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"Atrium"
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Atrium
\"Atrium charts the emergence of the atrium in architecture in the 1970s and 80s, and through it argues that it became the definitive typology for a contemporary understanding of the architect\"-- Provided by publisher.
BOOK
Cantharidin and sodium fluoride attenuate the negative inotropic effects of carbachol in the isolated human atrium
Carbachol, an agonist at muscarinic receptors, exerts a negative inotropic effect in human atrium. Carbachol can activate protein phosphatases (PP1 or PP2A). We hypothesized that cantharidin or sodium fluoride, inhibitors of PP1 and PP2A, may attenuate a negative inotropic effect of carbachol. During bypass-surgery trabeculae carneae of human atrial preparations (HAP) were obtained. These trabeculae were mounted in organ baths and electrically stimulated (1 Hz). Force of contraction was measured under isometric conditions. For comparison, we studied isolated electrically stimulated left atrial preparations (LA) from mice. Cantharidin (100 µM) and sodium fluoride (3 mM) increased force of contraction in LA (
n
= 5–8,
p
< 0.05) by 113% ± 24.5% and by 100% ± 38.2% and in HAP (
n
= 13–15,
p
< 0.05) by 625% ± 169% and by 196% ± 23.5%, respectively. Carbachol (1 µM) alone exerted a rapid transient maximum negative inotropic effect in LA (
n
= 6) and HAP (
n
= 14) to 46.9% ± 3.63% and 19.4% ± 3.74%, respectively (
p
< 0.05). These negative inotropic effects were smaller in LA (
n
= 4–6) and HAP (
n
= 9–12) pretreated with 100 µM cantharidin and amounted to 58.0% ± 2.27% and 59.2% ± 6.19% or 3 mM sodium fluoride to 63.7% ± 9.84% and 46.3% ± 5.69%, (
p
< 0.05). We suggest that carbachol, at least in part, exerts a negative inotropic effect in the human atrium by stimulating the enzymatic activity of PP1 and/or PP2A.
Journal Article
Idiopathic enlargement of the right atrium masking left atrial aneurysm in a neonate
An idiopathic enlargement of the right atrium is an extremely rare cardiac malformation. There are no established guidelines for the management of this disease, especially concerning medical versus surgical therapeutic approach and the timing for an operation. We report in this case about a neonate that first was treated conservatively until the age of 5 month and finally got an operative resection of the aneurysm. After surgery, unexpected complications occurred. A second aneurysm in the left atrium was demasked. Furthermore, a progressive dilatation of both atrial chambers after resection required regular follow-up and ongoing evaluation of treatment.
Journal Article
Clonidine stimulates force of contraction via histamine H2 receptors in the human atrium
Clonidine has various clinical effects mediated by agonism of α
1
- or α
2
-adrenoceptors and the blocking of hyperpolarization-activated-nucleotide-gated pacemaker channels (HCN). It is unknown whether clonidine can also stimulate human cardiac histamine H
2
receptors (hH
2
Rs). We used isolated electrically stimulated left and spontaneously beating right atrial preparations from mice overexpressing the hH
2
R specifically in the heart (H
2
-TG), and spontaneously beating right atrial preparations of guinea pigs for comparison. Moreover, we studied isolated electrically stimulated muscle strips from the human right atrium. Clonidine (1, 3, and 10 µM) increased force of contraction in isolated left atrial preparations from H
2
-TG mice. In contrast, clonidine reduced the spontaneous beating rate in right atrial preparations from H
2
-TG. Clonidine raised the beating rate in guinea pig right atrial preparations. Clonidine failed to increase the force of contraction but reduced beating rate in wild-type litter mate mice (WT). In WT, histamine failed to increase the force of contraction in left atrial preparations and beating rate in right atrial preparations. Clonidine (10 µM) increased the force of contraction in isolated human right atrial preparations. The positive inotropic effect in the human atrium was attenuated by cimetidine (10 µM). Clonidine increased the beating rate of the isolated spontaneously beating guinea pig right atrium and acted as a H
2
R partial agonist. Furthermore, clonidine showed binding to the guinea pig H
2
R (100 µM) using HEK cells in a recombinant expression system (p
K
i
< 4.5) but hardly to the human H
2
R. These data suggest that clonidine can functionally activate cardiac human H
2
R.
Journal Article
Cantharidin increases the force of contraction and protein phosphorylation in isolated human atria
Cantharidin, an inhibitor of protein phosphatase 1 (PP1) and protein phosphatase 2A (PP2A), is known to increase the force of contraction and shorten the time to relaxation in human ventricular preparations. We hypothesized that cantharidin has similar positive inotropic effects in human right atrial appendage (RAA) preparations. RAA were obtained during bypass surgery performed on human patients. These trabeculae were mounted in organ baths and electrically stimulated at 1 Hz. For comparison, we studied isolated electrically stimulated left atrial (LA) preparations and isolated spontaneously beating right atrial (RA) preparations from wild-type mice. Cumulatively applied (starting at 10 to 30 µM), cantharidin exerted a positive concentration-dependent inotropic effect that plateaued at 300 µM in the RAA, LA, and RA preparations. This positive inotropic effect was accompanied by a shortening of the time to relaxation in human atrial preparations (HAPs). Notably, cantharidin did not alter the beating rate in the RA preparations. Furthermore, cantharidin (100 µM) increased the phosphorylation state of phospholamban and the inhibitory subunit of troponin I in RAA preparations, which may account for the faster relaxation observed. The generated data indicate that PP1 and/or PP2A play a functional role in human atrial contractility.
Journal Article
Tegaserod Stimulates 5-HT4 Serotonin Receptors in the Isolated Human Atrium
Tegaserod (1-[(5-methoxy-1H-indol-3-yl)methyliden]amino-3-pentylguanidine) is a potent agonist at human recombinant 5-HT4 serotonin receptors. Consequently, tegaserod is utilized in the treatment of bowel diseases. The objective of this study was to test the hypothesis that tegaserod stimulates human cardiac atrial 5-HT4-receptors via cyclic adenosine monophosphate (cAMP)-dependent pathways. Tegaserod exerted positive inotropic effects (PIEs) and positive chronotropic effects (PCEs) in isolated left and right atrial preparations, respectively, from mice with cardiac-specific overexpression of the human 5-HT4 serotonin receptor (5-HT4-TG) in a concentration- and time-dependent manner. However, no effect was observed in the hearts of littermates of wild-type mice (WT). Western blot analysis revealed that the expression of 5-HT4 receptors was significantly higher in 5-HT4-TG mice compared to WT mice. The specificity of the signal for the 5-HT4 receptor was confirmed by the absence of the signal in the hearts of 5-HT4 receptor knockout mice. Furthermore, tegaserod increased the force of contraction (at concentrations as low as 10 nM), reduced the time of tension relaxation, and increased the rate of tension development in isolated electrically stimulated (at a rate of 60 beats per minute) human right atrial preparations (HAPs, obtained during open-heart surgery) when administered alone. The potency and efficacy of tegaserod to raise the force of contraction were enhanced in the presence of cilostamide, a phosphodiesterase III inhibitor. The positive inotropic effect of tegaserod in HAPs was found to be attenuated by the 5-HT4 serotonin receptor antagonist GR 125487 (0.1 µM). The efficacy of tegaserod (10 µM) in raising the force of contraction in HAPs was less pronounced than that of serotonin (10 µM) or isoprenaline (1 µM). Tegaserod shifted the concentration–response curve of the force of contraction to serotonin to the right in HAPs, indicating that it is a partial agonist at 5-HT4 serotonin receptors in this model. We propose that the mechanism of action of tegaserod in HAPs involves cAMP-dependent phosphorylation of cardiac regulatory proteins.
Journal Article
Mosapride stimulates human 5-HT4-serotonin receptors in the heart
Mosapride (4-amino-5-chloro-2-ethoxy-N-[[4-[(4-fluorophenyl) methyl]-2-morpholinyl]-methyl] benzamide) is a potent agonist at gastrointestinal 5-HT
4
receptors. Mosapride is an approved drug to treat several gastric diseases. We tested the hypothesis that mosapride also stimulates 5-HT
4
receptors in the heart. Mosapride increased the force of contraction and beating rate in isolated atrial preparations from mice with cardiac overexpression of human 5-HT
4
-serotonin receptors (5-HT
4
-TG). However, it is inactive in wild-type mouse hearts (WT). Mosapride was less effective and potent than serotonin in raising the force of contraction or the beating rate in 5-HT
4
-TG. Only in the presence of cilostamide (1 μM), a phosphodiesterase III inhibitor, mosapride, and its primary metabolite time dependently raised the force of contraction under isometric conditions in isolated paced human right atrial preparations (HAP, obtained during open heart surgery). In HAP, mosapride (10 μM) reduced serotonin-induced increases in the force of contraction. Mosapride (10 µM) shifted the concentration–response curves to serotonin in HAP to the right. These data suggest that mosapride is a partial agonist at 5-HT
4
-serotonin receptors in HAP.
Journal Article
Perioperative echocardiographic strain analysis: what anesthesiologists should know
Echocardiographic strain analysis by speckle tracking allows assessment of myocardial deformation during the cardiac cycle. Its clinical applications have significantly expanded over the last two decades as a sensitive marker of myocardial dysfunction with important diagnostic and prognostic values. Strain analysis has the potential to become a routine part of the perioperative echocardiographic examination for most anesthesiologist-echocardiographers but its exact role in the perioperative setting is still being defined.
This clinical report reviews the principles underlying strain analysis and describes its main clinical uses pertinent to the field of anesthesiology and perioperative medicine. Strain for assessment of left and right ventricular function as well as atrial strain is described. We also discuss the potential role of strain to aid in perioperative risk stratification, surgical patient selection in cardiac surgery, and guidance of anesthetic monitor choice and clinical decision-making in the perioperative period.
Echocardiographic strain analysis is a powerful tool that allows seeing what conventional 2D imaging sometimes fails to reveal. It often provides pathophysiologic insight into various cardiac diseases at an early stage. Strain analysis is readily feasible and reproducible thanks to the use of highly automated software platforms. This technique shows promising potential to become a valuable tool in the arsenal of the anesthesiologist-echocardiographer and aid in perioperative risk-stratification and clinical decision-making.
Journal Article
Ergotamine Stimulates Human 5-HT4-Serotonin Receptors and Human H2-Histamine Receptors in the Heart
Ergotamine (2′-methyl-5′α-benzyl-12′-hydroxy-3′,6′,18-trioxoergotaman) is a tryptamine-related alkaloid from the fungus Claviceps purpurea. Ergotamine is used to treat migraine. Ergotamine can bind to and activate several types of 5-HT1-serotonin receptors. Based on the structural formula of ergotamine, we hypothesized that ergotamine might stimulate 5-HT4-serotonin receptors or H2-histamine receptors in the human heart. We observed that ergotamine exerted concentration- and time-dependent positive inotropic effects in isolated left atrial preparations in H2-TG (mouse which exhibits cardiac-specific overexpression of the human H2-histamine receptor). Similarly, ergotamine increased force of contraction in left atrial preparations from 5-HT4-TG (mouse which exhibits cardiac-specific overexpression of the human 5-HT4-serotonin receptor). An amount of 10 µM ergotamine increased the left ventricular force of contraction in isolated retrogradely perfused spontaneously beating heart preparations of both 5-HT4-TG and H2-TG. In the presence of the phosphodiesterase inhibitor cilostamide (1 µM), ergotamine 10 µM exerted positive inotropic effects in isolated electrically stimulated human right atrial preparations, obtained during cardiac surgery, that were attenuated by 10 µM of the H2-histamine receptor antagonist cimetidine, but not by 10 µM of the 5-HT4-serotonin receptor antagonist tropisetron. These data suggest that ergotamine is in principle an agonist at human 5-HT4-serotonin receptors as well at human H2-histamine receptors. Ergotamine acts as an agonist on H2-histamine receptors in the human atrium.
Journal Article