Ketamine Preconditions Isolated Human Right Atrial Myocardium

2005 ◽  
Vol 102 (6) ◽  
pp. 1190-1196 ◽  
Author(s):  
Jean-Luc Hanouz ◽  
Lan Zhu ◽  
Emmanuel Persehaye ◽  
Massimo Massetti ◽  
Gerard Babatasi ◽  
...  
Keyword(s):  
Adenosine Triphosphate ◽  
Enhanced Recovery ◽  
Human Myocardium ◽  
Right Atrial ◽  
Control Group ◽  
Force Of Contraction ◽  
Human Right ◽  
Adrenoceptor Antagonist ◽  
Racemic Ketamine

Background The authors examined the effect of ketamine and its S(+) isomer on isolated human myocardium submitted to hypoxia-reoxygenation in vitro. Methods The authors studied isometric contraction of human right atrial trabeculae suspended in an oxygenated Tyrode's modified solution at 34 degrees C. Ten minutes before a 30-min hypoxic period followed by a 60-min reoxygenation, muscles were exposed for 15 min to racemic ketamine and its S(+) isomer at 10, 10, and 10 m alone or in the presence of 8.10 m 5-hydroxydecanoate, 10 m HMR 1098 (sarcolemmal adenosine triphosphate-sensitive potassium channel antagonist), 10 m phentolamine (alpha-adrenoceptor antagonist), and 10 m propranolol (beta-adrenoceptor antagonist). Force of contraction at the end of the 60-min reoxygenation period was compared between groups (mean +/- SD). Results Ketamine (10 m: 85 +/- 4%; 10 m: 95 +/- 10%; 10 m: 94 +/- 14% of baseline) and S(+)-ketamine (10-6 m: 85 +/- 4%; 10 m: 91 +/- 16%; 10 m: 93 +/- 14% of baseline) enhanced recovery of force of contraction at the end of the reoxygenation period as compared with the control group (47 +/- 10% of baseline; P < 0.001). Ketamine-induced preconditioning at 10 m was inhibited by 5-hydroxydecanoate (60 +/- 16%; P < 0.001), HMR 1098 (60 +/- 14%; P < 0.001), phentolamine (56 +/- 12%; P < 0.001), and propranolol (60 +/- 7%; P < 0.001). Conclusions In vitro, ketamine preconditions isolated human myocardium, at least in part, via activation of adenosine triphosphate-sensitive potassium channels and stimulation of alpha- and beta-adrenergic receptors.

Mechanisms of Desflurane-induced Preconditioning in Isolated Human Right Atria In Vitro 

2002 ◽  
Vol 97 (1) ◽  
pp. 33-41 ◽  
Author(s):  
Jean-Luc Hanouz ◽  
Alexandra Yvon ◽  
Massimo Massetti ◽  
Olivier Lepage ◽  
Gérard Babatasi ◽  
...  
Keyword(s):  
Human Myocardium ◽  
Adenosine A1 Receptor ◽  
Right Atrial ◽  
Control Group ◽  
Human Right ◽  
Beta Adrenoceptors ◽  
Adrenoceptor Antagonist ◽  
Adenosine A1 ◽  
A1 Receptor

Background The authors examined the role of adenosine triphosphate-sensitive potassium (K(ATP)) channels, adenosine A1 receptor, and alpha and beta adrenoceptors in desflurane-induced preconditioning in human myocardium, in vitro. Methods The authors recorded isometric contraction of human right atrial trabeculae suspended in oxygenated Tyrode's solution (34 degrees C; stimulation frequency, 1 Hz). Before a 30-min anoxic period, 3, 6, and 9% desflurane was administered during 15 min. Desflurane, 6%, was also administered in the presence of 10 microm glibenclamide, a K(ATP) channels antagonist; 10 microm HMR 1098, a sarcolemmal K(ATP) channel antagonist; 800 microm 5-hydroxy-decanoate (5-HD), a mitochondrial K(ATP) channel antagonist; 1 microm phentolamine, an alpha-adrenoceptor antagonist; 1 microm propranolol, a beta-adrenoceptor antagonist; and 100 nm 8-cyclopentyl-1,3-dipropylxanthine (DPX), the adenosine A1 receptor antagonist. Developed force at the end of a 60-min reoxygenation period was compared (mean +/- SD). Results Desflurane at 3% (95 +/- 13% of baseline), 6% (86 +/- 6% of baseline), and 9% (82 +/- 6% of baseline) enhanced the recovery of force after 60 min of reoxygenation as compared with the control group (50 +/- 11% of baseline). Glibenclamide (60 +/- 12% of baseline), 5-HD (57 +/- 21% of baseline), DPX (63 +/- 19% of baseline), phentolamine (56 +/- 20% of baseline), and propranolol (63 +/- 13% of baseline) abolished desflurane-induced preconditioning. In contrast, HMR 1098 (85 +/- 12% of baseline) did not modify desflurane-induced preconditioning. Conclusions In vitro, desflurane preconditions human myocardium against simulated ischemia through activation of mitochondrial K(ATP) channels, adenosine A1 receptor, and alpha and beta adrenoceptors.

Mechanisms of Sevoflurane-induced Myocardial Preconditioning in Isolated Human Right Atria In Vitro 

2003 ◽  
Vol 99 (1) ◽  
pp. 27-33 ◽  
Author(s):  
Alexandra Yvon ◽  
Jean-Luc Hanouz ◽  
Benoît Haelewyn ◽  
Xavier Terrien ◽  
Massimo Massetti ◽  
...  
Keyword(s):  
Potassium Channels ◽  
Potassium Channel ◽  
Adenosine Triphosphate ◽  
Human Myocardium ◽  
Right Atrial ◽  
Human Right ◽  
Myocardial Preconditioning ◽  
Right Atria

Background The authors examined the role of adenosine triphosphate-sensitive potassium channels and adenosine A(1) receptors in sevoflurane-induced preconditioning on isolated human myocardium. Methods The authors recorded isometric contraction of human right atrial trabeculae suspended in oxygenated Tyrode's solution (34 degrees C; stimulation frequency, 1 Hz). In all groups, a 30-min hypoxic period was followed by 60 min of reoxygenation. Seven minutes before hypoxia reoxygenation, muscles were exposed to 4 min of hypoxia and 7 min of reoxygenation or 15 min of sevoflurane at concentrations of 1, 2, and 3%. In separate groups, sevoflurane 2% was administered in the presence of 10 microm HMR 1098, a sarcolemmal adenosine triphosphate-sensitive potassium channel antagonist; 800 microm 5-hydroxy-decanoate, a mitochondrial adenosine triphosphate-sensitive potassium channel antagonist; and 100 nm 8-cyclopentyl-1,3-dipropylxanthine, an adenosine A(1) receptor antagonist. Recovery of force at the end of the 60-min reoxygenation period was compared between groups (mean +/- SD). Results Hypoxic preconditioning (90 +/- 4% of baseline) and sevoflurane 1% (82 +/- 3% of baseline), 2% (92 +/- 5% of baseline), and 3% (85 +/- 7% of baseline) enhanced the recovery of force after 60 min of reoxygenation compared with the control groups (52 +/- 9% of baseline). This effect was abolished in the presence of 5-hydroxy-decanoate (55 +/- 14% of baseline) and 8-cyclopentyl-1,3-dipropylxanthine (58 +/- 16% of baseline) but was attenuated in the presence of HMR 1098 (73 +/- 10% of baseline). Conclusions In vitro, sevoflurane preconditions human myocardium against hypoxia through activation of adenosine triphosphate-sensitive potassium channels and stimulation of adenosine A(1) receptors.

scholarly journals The Effect of Ivabradine on the Human Atrial Myocardial Contractility in an In Vitro Study

2019 ◽  
Vol 2019 ◽  
pp. 1-7
Author(s):  
Ryan Chaban ◽  
Katja Buschmann ◽  
Anna Krausgrill ◽  
Andres Beiras-Fernandez ◽  
Christian-Friedrich Vahl
Keyword(s):  
Myocardial Contractility ◽  
In Vitro Study ◽  
Right Atrial ◽  
Control Group ◽  
Force Of Contraction ◽  
Time To Peak ◽  
Before And After ◽  
The Right ◽  
Electrical Impulses

Purpose. Ivabradine has emerged as a new antiarrhythmic agent that could compete with the traditional ones, such as beta-blockers. This experimental study aims to ascertain whether ivabradine directly interferes with the myocardial contractility in an in vitro environment. Methods. Myocardial tissues from the right atrial appendages of patients undergoing cardiac surgery were dissected to obtain 40 specimens from 20 patients (length: 3 mm), which were exposed to electrical impulses at a frequency of 75 bpm for 30 min to reach a steady state. Specimens were then categorised into four groups (each including five patients). The first group was the control, whereas the second, third, and fourth were treated with 60 nM, 200 nM, and 2 μM ivabradine, respectively. We assessed five different contraction parameters before and after a 15 min treatment and calculated their relative changes, which were then compared to the control group. Results. Ivabradine has affected the force of contraction significantly in vitro (p=0.009). However, force of contraction decreased in both the control group (93.5 ± 4.7%) and the second group (94.1 ± 4.5%, p=0.8) and force of contraction remained unchanged in the third group (101.0 ± 4.1%, p=0.24) and increased significantly in the fourth group (108.9 ± 11.6%, p=0.008). There was no change in other contraction parameters, such as passive tension force (97.1 ± 5.1%, p=0.368), duration of contraction (99.1 ± 4.3%, p=0.816), time to peak (96.6 ± 3.0%, p=0.536), and time to relaxation (101.2 ± 7.0%, p=0.564). Conclusions. Ivabradine did not interfere with the contractile behaviour of human atrial tissue when it was used in therapeutic dosages in vitro. However, it increased the contractility slightly, when it was used in supratherapeutic dosage.

Desflurane-induced postconditioning of diabetic human right atrial myocardium in vitro

2010 ◽  
Vol 36 (1) ◽  
pp. 21-28 ◽  
Author(s):  
S. Lemoine ◽  
C. Durand ◽  
L. Zhu ◽  
C. Ivasceau ◽  
O. Lepage ◽  
...  
Keyword(s):  
Right Atrial ◽  
Atrial Myocardium ◽  
Human Right

scholarly journals EVALUATION OF BENEFICIAL EFFECTS OF LINUM USITATISSIMUM IN CONGESTIVE HEART FAILURE

2017 ◽  
Vol 9 (10) ◽  
pp. 62
Author(s):  
Pravin Tirgar ◽  
Limbasiya Kalpesh
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Linum Usitatissimum ◽  
Positive Inotropic Effect ◽  
Methanolic Extract ◽  
In Vitro Study ◽  
Control Group ◽  
Force Of Contraction ◽  
Beneficial Effects

Objective: Evaluation of beneficial effects of the seed of Linum usitatissimum in congestive heart failure.Methods: Methanolic extract of seeds of Linumusitatissimum (MELU) was prepared using soxhlet apparatus and oil of seed of Linumusitatissimum (OLU) was isolated using Clevenger apparatus. The positive inotropic action of methanolic extract of seeds of Linum usitatissimum was evaluated using Langendorff’s assembly (in vitro study). Beneficial effects of methanolic extract and oil of seeds of Linum usitatissimum were carried out by doxorubicin (1 mg/kg, i. p. within 3 w) to induce congestive heart failure (in vivo study). Parameters like electrocardiogram (ECG) recording and cytosolic Ca2+level and histopathology of the heart were carried out. In same study diuretic action was evaluated using Lipschitz model.Results: Methanolic extract of seeds of Linum usitatissimum showed significantly increased in positive inotropic effect (force of contraction 48.8±1.53 mm) as compared to control group (force of contraction 17.5±0.76 mm) on Langendorff”s study (in vitro study). In doxorubicin-induced congestive heart failure both MELU and OLU showed significant decreased QT (Note: In cardiology, the QT interval is a measure of the time between the start of the Q wave and the end of the T wave in the heart's electrical cycle. There is no full form for this medical word) interval. The histopathologic study indicated the least damage to the architecture of myocardial membrane. MELU and OLU increased urine output (5.66±0.16 ml and 6.58±0.15 ml respectively) significantly in Lipschitz model as compared to disease control group (4.58±0.15 ml).Conclusion: Present research work emphasizes that the seeds of Linum usitatissimum is beneficial in the management of congestive heart failure because of having positive inotropic effect, diuretic activity and control of rhythmicity of heart.

scholarly journals Mechanisms Involved in Cardioprotective Effects of Pravastatin Administered during Reoxygenation in Human Myocardium In Vitro 

2012 ◽  
Vol 116 (4) ◽  
pp. 824-833 ◽  
Author(s):  
Sandrine Lemoine ◽  
Stéphane Allouche ◽  
Laurent Coulbault ◽  
Valérie Cornet ◽  
Massimo Massetti ◽  
...  
Keyword(s):  
Caspase 3 ◽  
Mitochondrial Permeability Transition Pore ◽  
Mitochondrial Permeability Transition ◽  
Permeability Transition Pore ◽  
Permeability Transition ◽  
Human Myocardium ◽  
Control Group ◽  
Force Of Contraction ◽  
Mitochondrial Permeability ◽  
Oxide Synthase

Background The authors investigated the effect of pravastatin during reoxygenation after myocardial hypoxia and examined the involvement of nitric oxide synthase, mitochondrial permeability transition pore, and expression of markers of apoptosis in human myocardium in vitro. Methods Human atrial trabeculae were exposed to hypoxia for 30 min and reoxygenation for 60 min (control group; n = 10). Pravastatin (5, 10, 50, 75 μM; n = 6 in each group) was administered throughout the reoxygenation. In separate groups (n = 6 in each group), pravastatin 50 μM was administered in the presence of 200 μM L-NG-nitroarginine methyl ester, a nitric oxide synthase inhibitor, and 50 μM atractyloside, the mitochondrial permeability transition pore opener. The primary endpoint was the developed force of contraction at the end of reoxygenation, expressed as a percentage of baseline (mean ± SD). Protein expression of BAD, phospho-BAD, caspase 3, Pim-1 kinase, and Bcl-2 were measured using Western immunoblotting. Results The administration of 10 (77 ± 5% of baseline), 50 (86 ± 6%), and 75 μM (88 ± 13%) pravastatin improved the force of contraction at the end of reoxygenation, compared with that of the control group (49 ± 11%; P < 0.001). These beneficial effects were prevented by L-NG-nitroarginine methyl ester and atractyloside. Compared with control group, the administration of 5 μM pravastatin did not modify the force of contraction. Pravastatin increased the phosphorylation of BAD, activated the expression of Pim-1 kinase and Bcl-2, and maintained the caspase 3 concentration relative to that of the respective untreated controls. Conclusions Pravastatin, administered at reoxygenation, protected the human myocardium by preventing the mitochondrial permeability transition pore opening, phosphorylating BAD, activating nitric oxide synthase, Pim-1 kinase, and Bcl-2, and preserving the myocardium against the caspase 3 activation.

In Vitro  Effects of Desflurane, Sevoflurane, Isoflurane, and Halothane in Isolated Human Right Atria

2000 ◽  
Vol 92 (1) ◽  
pp. 116-116 ◽  
Author(s):  
Jean-Luc Hanouz ◽  
Massimo Massetti ◽  
Géraldine Guesne ◽  
Stéphane Chanel ◽  
Gérard Babatasi ◽  
...  
Keyword(s):  
Isometric Force ◽  
Coupling Parameter ◽  
Coronary Bypass ◽  
Negative Inotropic Effect ◽  
Peak Force ◽  
Right Atrial ◽  
Human Right ◽  
Time To Peak ◽  
Positive Force

Background Direct myocardial effects of volatile anesthetics have been studied in various animal species in vitro. This study evaluated the effects of equianesthetic concentrations of desflurane, sevoflurane, isoflurane, and halothane on contractile parameters of isolated human atria in vitro. Methods Human right atrial trabeculae, obtained from patients undergoing coronary bypass surgery, were studied in an oxygenated (95% O2-5% CO2) Tyrode's modified solution ([Ca2+]o = 2.0 mM, 30 degrees C, stimulation frequency 0.5 Hz). The effects of equianesthetic concentrations (0.5, 1, 1.5, 2, and 2.5 minimum alveolar concentration [MAC]) of desflurane, sevoflurane, isoflurane, and halothane on inotropic and lusitropic parameters of isometric twitches were measured. Results Isoflurane, sevoflurane, and desflurane induced a moderate concentration-dependent decrease in active isometric force, which was significantly lower than that induced by halothane. In the presence of adrenoceptor blockade, the desflurane-induced decrease in peak of the positive force derivative and time to peak force became comparable to those induced by isoflurane. Halothane induced a concentration-dependent decrease in time to half-relaxation and a contraction-relaxation coupling parameter significantly greater than those induced by isoflurane, sevoflurane and desflurane. Conclusions In isolated human atrial myocardium, desflurane, sevoflurane, and isoflurane induced a moderate concentration-dependent negative inotropic effect. The effect of desflurane on time to peak force and peak of the positive force derivative could be related to intramyocardial catecholamine release. At clinically relevant concentrations, desflurane, sevoflurane, and isoflurane did not modify isometric relaxation.

scholarly journals Characterization of an in vitro model for the study of the short and prolonged effects of myocardial ischaemia and reperfusion in man

2000 ◽  
Vol 99 (5) ◽  
pp. 443-453 ◽  
Author(s):  
Jin-Gang ZHANG ◽  
Sudip GHOSH ◽  
Colin D. OCKLEFORD ◽  
Manuel GALIÑANES
Keyword(s):  
Myocardial Ischaemia ◽  
In Vitro Model ◽  
Human Myocardium ◽  
Right Atrial ◽  
Tissue Viability ◽  
Ischaemia And Reperfusion ◽  
Mtt Reduction ◽  
Vitro Model

The mechanisms underlying myocardial ischaemia and reperfusion-induced injury have been investigated, mainly by using animal experimental preparations in vitro and in vivo, but little is known of the process in human myocardium. The present studies characterize an in vitro model using human myocardium for the study of early and delayed effects of ischaemia and reperfusion. The right atrial appendage was manually sliced and incubated in buffer through which was bubbled O2/CO2 (19:1, v/v) for various time periods. Lactate dehydrogenase (LDH) leakage, 3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl-2H-tetrazolium bromide (MTT) reduction, oxygen consumption, nucleotide levels and tissue morphology were all investigated as markers of myocardial injury. The specimens remained stable and viable up to 24 h, but had significantly deteriorated by 48 h. The preparation responded to ischaemia in a time-related manner. Tissue viability was reduced by 25% after 30 min ischaemia, declined to 60% after 60 min ischaemia and to 75% after 120 min ischaemia. Interestingly, the tissue was more susceptible when ischaemia was induced after 24 h of aerobic incubation. The effects of the duration of reperfusion were investigated after a fixed 60 min ischaemic insult. The results of LDH leakage suggest that reperfusion injury is mainly sustained within the first 2 h of reperfusion. However, the results of MTT reduction show that there is a progressive decrease in tissue viability over the 24 h reperfusion period, possibly reflecting the occurrence of tissue necrosis and apoptosis at different reperfusion times. In conclusion, the data provide evidence that the incubation of human atrial tissue in vitro is stable, and slices are viable for at least 24 h, which permits the study of early and delayed consequences of ischaemia and reperfusion in the human myocardium.

46 VITRIFICATION AT THE GERMINAL VESICLE STAGE TRIGGERS PRECOCIOUS MEIOTIC RESUMPTION BUT DOES NOT AFFECT CYTOPLASMIC MATURATION IN CUMULUS-ENCLOSED PORCINE OOCYTES DURING IN VITRO MATURATION

2016 ◽  
Vol 28 (2) ◽  
pp. 153
Author(s):  
T. Somfai ◽  
N. T. Men ◽  
H. Kaneko ◽  
J. Noguchi ◽  
S. Haraguchi ◽  
...  
Keyword(s):  
Adenosine Triphosphate ◽  
In Vitro Maturation ◽  
Germinal Vesicle ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Control Group ◽  
Control Groups ◽  
Porcine Oocyte ◽  
And Control

Previously we have reported a vitrification protocol that allows preservation of immature porcine oocytes in large numbers (Somfai et al. 2014 PLoS One 9, e97731). However, despite high survival rates, embryo development rates have remained low. The aim of our current research is to reveal factors potentially responsible for reduced developmental competence of vitrified oocytes. As a first step, we investigated the effects of vitrification at the germinal vesicle stage on subsequent nuclear progression and the normality of cytoplasmic functions during in vitro maturation (IVM). Cumulus-enclosed porcine oocytes were vitrified in microdrops, stored, and then warmed by our method (Somfai et al. 2015 Reprod. Fertil. Dev. 27, 124). Then the oocytes were subjected to IVM for 46 h in a chemically defined porcine oocyte medium. During the first 22 h of IVM, the medium was supplemented with 1 mM dibutyryl cyclic adenosine monophosphate, 10 IU mL–1 of eCG, and 10 IU mL–1 of hCG. The following 24 h of IVM was performed in porcine oocyte medium without any supplementation. We compared vitrified/warmed oocytes (vitrified group) with freshly collected immature oocytes (control group) in terms of (1) nuclear progression, (2) intracellular glutathione (GSH), and (3) adenosine triphosphate levels throughout IVM. Each experiment was replicated at least 3 times. Results were analysed by one-way ANOVA and Tukey’s multiple comparison test. A total of 510 oocytes were vitrified of which 422 (82.3%) survived. Only live oocytes were subjected to subsequent assays. Orcein staining revealed that after 22 h of IVM, a significantly higher percentage (P < 0.05) of vitrified oocytes showed germinal vesicle breakdown compared with the control group (22.0 v. 0.9%, respectively). In a similar fashion, after 30 h IVM, a significantly higher (P < 0.05) percentage of oocytes reached the metaphase-II (MII) stage in the vitrified group than in the control group (21.8 v. 0%, respectively). After 46 h of IVM, there was no difference between the vitrified and control groups in terms of the percentage of MII stage oocytes (93.9 and 86.3%, respectively). Analysis of GSH levels in oocytes by the 5,5′-dithio-bis-2-nitrobenzoic acid-glutathione disulfide reductase recycling assay showed no significant difference between the vitrified and control groups at 0 h (6.7 and 7.0 pmol, respectively), 22 h (5.5 and 5.5 pmol, respectively), and 46 h (6.9 and 7.9 pmol, respectively) of IVM. Adenosine triphosphate assay (FL-ASC; Sigma-Aldrich Co., St. Louis, MO) revealed similar adenosine triphosphate contents in the oocytes of the vitrified and control groups at 0 h (1.53 and 1.61 pmol, respectively), 22 h (1.67 and 1.70 pmol, respectively), and 46 h (1.65 and 1.83 pmol, respectively) of IVM. In conclusion, vitrification triggered precocious nuclear maturation even in the presence of dibutyryl cyclic adenosine monophosphate; however, it did not affect GSH levels and overall metabolism. This work was supported by JSPS KAKENHI (Grant Number: 26870839) and JST/JICA SATREPS.

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