Effects of hypoxia, simulated ischemia and reoxygenation on the contractile function of human atrial trabeculae

1996 ◽  
Vol 160-161 (1) ◽  
pp. 143-151 ◽  
Author(s):  
Andreas Lammerich ◽  
J�rgen Bohm ◽  
Ingolf Schimke ◽  
Kay-Dietrich Wagner ◽  
Eberhard Storch ◽  
...  
Keyword(s):  
Contractile Function ◽  
Simulated Ischemia ◽  
Human Atrial Trabeculae

Effects of hypoxia, simulated ischemia and reoxygenation on the contractile function of human atrial trabeculae

1996 ◽  
pp. 143-151
Author(s):  
Andreas Lammerich ◽  
Jürgen Böhm ◽  
Ingolf Schimke ◽  
Kay-Dietrich Wagner ◽  
Eberhard Storch ◽  
...  
Keyword(s):  
Contractile Function ◽  
Simulated Ischemia ◽  
Human Atrial Trabeculae

Annexin V staining during reperfusion detects cardiomyocytes with unique properties

2001 ◽  
Vol 281 (5) ◽  
pp. H1931-H1937 ◽  
Author(s):  
Prakash Narayan ◽  
Robert M. Mentzer ◽  
Robert D. Lasley
Keyword(s):  
Propidium Iodide ◽  
Ventricular Myocytes ◽  
Contractile Function ◽  
Ischemia Reperfusion ◽  
Annexin V ◽  
Cell Width ◽  
Simulated Ischemia ◽  
Propidium Iodide Staining ◽  
Membrane Blebs ◽  
Apoptosis And Necrosis

With the use of markers of sarcolemmal membrane permeability, cardiomyocyte models of ischemic injury have primarily addressed necrotic death during ischemia. In the present study, we used annexin V-propidium iodide staining to examine apoptosis and necrosis after simulated ischemia and simulated reperfusion in rat ventricular myocytes. Annexin V binds phosphatidylserine, a phosphoaminolipid thought to be externalized during apoptosis or programmed cell death. Propidium iodide is a marker of cell necrosis. Under baseline conditions, <1% of cardiomyocytes stained positive for annexin V. After 20 or 60 min of simulated ischemia, there was no increase in annexin V staining, although 60-min simulated ischemia resulted in significant propidium iodide staining. Twenty minutes of simulated ischemia, followed by 20 or 60 min of simulated reperfusion, resulted in 8–10% of myocytes staining positive for annexin V. Annexin V-positive cells retained both rod-shaped morphology and contractile function but exhibited the decreased cell width indicative of cell shrinkage. Baseline mitochondrial free Ca2+(111 ± 14 nM) was elevated in reperfused annexin V-negative cells (214 ± 22 nM), and further elevated in annexin V-positive myocytes (382 ± 9 nM). After 60 min of simulated reperfusion, caspase-3-like activity was observed in ∼3% of myocytes, which had a rounded appearance and membrane blebs. These results suggest that the use of annexin V after simulated ischemia-reperfusion uncovers a population of cardiomyocytes whose characteristics appear to be consistent with cells undergoing apoptosis.

Role of AMPK in the protective effects exerted by triiodothyronine in ischemic-reperfused myocardium

2021 ◽  
Vol 66 (3) ◽  
pp. 207-221
Author(s):  
Romina Hermann ◽  
Victoria Evangelina Mestre Cordero ◽  
María de las Mercedes Fernández Pazos ◽  
Mailen Florencia Córdoba ◽  
Federico Joaquín Reznik ◽  
...  
Keyword(s):  
Acute Treatment ◽  
Mitochondrial Permeability Transition ◽  
Contractile Function ◽  
Ischemia Reperfusion ◽  
Protective Effects ◽  
Cellular Viability ◽  
Retention Capacity ◽  
Atp Production ◽  
Simulated Ischemia ◽  
Compound C

Recent studies have provided evidence that triiodothyronine (T3) might play an effective role in the recovery of ischemic myocardium, through the preservation of mitochondrial function and the improvement of energy substrate metabolism. To this respect, it has been suggested that T3 could activate AMP-activated protein kinase (AMPK), the cellular ‘fuel-gauge’ enzyme, although its role has yet to be elucidated. The aim of the present study was to investigate the effects produced by acute treatment with T3 (60 nM) and the pharmacological inhibition of AMPK by compound C on isolated rat left atria subjected to 75 min simulated ischemia-75 min reperfusion. Results showed that T3 increased AMPK activation during simulated ischemia-reperfusion, while compound C prevented it. At the end of simulated reperfusion, acute T3 treatment increased contractile function recovery and cellular viability conservation. Mitochondrial ultrastructure was better preserved in the presence of T3 as well as mitochondrial ATP production rate and tissue ATP content. Calcium retention capacity, a parameter widely used as an indicator of the resistance of mitochondrial permeability transition pore (MPTP) to opening, and GSK-3β phosphorylation, a master switch enzyme that limits MPTP opening, were increased by T3 administration. All these beneficial effects exerted by T3 acute treatment were prevented when compound C was co-administrated. The present study provided original evidence that T3 enhances intrinsic activation of AMPK during myocardial ischemia-reperfusion, being this enzyme involved, at least in part, in the protective effects exerted by T3, contributing to mitochondrial structure and function preservation, post-ischemic contractile recovery and conservation of cellular viability.

Luteolin Inhibits Apoptosis and Improves Cardiomyocyte Contractile Function through the PI3K/Akt Pathway in Simulated Ischemia/Reperfusion

Pharmacology ◽  
2011 ◽  
Vol 88 (3-4) ◽  
pp. 149-158 ◽  
Author(s):  
Fang Fang ◽  
Dongye Li ◽  
Huanjun Pan ◽  
Dan Chen ◽  
Lingling Qi ◽  
...  
Keyword(s):  
Contractile Function ◽  
Ischemia Reperfusion ◽  
Akt Pathway ◽  
Simulated Ischemia

Further study on the role of HSP70 on Ca2+ homeostasis in rat ventricular myocytes subjected to simulated ischemia

2006 ◽  
Vol 290 (2) ◽  
pp. C583-C591 ◽  
Author(s):  
Jing Liu ◽  
Kenneth W. L. Kam ◽  
Gudrun H. Borchert ◽  
Gennadi M. Kravtsov ◽  
Heather J. Ballard ◽  
...  
Keyword(s):  
Antisense Oligonucleotide ◽  
Ventricular Myocytes ◽  
Contractile Function ◽  
Rat Ventricular Myocytes ◽  
Simulated Ischemia ◽  
Opioid Receptor Agonist ◽  
Plasmic Reticulum ◽  
Rat Ventricular Myocyte ◽  
Hsp70 Synthesis

We hypothesized that activation of heat shock protein 70 (HSP70) by preconditioning, which is known to confer delayed cardioprotection, attenuates the impaired handling of Ca2+ at multiple sites. To test the hypothesis, we determined how the ryanodine receptor (RyR), sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA), and Na+/Ca2+ exchanger (NCX) handled Ca2+ in rat ventricular myocytes preconditioned with a κ-opioid receptor agonist, U50488H (UP), followed by blockade of HSP70 with a selective antisense oligonucleotide and subsequently subjected to simulated ischemia. We determined the following: 1) the Ca2+ transients induced by electrical stimulation and caffeine, which provide the overall picture of Ca2+ homeostasis; 2) expression of RyR, SERCA, and NCX; and 3) Ca2+ fluxes via NCX by the use of 45Ca2+ in the rat ventricular myocyte. We found that UP increased the activity of RyR, SERCA, and NCX and the expression of RyR and SERCA. These effects led to increases in the release of Ca2+ from the sarcoplasmic reticulum via RyR and in the removal of Ca2+ from the cytoplasm by reuptake of Ca2+ to the SR via SERCA and by extrusion of Ca2+ out of the cell via NCX. UP also reduced mitochondrial Ca2+ accumulation. All of the effects of UP were either abolished or significantly attenuated by blockade of HSP70 synthesis with a selective antisense oligonucleotide. The results are evidence that activation of HSP70 by preconditioning improves the ischemia-impaired Ca2+ homeostasis at multiple sites in the heart, which may be responsible, at least partly, for attenuated Ca2+ overload, improved recovery in contractile function, and cardioprotection.

scholarly journals Effects of ischemia and reperfusion on isolated ventricular myocytes from young adult and aged Fischer 344 rat hearts

2008 ◽  
Vol 294 (5) ◽  
pp. H2174-H2183 ◽  
Author(s):  
J. Darcy O'Brien ◽  
Jessica H. Ferguson ◽  
Susan E. Howlett
Keyword(s):  
Young Adult ◽  
Cell Viability ◽  
Ventricular Myocytes ◽  
Contractile Function ◽  
Ischemia And Reperfusion ◽  
Early Reperfusion ◽  
Aging Heart ◽  
Fischer 344 ◽  
Simulated Ischemia ◽  
The Impact

This study examined the impact of age on contractile function, Ca2+ homeostasis, and cell viability in isolated myocytes exposed to simulated ischemia and reperfusion. Ventricular myocytes were isolated from anesthetized young adult (3 mo) and aged (24 mo) male Fischer 344 rats. Cells were field-stimulated at 4 Hz (37°C), exposed to simulated ischemia, and reperfused with Tyrode solution. Cell shortening and intracellular Ca2+ were measured simultaneously with an edge detector and fura-2. Cell viability was assessed by Trypan blue exclusion. Ischemia (20–45 min) depressed amplitudes of contraction equally in isolated myocytes from young adult and aged animals. The degree of postischemic contractile depression (stunning) was comparable in both groups. Ca2+ transient amplitudes were depressed in early reperfusion in young adult and aged cells and then recovered to preischemic levels in both groups. Cell viability also declined equally in reperfusion in both groups. In short, some cellular responses to simulated ischemia and reperfusion were similar in both groups. Even so, aged myocytes exhibited a much greater and more prolonged accumulation of diastolic Ca2+ in ischemia and in early reperfusion compared with myocytes from younger animals. In addition, the degree of mechanical alternans in ischemia increased significantly with age. The observation that there is an age-related increase in accumulation of diastolic Ca2+ in ischemia and early reperfusion may account for the increased sensitivity to ischemia and reperfusion injury in the aging heart. The occurrence of mechanical alternans in ischemia may contribute to contractile dysfunction in ischemia in the aging heart.

scholarly journals Insulin improves cardiomyocyte contractile function through enhancement of SERCA2a activity in simulated ischemia/reperfusion1

2006 ◽  
Vol 27 (7) ◽  
pp. 919-926 ◽  
Author(s):  
Jie YU ◽  
Hai-feng ZHANG ◽  
Feng WU ◽  
Qiu-xia LI ◽  
Heng MA ◽  
...  
Keyword(s):  
Contractile Function ◽  
Simulated Ischemia

Insulin improves cardiac myocytes contractile function recovery in simulated ischemia-reperfusion: Key role of Akt

2003 ◽  
Vol 48 (13) ◽  
pp. 1364-1369 ◽  
Author(s):  
Bo Zhang ◽  
Haifeng Zhang ◽  
Qian Fan ◽  
Xinliang Ma ◽  
Feng Gao
Keyword(s):  
Cardiac Myocytes ◽  
Contractile Function ◽  
Ischemia Reperfusion ◽  
Simulated Ischemia ◽  
Function Recovery
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