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K Emilsson

Publications and source records attributed to K Emilsson.

13 recordsLinked to original sources
PubMed2001

The mode of left ventricular pumping: is there an outer contour change in addition to the atrioventricular plane displacement?

The outer contour of the heart has in some studies been shown to be constant during the heart cycle and the epicardial apex almost stationary whilst the base of the ventricles moves towards apex during systole. The base of the left ventricle has been regarded as a cylinder with constant cross-sectional area with changes in height during the heart cycle, the latter corresponding to the amplitude of mitral annulus motion (MAM). In this echocardiographic study, including 20 healthy adults, the stroke volume calculated by the cylinder model was significantly lower than by a reference method (modified Simpson's rule). MAM explained 82% of the stroke volume and 18% must, therefore, be explained by an inward motion of the outer left ventricular wall. A mean outer diameter shortening of about 3% (about 2 mm) was calculated.

Adolescent↗
PubMed2001

Comparison between circumflex artery motion and mitral annulus motion.

OBJECTIVE: To compare mitral annulus motion (MAM) with circumflex artery motion (CXM) and the motion amplitude at an endocardial site (representing MAM) with an epicardial site (representing CXM) at the most basal lateral part of the atrioventricular plane (AVP). DESIGN: MAM and CXM were obtained in 28 patients examined by echocardiography and coronary angiography. The motion amplitude epicardially and endocardially was recorded by echocardiography in 13 patients with normal ejection fraction (EF) (> or = 0.50) and in 13 patients with decreased EF (<0.50). RESULTS: CXM was higher than MAM in most patients with normal EF but lower than MAM in most patients with decreased EF. The motion amplitude epicardially was significantly higher (p < 0.001) than endocardially in patients with normal EF. while there was no significant difference in patients with decreased EF. CONCLUSION: CXM represents the motion of the epicardial part of the AVP and differs from MAM, which represents the endocardial part of the wall. This must be considered when CXM is used for assessment of left ventricular systolic function.

Adult↗
PubMed2000

The relation between mitral annulus motion and ejection fraction changes with age and heart size.

Mitral annulus motion (MAM) has recently been introduced as an index of left ventricular function. Several echocardiographic studies have shown good agreement between ejection fraction (EF) and MAM x 5, where MAM is the total mitral annulus motion, measured in mm, and EF is expressed as a percentage. This means that if MAM is used for estimation of left ventricular function, the conversion factor 5 is used, if the function is expressed as EF. In these studies, the mean age of the patients was over 60 years. The present study, including 102 patients, shows that in patients aged 20-40 years, the conversion factor is about 4.3, in patients aged 41-60 years it is about 4.6 and in patients aged 61-80 years it is about 5.0. It was also found that the ratio EF/MAM decreases with increasing height and left ventricular diameter, both variables closely connected to heart size. The results suggest that when MAM is used in assessment of left ventricular function, it is unwise to express the function in terms of EF. It is preferable to use MAM as a direct index of ventricular function, using reference values referred to aged and height. If the estimated function is expressed in terms of EF, different converting factors must be used depending on the age of the patients.

Adult↗
PubMed2000

The relation between mitral annulus motion and left ventricular ejection fraction in atrial fibrillation.

Mitral annulus motion (MAM) has recently been introduced as an index of left ventricular function. Previous studies have shown a good agreement between MAM (mm) x 5 and ejection fraction in middle-aged and elderly patients. These studies only included patients with sinus rhythm, while patients with atrial fibrillation were excluded. In the present study, MAM was reduced in patients with atrial fibrillation while ejection fraction (EF) did not differ from age-matched control patients with sinus rhythm. The 'conversion factor' (EF/MAM) was 7.2 in the group with atrial fibrillation and 5. 1 in controls with sinus rhythm. This difference must be taken into account when MAM is used to estimate left ventricular function in patients with atrial fibrillation. Patients with atrial fibrillation had lower stroke volume and higher heart rate than patients with sinus rhythm. A decreased systolic long-axis shortening was found (P<0.005) compared to patients with sinus rhythm, but no difference in short-axis diameter shortening.

Aged↗
PubMed2000

The relation between ejection fraction and mitral annulus motion before and after direct-current electrical cardioversion.

Mitral annulus motion (MAM) and the relation between left ventricular ejection fraction (EF) and MAM has been shown to differ between patients with sinus rhythm and patients with atrial fibrillation. However, it has not been investigated how the relation between EF and MAM changes on direct-current (DC) electrical cardioversion to sinus rhythm. Therefore, 31 consecutive patients on the waiting list for DC electrical cardioversion were examined by echocardiography before DC electrical cardioversion, and those who maintained sinus rhythm (13 patients) were examined again 4-8 weeks after cardioversion. The conversion factor (CF) (ratio EF/MAM) decreased from 8.4 +/- 1.7 before to 5.8 +/- 0.8 SD after cardioversion (P<0.001). The EF increased slightly (P<0.05) but the MAM had a much greater increase (P<0.001), resulting in the decrease in CF. There was no significant difference in CF between patients after cardioversion and age- and gender-matched control patients with sinus rhythm, indicating that CF is normalized or almost normalized 4-8 weeks after cardioversion. This indicates that when MAM is used for investigation of the left ventricular function, and the function is expressed as EF, the same CF as in other patients with sinus rhythm can be used 4-8 weeks after DC electrical cardioversion.

Aged↗
PubMed2000

The relation between mitral annulus motion and ejection fraction: a nonlinear function.

In previous studies of the relation between mitral annulus motion (MAM) and left ventricular ejection fraction (EF), a linear relationship has been suggested. In this meta-analysis of 434 patients, we show that the relation is nonlinear and that a linear regression model overestimates EF in the lower range of MAM. The relation is better described by an S function and is influenced by age and heart size.

Adolescent↗
PubMed1996

Ligand cross-reactivity within the protease-activated receptor family.

Recently, a second member of the protease-activated receptor (PAR) family, named PAR-2, has been identified. Similar to the thrombin receptor, PAR-2 appears to be activated by proteolytic-mediated exposure of a "tethered ligand" sequence and can also be activated by the corresponding synthetic peptides. Similarities in the amino acid sequence of the receptors' tethered ligand sequences suggest that their respective agonist peptides might not be absolutely specific for their particular receptors. To test this, the receptor specificity of each agonist has been determined by measuring the responses of Xenopus oocytes expressing the thrombin receptor or PAR-2 to agonist peptides or enzymes. Thrombin receptors responded to thrombin, the human thrombin receptor-activating peptide SFLLRNP-NH2 (TRAP) (EC50 = 0.1 microM), and Xenopus TRAP, TFRIFD-NH2 (EC50 = 1 microM), but did not show any increase in calcium efflux over control levels with trypsin (50 nM) or PAR-2 agonist peptides (100 microM). Human and murine PAR-2 receptors responded comparably to human and murine PAR-2 agonist peptides (SLIGKVD and SLIGRL, respectively) (EC50 = 0.5-2.0 microM) and trypsin, but not to thrombin. PAR-2 was also found to be responsive to TRAP (EC50 = 1 microM) but was unresponsive to Xenopus TRAP (50 microM). Responses to additional peptide agonist analogs suggest that an amino-terminal serine is critical for PAR-2 agonist activity.

Amino Acid Sequence↗
PubMed1995

Molecular cloning and functional expression of the gene encoding the human proteinase-activated receptor 2.

We previously reported the molecular cloning of a mouse guanosine-nucleotide-binding-protein-coupled receptor similar to the thrombin receptor. Since the physiological agonist was unknown, the receptor was named proteinase-activated receptor 2. We describe here the cloning and functional expression of the gene encoding the corresponding human receptor. The gene is divided into two exons separated by about 14 kb intronic DNA. The deduced protein sequence is 397 amino acids long and 83% identical to the mouse receptor sequence. Within the extracellular amino terminus, the residues predicted to form the tethered agonist ligand differ between the two receptors; of the first six residues only four are conserved. At positions five and six, a lysine residue and a valine residue, respectively, have replaced arginine and leucine residues found in the mouse sequence. When the human receptor is expressed in Chinese hamster ovary cells, it can be activated by low nanomolar concentrations of the serine proteinase trypsin and by peptides made from the receptor sequence. Northern-blot analysis of receptor expression showed that the receptor transcript is widely expressed in human tissues with especially high levels in pancreas, liver, kidney, small intestine and colon. Moderate expression was detected in many organs but none in brain or skeletal muscle. By fluorescence in situ hybridization, the human proteinase-activated receptor 2 gene was mapped to chromosomal region 5q13, where, previously, the related thrombin receptor gene has been located.

Amino Acid Sequence↗
PubMed1994

Molecular cloning of a potential proteinase activated receptor.

A DNA sequence encoding a G-protein-coupled receptor was isolated from a mouse genomic library. The predicted protein is similar in structure to the thrombin receptor and has a similar activation mechanism. When expressed in Xenopus laevis oocytes, the receptor was activated by low concentrations of trypsin (EC 3.4.21.4) and by a peptide (SLIGRL) derived from the receptor sequence, but was not activated by thrombin (EC 3.4.21.5). Trypsin failed to activate a mutant receptor in which the presumed cleavage site Arg-34-Ser-35 was changed to an Arg-Pro sequence. The agonist peptide (SLIGRL) activated equally well mutant and wild-type receptors. Northern blot analysis demonstrated receptor transcripts in highly vascularized tissues such as kidney, small intestine, and stomach. Because this, to our knowledge, is the second example, besides the thrombin receptor, of a proteolytically activated seven-transmembrane G-protein-coupled receptor, we have provisionally named it proteinase activated receptor 2.

Amino Acid Sequence↗
PubMed1992

Uptake and release of serotonin in rat cerebrovascular nerves after subarachnoid hemorrhage.

BACKGROUND AND PURPOSE: Serotonin released from platelets has been suggested as one substance causing the vasospasm following subarachnoid hemorrhage. We studied whether such serotonin is able to constrict pial vessels. METHODS: We studied the uptake of serotonin in pial perivascular nerves by immunohistochemistry. We measured the contractile response in rat basilar artery after in vitro incubation with serotonin and during electrical field stimulation of perivascular nerves following experimental subarachnoid hemorrhage. RESULTS: After incubation with serotonin, electrical field stimulation caused a tetrodotoxin- and ketanserin-blockable contractile response. We observed no such response in vessels from rats treated with 6-hydroxydopamine or after blockade of serotonin uptake. After subarachnoid hemorrhage, a pronounced network of serotonin-immunoreactive nerve fibers was demonstrated in the vessel wall. In vessels from control rats, no serotonin fibers were seen, and in vessels from 6-hydroxydopamine-treated animals with subarachnoid hemorrhage only a few such fibers were seen. Electrical field stimulation of the basilar artery from rats tested 2 or 16 hours (but not 10 minutes or 24 hours) after subarachnoid hemorrhage showed contractile responses that were prevented by tetrodotoxin, ketanserin, and prior 6-hydroxydopamine treatment. CONCLUSIONS: Our study demonstrates a capacity of the perivascular sympathetic nerves to take up serotonin both in vitro and during the early phase of subarachnoid hemorrhage. Such uptake may help to remove excess serotonin from the subarachnoid space. Only if serotonin is subsequently released upon nerve activation may minor smooth muscle contraction develop.

Animals↗
PubMedDate not supplied

Vascular effects of proteinase-activated receptor 2 agonist peptide.

Proteinase-activated receptor 2 (PAR-2) is a G protein-coupled receptor related to the thrombin receptor. PAR-2 can be activated by trypsin and by synthetic peptides corresponding to the new amino terminus generated by activating proteolytic cleavage. We show in this report that intravenous injection of PAR-2 agonist peptides has dramatic effects on arterial blood pressure in anesthetized rats. The peptide SLIGRLETQPPI, at 150 nmol/kg, transiently decreased the mean arterial pressure from 104 to 60 mm Hg. The hypotensive response was dose-dependent, and was not secondary to effects on central vasoregulatory systems, heart rate, or the kidneys. A nitric oxide synthase inhibitor attenuated the hypotensive response induced by the PAR-2 agonist peptide. Further experiments in vitro, on preparations of rat femoral artery and vein, showed that PAR-2 agonist peptide elicited a dose-dependent relaxation of both types of vessel. Removal of the endothelium abolished the agonist peptide-induced relaxation. Our results demonstrate that activation of PAR-2 can modulate vascular tone, and that this response was an effect mediated at least partly by nitric oxide. The effect on blood vessels further suggests that the physiological activator of this proteolytically activated receptor is an enzyme present and active in the blood, possibly after a vascular injury.

Amino Acid Sequence↗