S. Eriksson
Karolinska Institutet
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Featured researches published by S. Eriksson.
Journal of Neurochemistry | 1983
Ulf Tossman; S. Eriksson; Anders Delin; Lars Hagenfeldt; David Law; Urban Ungerstedt
Abstract: Changes in brain amino acid uptake and metabolism have been proposed as a possible etiological factor in hepatic encephalopathy. By use of a brain dialysis technique (a thin tube implanted in the brain of the living animal), the extracellular amino acid concentrations in the striatum of portacaval (PC)‐shunted and shamoperated rats were measured. Leucine, phenylalanine, methionine, and glutamine were increased two‐ to sixfold in the PC‐shunted rats, whilst no changes were seen for GABA, valine, glutamate, or isoleucine, confirming previous reports. Aspartate levels were 350% higher in the PC‐shunted rats, and this rise, as well as that of phenylalanine, was significantly correlated with the lower motor activity observed in the PC‐shunted rats, suggesting a possible importance of these amino acids in the etiology of hepatic encephalopathy. The amino acid concentrations measured in whole blood demonstrated the well‐known pattern of low levels of branched‐chain amino acids and increased concentrations of phenylalanine, glutamine, and histidine.
Acta Anaesthesiologica Scandinavica | 2011
Robert Frithiof; Oliver Soehnlein; S. Eriksson; Johan Fenhammar; Hans Hjelmqvist; Lennart Lindbom; M. Rundgren
Background: Isoflurane is a common anesthetic agent used in human surgery and in animal models of sepsis. It has been suggested to have beneficial anti‐inflammatory properties and to protect kidney function. Here, we investigated the effect of isoflurane on the development of kidney injury and dysfunction during 48‐h endotoxemia in sheep.
Journal of Hepatology | 1992
Anders Thörne; Ulla Johansson; John Wahren; S. Eriksson
Energy expenditure was determined using continuous indirect calorimetry in the basal state and during 3 h of total parenteral nutrition (TPN) in 8 patients with cirrhosis and 8 healthy volunteers. TPN consisted of glucose, fat and amino acids and had a glucose/fat ratio of 50:50. The infusion rate was set to provide energy corresponding to 62.5% of the individually measured 24-h resting energy expenditure. In the basal state energy expenditure was similar in patients and controls while the respiratory quotient (RQ) was lower in the patients (0.78 +/- 0.01 vs. 0.82 +/- 0.01, mean +/- SEM, p < 0.05). During TPN, energy expenditure increased progressively during the 3-h infusion period. The average rise in energy expenditure was similar in patients (19.1 +/- 1.2%) and in controls (21.4 +/- 1.6%, n.s.). The RQ rose in both groups, but more in the patients with cirrhosis. At the end of the study, RQ was higher in patients (0.89 +/- 0.01) than in controls (0.85 +/- 0.01, p < 0.05). It is concluded that the nutrient-induced rise in energy expenditure during TPN is not significantly different in patients with cirrhosis and control subjects. Furthermore, the results indicate that the increased fat utilization in overnight fasting cirrhotic patients is rapidly shifted to an augmented carbohydrate oxidation during TPN, possibly as a consequence of marked hyperinsulinemia.
Acta Anaesthesiologica Scandinavica | 2001
J. Ullman; S. Eriksson; M. Rundgren
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.
General Pharmacology-the Vascular System | 1983
S. Eriksson; L. Hagenfeldt; D. Law; C. Patrono; E. Pinca; Å. Wennmalm
Abstract The present data do not provide evidence that basal or CO 2 -stimulated human cerebral blood flow is under control of locally formed PG. It is suggested that the CBF decreasing effect elicited by indomethacin is separated from its inhibitory effect on PG formation.
Acta Anaesthesiologica Scandinavica | 2003
J. Ullman; R. Härgestam; S. Lindahl; S. H. H. Chan; S. Eriksson; M. Rundgren
Background: General anaesthesia may stimulate the renin‐angiotensin system. Exogenous administration of angiotensin II elevates blood pressure mainly via increased total peripheral resistance caused by direct vasoconstrictor actions. It is also well established that the hypertensive effect of angiotensin II involves a cerebrally mediated component. The hypertensive effect of an intravascular infusion of angiotensin II is substantially reduced by isoflurane anaesthesia. A likely mechanism is that isoflurane anaesthesia reduces the cerebral component of the angiotensin II effect on blood pressure, which involves influences on autonomic nervous activity. In an experimental study in sheep we used real‐time spectral analysis of arterial blood pressure signals to obtain information on parasympathetic, respectively, sympathetic autonomic nervous activity in response to angiotensin II administration during isoflurane anaesthesia.
Brain Research | 1988
S. Eriksson; Christa Simon-Oppermann; Eckhart Simon; David A. Gray
Dogs were implanted with a device for chronic cannulation of the anterior part of the 3rd ventricle (A3V). Intracerebroventricular (i.c.v.) infusion of artificial cerebrospinal fluid (CSF) containing 0.35 M NaCl into the A3V of 7 normally hydrated dogs induced thirst (average water intake 11.8 +/- 2.0 ml.kg-1 b. wt.) and significantly increased arginine-vasopressin (AVP) concentration in the blood plasma from 3.4 +/- 0.3 to 8.2 +/- 1.2 pg.ml-1. When repeating the i.c.v. hypertonic infusion at intervals of one week or more in two dogs, its dipsogenic effect vanished within 3-5 months. X-ray analysis revealed an occlusion of the rostroventral part of the A3V. Subsequent controls on 3 other dogs confirmed that the dipsogenic response to i.c.v. osmotic stimulation was abolished in association with similar partial occlusions of the A3V. However, this stimulus still produced a significant increase of plasma AVP from 3.7 +/- 0.5 to 5.7 +/- 0.7 pg.ml-1 in the 5 dogs. Control of drinking in these dogs was otherwise unimpaired as indicated by their normal plasma osmolalities. Histological examination revealed that the loss of the dipsogenic response to i.c.v. infusion of 0.35 M NaCl was in each case associated with fibrinous occlusion of the A3V between its rostral wall and the mass intermedia, preventing the passage of the infusate to the supraoptic and infundibular recesses.
Archive | 1987
Eckhart Simon; S. Eriksson; Rüdiger Gerstberger; David A. Gray; Christa Simon-Oppermann
Salt and fluid homeostasis in vertebrates involves two important peptide hormones with well-defined systemic sites of action: 8Arg-vasopressin/vasotocin (AVP/AVT) and 5I1e-/5Val-angiotensin II (ANG II). Neuronal systems producing AVP/AVT are, however, not confined to the hypothalamo-neurohypophyseal system but establish numerous extrahypothalamic connections (Zimmerman 1981; Berk et al. 1982). More recently ANG II has also been identified as a neuropeptide by biochemical and immunocytochemical techniques (Ganong 1984; Lind et al. 1985).
Clinical Physiology | 1981
Åke Wennmalm; S. Eriksson; John Wahren
Acta Physiologica Scandinavica | 1983
S. Eriksson; L. Hagenfeldt; D. Law; C. Patrono; E. Pinca; Å. Wennmalm