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S Egert

Publications and source records attributed to S Egert.

11 recordsLinked to original sources
PubMed1999

Contribution of alpha-adrenergic and beta-adrenergic stimulation to ischemia-induced glucose transporter (GLUT) 4 and GLUT1 translocation in the isolated perfused rat heart.

The intracellular signaling mechanism of the ischemia-stimulated glucose transporter (GLUT) translocation in the heart is not yet characterized. It has been suggested that catecholamines released during ischemia may be involved in this pathway. The purpose of this study was to evaluate the contribution of alpha-adrenoceptors and beta-adrenoceptors to ischemia-mediated GLUT4 and GLUT1 translocation in the isolated, Langendorff-perfused rat heart. Additionally, GLUT translocation was studied in response to catecholamine stimulation with phenylephrine (Phy) and isoproterenol (Iso). The results were compared with myocardial uptake of glucose analogue [18F]fluorodeoxyglucose (FDG). Subcellular analysis of GLUT4 and GLUT1 protein on plasma membrane vesicles (PM) and intracellular membrane vesicles (IM) using membrane preparation and immunoblotting revealed that alpha- and beta-receptor agonists stimulated GLUT4 translocation from IM to PM (2.5-fold for Phy and 2.1-fold for Iso, P<0.05 versus control), which was completely inhibited by phentolamine (Phe) and propranolol (Pro), respectively. Plasmalemmal GLUT1 moderately rose after Iso exposure, and this was prevented by Pro. In contrast, ischemia-stimulated GLUT4 translocation (2.2-fold, P<0.05 versus control) was only inhibited by alpha-adrenergic antagonist Phe but not by beta-adrenergic antagonist Pro. Similarly, Phe but not Pro inhibited ischemia-stimulated GLUT1 translocation. GLUT data were confirmed by FDG uptake monitored using bismuth germanate detectors. The catecholamine-stimulated FDG uptake (6.9-fold for Phy and 8.9-fold for Iso) was significantly inhibited by Phe and Pro; however, only Phe but not Pro significantly reduced the ischemia-induced 2.5-fold increase in FDG uptake (P<0.05 versus ischemia). This study suggests that alpha-adrenoceptor stimulation may play a role in the ischemia-mediated increase in glucose transporter trafficking leading to the stimulation of FDG uptake in the isolated, perfused rat heart, whereas beta-adrenergic activation does not participate in this signaling pathway.

Adrenergic alpha-Agonists↗
PubMed1999

Myocardial glucose transporter GLUT1: translocation induced by insulin and ischemia.

Myocardial glucose transport is not only facilitated by the insulin sensitive glucose transporter (GLUT) 4 but also by GLUT1. It was recently demonstrated that ischemia induces GLUT4 translocation by a mechanism distinct from the insulin-induced signaling pathway. However, the role of ischemia-mediated GLUT1 translocation and the signaling pathway involved is not yet defined. This study investigated the effects of wortmannin, a phosphatidylinositol-3 kinase (PI3kinase) inhibitor, on basal, ischemia- and insulin-stimulated GLUT1 redistribution. PI3kinase is known to participate in insulin-mediated GLUT4 translocation. Rat hearts were perfused with Krebs-Henseleit buffer containing 10 mmol/l glucose according to Langendorff and treated with/without 1 micromol/l wortmannin, 100 nmol/l insulin and 15 min no-flow ischemia. Relative subcellular distribution of GLUT1 protein was analysed using membrane fractionation and subsequent Western blotting. Both ischemia and insulin significantly increased the relative amount of GLUT1 in the plasma membrane (PM) compared to controls (41.6+/-2.8% in controls v 46.0+/-2.3% in ischemic and 51.4+/-3.9% in insulin hearts, both P<0.05) with a concomitant decrease of GLUT1 in intracellular membranes. However, the increases were moderate in view of the more than 2-fold stimulated GLUT4 translocation shown for ischemia and insulin. Although wortmannin completely inhibited insulin-induced GLUT1 translocation (42.0+/-2.0% GLUT1 on PM), it had no effect on the ischemia-induced translocation of GLUT1 (45. 4+/-1% GLUT1 on PM). Treatment with the inhibitor alone did not influence basal GLUT1 distribution. Results show that in the perfused rat heart, PI3 kinase is involved in the insulin-induced signaling leading to GLUT1 translocation but not in the ischemia-mediated signaling and basal GLUT1 trafficking. This suggests two different pathways for ischemia- and insulin-induced GLUT1 translocation as recently shown for GLUT4.

Androstadienes↗
PubMed1997

Increased sarcolemmal glucose transporter abundance in myocardial ischemia.

Many clinical and laboratory studies suggest that an increase in glucose uptake and metabolism by ischemic myocardium helps protect myocardial cells from irreversible injury. We have examined whether increased sarcolemmal abundance of cardiomyocyte glucose transporters plays a role in this adaptive response. We have shown that acute myocardial ischemia in perfused rat hearts results in increased sarcolemmal abundance of the major glucose transporter, GLUT4, by causing translocation of GLUT4 molecules from an intracellular compartment to the sarcolemma. In nonischemic control hearts only 18 +/- 2.8% of GLUT4 molecules were on the sarcolemma whereas in ischemic hearts this increased to 41 +/- 9.3%. Insulin also caused translocation of GLUT4 molecules to the sarcolemma, and resulted in 61 +/- 2.6% of GLUT4 molecules on the sarcolemma. The combination of ischemia and insulin did not result in additive increases in sarcolemmal GLUT4 abundance. In more persistent or chronic ischemia, the other major myocardial glucose transporter, GLUT1, appears to play an important role. The mRNA for this transporter, which is constitutively expressed on cardiomyocyte sarcolemma, was increased 2.0-fold in regions of hibernating myocardium in humans with coronary heart disease as well as in persistently hypoxic rat neonatal cardiomyocytes in primary culture. In neither of these conditions was GLUT4 mRNA expression increased. Thus, acute myocardial ischemia increases sarcolemmal glucose transporter abundance mainly by translocating previously synthesized GLUT4 molecules from an intracellular compartment, whereas more chronic ischemia also increases GLUT1 abundance via enhanced mRNA expression. Increased GLUT1 and GLUT4 abundance may participate in the augmented glucose uptake of ischemic myocardium and therefore may help protect ischemic myocardium from irreversible injury.

Animals↗
PubMed1997

Effects of wortmannin on insulin- and ischemia-induced stimulation of GLUT4 translocation and FDG uptake in perfused rat hearts.

OBJECTIVE: Myocardial glucose transport is enhanced by hormonal and other stimuli such as ischemia and hypoxia which induce glucose transporter 4 (GLUT4) translocation. Whether insulin and ischemia share a common signaling mechanism is not yet known. This study investigated whether phosphatidylinositol 3-kinase (PI3K), a signaling intermediate of the insulin-responsible pathway, also participates in the ischemia-induced stimulation of glucose. METHODS: Isolated Langendorff-perfused Sprague-Dawley rat hearts were subjected to 100 nmol/l insulin or 15 min of no-flow ischemia with/without 1 mumol/l wortmannin, an inhibitor of PI3K. After perfusion, relative subcellular glucose transporter GLUT4 distribution was assessed by membrane fractionation and immunoblotting and compared to controls. Uptake kinetics of the glucose analog [18F]fluoro-deoxyglucose (FDG) were also studied during perfusion of rat hearts. RESULTS: GLUT4 translocation to the plasma membrane (PM) was increased by insulin 1.8-fold and by ischemia 2.4-fold (P < 0.05). FDG uptake was increased by insulin 6.0-fold and by ischemia 6.2-fold (P < 0.05). Wortmannin 1 mumol/l inhibited insulin-mediated translocation of GLUT4 and increase in FDG uptake completely. However, it did not show any effect on ischemia-stimulated GLUT4 translocation or on ischemia-induced increase in FDG utilization. A significant correlation was found between relative GLUT4 translocation and FDG uptake in hearts of the insulin series (r = 0.9, P < 0.05) and of the ischemia series (r = 0.8, P < 0.05). CONCLUSIONS: Our results demonstrate that wortmannin did not inhibit ischemia-induced stimulation of myocardial glucose transport, supporting the hypothesis of different signaling pathways for ischemia and insulin.

Androstadienes↗
PubMed1996

Chondropathia patellae and knee muscle control. An electromyographic study.

The activity of knee-related muscles was registered via exercising on a bicycle ergometer by 17 patients with clinically diagnosed chondropathia patellae. M. quadriceps activity was shorter and the hamstring activity longer in the chondropathy group compared with a matched healthy control group. The changes in m. quadriceps occurred to an almost equal extent in lateral and medial sections. In five patients with unilateral complaints, the electromyographic changes were nevertheless noted on both sides. The study shows that chondropathia patellae involves a change in muscle control affecting not only the knee extensors but also the hamstrings. Through the changed innervation pattern the coactivation phase, i.e. the phase of simultaneous activation of knee flexors and extensors at the end of the extension phase, takes place at a higher angle of flexion. Physiotherapy should involve all knee-related muscles and should include not only isometric but also dynamic exercises.

Adult↗
PubMed1995

[Scintigraphic evaluation of the ischemically damaged myocardium in patients with reduced left ventricular function. From clinical aspects to the cell].

Identification of viable myocardium in patients with impaired left ventricular function, who are possible candidates for revascularization, represents an important clinical question. Modern methods of revascularization provide a therapeutic alternative to conventional pharmacological therapy even in patients with advanced ischemic heart disease. Modern diagnostic techniques make it possible to assess not only the extent of ischemia under exercise conditions, but also the presence of viable tissue in patients with severe coronary artery disease and impaired ventricular function. Currently, the most accurate methods for scintigraphic quantification of viable myocardial tissue are metabolic investigations with positron emission tomography (PET). Because of the limited availability of PET other methods like thallium-201-scintigraphy play an important clinical role. Modifications of thallium-201-scintigraphy, for example the introduction of reinjection protocols have improved the recognition of viable tissue and decreased the diagnostic difference to PET. We recommend as standard diagnostic procedure for assessment of tissue viability thallium-201-scintigraphy with reinjection. In patients with severely depressed left ventricular function and equivocal thallium-201-scintigraphy findings, PET should be considered as further diagnostic test. Low dose dobutamine-echocardiography is emerging as alternative test for evaluation of contractile reserve in dysfunctioning left ventricular segments. Its clinical role, however, remains to be determined. Besides the clinical application of these methods, newly developed radiotracers, together with PET, may provide insights into the mechanism of metabolic adaptations in patients with repeated episodes of ischemia. Furthermore, correlation of clinical data with in vitro histological and biological tissue analysis in the same patients may provide a better understanding of metabolic alterations observed in chronic ischemic heart disease.

Cell Hypoxia↗
PubMed1981

Psychiatric interviewing techniques. IV. Experimental study: Four contrasting styles.

The development and definition of four contrasting interview styles is described. The four styles were designed using different permutations of techniques which, on the basis of an earlier naturalistic study, appeared to be most effective in eliciting either factual information or feelings. A 'sounding board' style utilized a minimal activity approach; an 'active psychotherapy' style actively sought to explore feelings and to bring out emotional links and meanings; a 'structured' style adopted an active cross-questioning approach, and a 'systematic exploratory' style aimed to combine a high use of both fact-oriented and feeling-oriented techniques. Quantitative measures based on video-tape and audio-tape analysis showed that two experienced interviewers could be trained to adopt these four very different styles and yet remain feeling and appearing natural. An experimental design to compare the four styles is described.

Attitude↗
PubMed1976

The cohesiveness of alcoholism-complicated marriages and its influence on treatment outcome.

One-hundred husbands, diagnosed as suffering from alcoholism, and their wives, were followed up twelve months after initial consultation and assessment. Follow-up information was complete in 89 cases. On the basis of both husband and wife accounts of the husband's drinking behaviour during the follow-up period, and their assessment of the drinking problem at twelve-months follow-up, 28 were classified as having a 'good' outcome and 29 as having a 'bad' outcome. In the remaining 32 cases outcome was considered 'equivocal'. A composite measure of marital cohesion was predictive of twelve-month outcome classification, cohesive marriages being significantly more likely to have a good outcome. The measure of marital cohesion was based upon husband and wife reports of mutual affection and of husband involvement in family tasks, favourable spouse perceptions and meta-perceptions, and optimism about the future of the marriage. Composite measures of dominance balance within the marriage were not predictive of outcome. Husband's job status, husband's self-esteem, and wife's reported hardship were not independent of marital cohesion, and were themseleves predictive of twelve-months outcome. When these variables were partially controlled it was found that marital cohesion remained predictive for husbands with relatively low status jobs and husbands with relatively low levels of self-esteem. It is an over-simplification to state that either the marriage, the spouse, or the severity of the patient's condition is alone the cause of variation in outcome. It is possible to integrate these findings with those of other studies on the influence of family variables on the outcom of conditions other than alcoholism. Together these studies suggest a general hypothesis linking a breakdown in the cohesiveness, or mutual rewardingness, of family relationships and unfavourable outcomes following treatment or consultation for psychological disorder.

Adult↗