1111 CARDIOMYOCYTE REGENERATION IN MAMMALIAN MYOCARDIUM

2012 ◽  
Vol 30 ◽  
pp. e324-e325
Author(s):  
Richard T. Lee
Keyword(s):  
Mammalian Myocardium

scholarly journals Effects of acidosis on resting cytosolic and mitochondrial Ca2+ in mammalian myocardium.

1993 ◽  
Vol 102 (3) ◽  
pp. 575-597 ◽  
Author(s):  
G Gambassi ◽  
R G Hansford ◽  
S J Sollott ◽  
B A Hogue ◽  
E G Lakatta ◽  
...  
Keyword(s):  
Lactic Acid ◽  
Ventricular Myocytes ◽  
Free Acid ◽  
Left Ventricular ◽  
Ruthenium Red ◽  
Acetoxymethyl Ester ◽  
Cytosolic Ph ◽  
Bicarbonate Buffer ◽  
Adult Rat ◽  
Mammalian Myocardium

Acidosis increases resting cytosolic [Ca2+], (Cai) of myocardial preparations; however, neither the Ca2+ sources for the increase in Cai nor the effect of acidosis on mitochondrial free [Ca2+], (Cam) have been characterized. In this study cytosolic pH (pHi) was monitored in adult rat left ventricular myocytes loaded with the acetoxymethyl ester (AM form) of SNARF-1. A stable decrease in the pHi of 0.52 +/- 0.05 U (n = 16) was obtained by switching from a bicarbonate buffer equilibrated with 5% CO2 to a buffer equilibrated with 20% CO2. Electrical stimulation at either 0.5 or 1.5 Hz had no effect on pHi in 5% CO2, nor did it affect the magnitude of pHi decrease in response to hypercarbic acidosis. Cai was measured in myocytes loaded with indo-1/free acid and Cam was monitored in cells loaded with indo-1/AM after quenching cytosolic indo-1 fluorescence with MnCl2. In quiescent intact myocytes bathed in 1.5 mM [Ca2+], hypercarbia increased Cai from 130 +/- 5 to 221 +/- 13 nM. However, when acidosis was effected in electrically stimulated myocytes, diastolic Cai increased more than resting Cai in quiescent myocytes, and during pacing at 1.5 Hz diastolic Cai was higher (285 +/- 17 nM) than at 0.5 Hz (245 +/- 18 nM; P < 0.05). The magnitude of Cai increase in quiescent myocytes was not affected either by sarcoplasmic reticulum (SR) Ca2+ depletion with ryanodine or by SR Ca2+ depletion and concomitant superfusion with a Ca(2+)-free buffer. In unstimulated intact myocytes hypercarbia increased Cam from 95 +/- 12 to 147 +/- 19 nM and this response was not modified either by ryanodine and a Ca(2+)-free buffer or by 50 microM ruthenium red in order to block the mitochondrial uniporter. In mitochondrial suspensions loaded either with BCECF/AM or indo-1/AM, acidosis produced by lactic acid addition decreased both intra- and extramitochondrial pH and increased Cam. Studies of mitochondrial suspensions bathed in indo-1/free acid-containing solution showed an increase in extramitochondrial Ca2+ after the addition of lactic acid. Thus, in quiescent myocytes, cytoplasmic and intramitochondrial buffers, rather than transsarcolemmal Ca2+ influx or SR Ca2+ release, are the likely Ca2+ sources for the increase in Cai and Cam, respectively; additionally, Ca2+ efflux from the mitochondria may contribute to the raise in Cai. In contrast, in response to acidosis, diastolic Cai in electrically stimulated myocytes increases more than resting Cai in quiescent cells; this suggests that during pacing, net cell Ca2+ gain contributes to enhance diastolic Cai.

Mechanical response of the mammalian myocardium to modifications of the action potential

1971 ◽  
Vol 5 (supp1) ◽  
pp. 64-70 ◽  
Author(s):  
R. L. Kaufmann ◽  
H. Antoni ◽  
R. Hennekes ◽  
R. Jacob ◽  
M. Kohlhardt ◽  
...  
Keyword(s):  
Action Potential ◽  
Mechanical Response ◽  
Mammalian Myocardium

scholarly journals Studies of the contractility of mammalian myocardium at low rates of stimulation.

1976 ◽  
Vol 254 (1) ◽  
pp. 1-17 ◽  
Author(s):  
D G Allen ◽  
B R Jewell ◽  
E H Wood
Keyword(s):  
Mammalian Myocardium

scholarly journals Forced expression of the cyclin B1–CDC2 complex induces proliferation in adult rat cardiomyocytes

2004 ◽  
Vol 382 (2) ◽  
pp. 411-416 ◽  
Author(s):  
Katrina A. BICKNELL ◽  
Carmen H. COXON ◽  
Gavin BROOKS
Keyword(s):  
Cell Division ◽  
Cyclin B1 ◽  
Cell Division Cycle ◽  
Myocardial Regeneration ◽  
Rat Cardiomyocytes ◽  
Adult Rat ◽  
Adult Cardiomyocytes ◽  
Mammalian Myocardium

Repair of the mature mammalian myocardium following injury is impaired by the inability of the majority of cardiomyocytes to undergo cell division. We show that overexpression of the cyclin B1–CDC2 (cell division cycle 2 kinase) complex re-initiates cell division in adult cardiomyocytes. Thus strategies targeting the cyclin B1–CDC2 complex might re-initiate cell division in mature cardiomyocytes in vivo and facilitate myocardial regeneration following injury.

The “end-systolic” length-tension relation in mammalian myocardium

1985 ◽  
Vol 80 (6) ◽  
pp. 636-641 ◽  
Author(s):  
R. W. Gülch
Keyword(s):  
Mammalian Myocardium
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