| 1. |
- Andersson, Bert, 1952, et al.
(author)
-
Heart rate dependency of cardiac performance in heart failure patients treated with metoprolol.
- 1999
-
In: European heart journal. - 0195-668X. ; 20:8, s. 575-83
-
Journal article (peer-reviewed)abstract
- To investigate whether a low heart rate is necessary to maintain improvement in myocardial function after long-term treatment with a beta-blocker in patients with heart failure.Forty-eight patients with congestive heart failure were investigated: 30 patients with dilated cardiomyopathy participating in a placebo-controlled trial (15 on placebo, 15 on metoprolol), and 18 patients treated by metoprolol in an open protocol. Investigations of spontaneous heart rate and of matched paced heart rates were performed at baseline and after 3, 6 and 12 months of follow-up by radionuclide angiography. There were significant signs of improvement in systolic indices of the spontaneous heart rate in the metoprolol-treated group (peak ejection rate: 0.98 to 1.32 end-diastolic volume.s-1, P = 0.015) as compared to placebo (1.14 to 1.19 end-diastolic volume.s-1, not significant). Similar effects were observed during the matched paced heart rate (peak ejection rate: metoprolol 0.91 to 1.38 end-diastolic volume.s-1, P = 0.037; placebo 1.22 to 1.12 end-diastolic volume.s-1, not significant). No effects were observed in the early peak filling rate. Left ventricular volumes decreased during metoprolol treatment, both for the spontaneous heart rate and during matched pacing.These data imply that beta-blocker treatment improves the force-frequency relationship of myocardial performance. A lower heart rate is not necessary to maintain cardiac function on a short-term basis, once myocardial recovery has occurred.
|
|
| 2. |
|
|
| 3. |
|
|
| 4. |
|
|
| 5. |
- Andersson, Sven, et al.
(author)
-
Tissue and intracellular pH in normal periarticular soft tissue and during different phases of antigen induced arthritis in the rat
- 1999
-
In: Journal of Rheumatology. - 0315-162X. ; 26:9, s. 2018-2024
-
Journal article (peer-reviewed)abstract
- OBJECTIVE: To measure intracellular and tissue pH in periarticular soft tissue during different phases of antigen induced arthritis in the rat. METHODS: pH was calculated using the following values: (1) the distribution of [14C]-dimethyl-oxazolidinedione; (2) the total tissue water and the extracellular space water volume, which was measured as [14C]-sucrose distribution in nephrectomized rats. Experiments were performed during both maximal inflammation (Day 3) and the restorative phase (Day 14). RESULTS: In all animals both tissue (pHt) and intracellular (pHi) pH were lower in arthritic joints than in the contralateral control. Mean pHt in control joints was 7.37+/-0.03. In arthritic rats it was 7.30+/-0.05 on Day 3 after challenge and 7.27+/-0.03 on Day 14. The pHi ranges were 6.86-7.81 for controls, 6.65-7.28 for arthritis Day 3, and 5.66-6.91 for arthritis Day 14. CONCLUSION: In this model there is a reduction in pH in the periarticular tissue of arthritic joints. The magnitude is, however, relatively small and the pannus tissue is not uniquely acidic in comparison with other compartments. There does not seem to be a correlation between pH and changes in metabolic balance, pannus formation, or healing.
|
|
| 6. |
- Berggren, Magnus, et al.
(author)
-
Controlling inter-chain and intra-chain excitations of a poly(thiophene) derivative in thin films
- 1999
-
In: Chemical Physics Letters. - : Elsevier. - 0009-2614 .- 1873-4448. ; 304:1-2, s. 84-90
-
Journal article (peer-reviewed)abstract
- The decay of photoexcitations in polythiophene chains has been studied in solid solutions of the polymer from room temperature to 4 K. A strong blue shift of the emission spectrum is observed in the polymer blend, as compared to the homopolymer. Dispersion of the polythiophene suppresses the non-radiative processes, which are suggested to be correlated to close contacts of polymer chains. Quantum chemistry modeling of the excited state distributed on two chains corroborate this conclusion.
|
|
| 7. |
- Laan, Martti, 1971, et al.
(author)
-
Increased levels of interleukin-16 in the airways of tobacco smokers: relationship with peripheral blood T lymphocytes
- 1999
-
In: Thorax. - 0040-6376. ; 54:10, s. 911-6
-
Journal article (peer-reviewed)abstract
- BACKGROUND: The mechanisms behind the development of systemic immunomodulation among tobacco smokers are not fully understood, but several studies have indicated a role for CD8+ and/or CD4+ T cells. Interleukin (IL)-16, a cytokine released from inflammatory cells as well as bronchial epithelial cells, can recruit and activate CD4+ T cells. A study was undertaken to establish whether the IL-16 level is increased in the airways of tobacco smokers and to determine whether airway levels of IL-16 are related to the number and function of systemic T lymphocytes. METHODS: Bronchoalveolar lavage (BAL) fluid was collected from eight never smokers and 18 tobacco smokers without clinical airway symptoms, and from 16 tobacco smokers with clinical airway symptoms. Interleukin-16 protein levels in BAL fluid were determined using enzyme-linked immunosorbent assay (ELISA). Peripheral blood was collected for determination of CD4+ T cell content using flow cytometry. The responsiveness of systemic lymphocytes in smokers was assessed by measuring the proliferative response of peripheral blood lymphocytes to the superantigen staphylococcus enterotoxin A (SEA). RESULTS: The IL-16 protein level in the BAL fluid was significantly higher in tobacco smokers than in non-smokers. However, among tobacco smokers the IL-16 level was similar in asymptomatic smokers and in those with airway symptoms. The level of IL-16 in the BAL fluid of smokers correlated negatively with the percentage of CD4+ T cells and positively with superantigen stimulated lymphocyte proliferation in peripheral blood. CONCLUSIONS: In tobacco smokers the airway IL-16 level is increased and it is possible that this increase in IL-16 influences systemic immunomodulation by altering the number and responsiveness of systemic T lymphocytes.
|
|
