuli. Based on results from experimental research, we will give an overview of intracellular mechanisms that is currently in focus. Secondly, we want to address the potential role of preconditioning in clinical practice. We will present results from studies in patients with coronary artery disease and discuss possible clinical implications. Results show that the phenomenon probably exists in the human myocardium. In the future, this might be exploited in patients with acute coronary syndromes, especially since advanced techniques are now available for acute revascularization. Additionally, identification of possible mechanisms involved may influence the choice of medical treatment in high‐risk patients with stable coronary artery disease. Preconditioning can also be exploited during elective surgical procedures. This should be of great interest, as the extent of elective surgery in patients at high‐risk for coronary events is increasing. In this respect it is important to note that opioid‐receptors are probably involved in preconditioning in humans. The last part of this review will address the possible relation between preconditioning and different anesthetic agents and sedatives.
Effect of hemodiafiltration and sepsis on chemotaxis of granulocytes and the release of IL‐8 and IL‐10
Authors: Toft P. , Brix‐Christensen V. , Bæch J. , Krog J. , Jørgensen H. S. , Tønnesen E. , Petersen T. K. , Dagnæs‐Hansen F. 
Published: March 2003

Background: Extracorporeal circulation, such as cardiopulmonary bypass and hemodialysis, has been associated with an activation of the immune system. Continuous veno venous hemodiafiltration (CVVHD) is used in critically ill septic patients. During CVVHD, cytokines are excreted in ultrafiltrate. When the membranes, used in CVVHD, are incubated with leukocytes in vitro a slight production of cytokines is observed. Due to the underlying disease it is difficult to investigate the effect of CVVHD in septic patients. We therefore studied the separate effect of CVVHD on the chemotaxis of granulocytes, the proliferation of lymphocytes and the release of IL‐8 and IL‐10 in healthy pigs compared to an endotoxin and a control group.Methods: Thirty‐one pigs were anesthetized and mechanically ventilated. CVVHD was performed in 10 pigs. Eleven pigs received an infusion of Escherichia coli endotoxin 30 µg/kg, and 10 pigs served as a control group. The chemotaxis of granulocytes was measured in an assay chamber, and the cytokines IL‐8 and IL‐10 with an enzyme‐linked immunosorbent assay. The adhesion molecules CD18 and CD62 on lymphocytes were measured using monoclonal antibodies, and the lymphocyte proliferation was measured without stimulation and in response to mitogens.Results: CVVHD was accompanied by lymphocytopenia and increased spontaneous lymphoproliferative response, but no change in adhesion molecules on lymphocytes or cytokine levels in plasma, and no decrease in the chemotaxis of granulocytes. Following endotoxin we observed a pronounced lymphocytopenia and an increased secretion of IL‐8 and IL‐10, a decrease in the expression of CD18 on lymphocytes and in the stimulated lymphocyte proliferation and in the chemotaxis of granulocytes.Conclusion: CVVHD does not, in contrast to endotoxin‐induced sepsis, influence chemotaxis of granulocytes, the production of IL‐8 and IL‐10 or the proliferation of lymphocytes.
Adrenocortical function and multiple organ failure in severe sepsis
Authors: Loisa P. , Rinne T. , Kaukinen S. 
Published: March 2003

Background: Some patients with severe sepsis may have relative adrenocortical insufficiency, although not all studies confirm this finding. Corticosteroids play an important role in controlling excessive immune response, and they may reduce the severity of organ dysfunction in critical illness. In this prospective study, we investigated the incidence of adrenal insufficiency in severe sepsis and its relation to the development of multiple organ failure.Methods: Forty‐one patients meeting the criteria for severe sepsis were studied. A short ACTH stimulation test was carried out within 24 h of the diagnosis of sepsis. Peak serum cortisol level < 680 nmol/L and a rise of less than 260 nmol/L were used as the criteria for relative adrenocortical insufficiency.Results: Relative adrenocortical insufficiency was detected in six patients. Duration of the ICU stay (P = 0.002) and mechanical ventilation (P = 0.024) were significantly longer in patients with impaired adrenal function. In the survivors, SOFA scores were significantly higher in patients with impaired adrenal function. The plasma ACTH levels were normal in most of the patients with relative adrenal insufficiency, whereas most patients with normal adrenal function had extremely low plasma ACTH levels.Conclusion: The ICU stay was longer and multiple organ failure more severe in patients with impaired adrenocortical function. There was a clear dissociation between ACTH and cortisol levels in AAR patients. This finding suggests that the integrity of the hypothalamic–pituitary–adrenal axis may be impaired in severe sepsis.
Albumin extravasation and tissue washout of hyaluronan after plasma volume expansion with crystalloid or hypooncotic colloid solutions
Authors: Berg S. , Golster M. , Lisander B. 
Published: March 2003

Background: Intravascular volume expansion is followed by loss of fluid from the circulation. The extravasation of albumin in this readjustment is insufficiently known.Methods: Twelve male volunteers participated, each in three separate sessions, in a controlled, randomised, open fashion. They received one of the following: albumin 40 g/L,(7.1 mL/kg, i.e. 500 mL per 70 kg); Ringer's acetate (21.4 mL/kg), or dextran 30 g/L (7.1 mL/kg). The fluids were infused during 30 min and the subjects were followed for 180 min. ECG, arterial oxygen saturation and non‐invasive arterial pressure were recorded. Haemoglobin, haematocrit, serum albumin and osmolality, plasma colloid osmotic pressure and hyaluronan concentration were determined in venous samples.Results: The serum albumin concentration decreased (P < 0.05, anova) following Ringer's acetate or dextran, whereas serum osmolality was unchanged in all groups. The colloid osmotic pressure decreased (P < 0.05) after the Ringer solution. The blood volume increase was estimated from the decrease in haemoglobin concentration and did not differ between the three fluids. The cumulated extravasation of albumin was largest following albumin (10.4 ± 5.4 g, mean ± SD), less following dextran (5.6 ± 5.0 g) and negligible in the Ringer group (0.5 ± 10.0 g; P < 0.05 against albumin). However, the Ringer solution increased the plasma concentration of hyaluronan drastically.Conclusions: Infusion of hypotonic colloidal solutions entails net loss of albumin from the vascular space. This is not the case after Ringer's acetate. Increased interstitial hydration from the latter fluid is followed by lymphatic wash out of hyaluronan.
Pharmacokinetics of a 24‐hour intravenous ketoprofen infusion in children
Authors: Kokki H. , Karvinen M. , Jekunen A. 
Published: March 2003

Background: No pharmacokinetic data are available with respect to the plasma concentration of ketoprofen during intravenous infusion in children.Methods: We present here the pharmacokinetics of ketoprofen after a 10‐min intravenous infusion of 1 mg/kg followed by a 24‐h infusion of 4 mg/kg in 18 children aged 7 months to 16 years. Venous blood samples were collected at 5 min, 1, 2, 4, 24 h following the loading dose, and then 1, 2 and 4 h after the end of the infusion. A validated HPLC method was used to measure plasma levels of ketoprofen.Results: The steady state plasma concentration of ketoprofen was 2.0 µg/mL (range 1.3–2.7 µg/mL). The clearance of ketoprofen was 0.09 L·h−1·kg−1 (range 0.06–0.13 L·h−1·kg−1). The distribution volume was 0.16 L/kg (range 0.12–0.21 L/kg). The terminal half‐life was 1.3 h (range 0.8–1.7 h).Conclusion: The pharmacokinetics of ketopofen in children is similar to that reported in adults. Our results indicate that ketoprofen is a feasible drug for continuous intravenous infusion in acute pain treatment in children.