Spermine prevent iron accumulation and depress lipofuscin accumulation in cultured myocardial cells

1996 ◽  
Vol 21 (3) ◽  
pp. 375-381 ◽  
Author(s):  
Massoud R. Marzabadi ◽  
Erik Løvaas
1983 ◽  
Vol 245 (1) ◽  
pp. H60-H65 ◽  
Author(s):  
J. L. Jones ◽  
R. E. Jones

Excitation thresholds and arrhythmias were studied in "adult-type" cultured chick embryo myocardial cells after electric field stimulation with biphasic, truncated, and rectified underdamped RLC (resistance-inductance-capacitance) type waveforms, to test the hypothesis that the negative phase of biphasic waveforms ameliorates membrane dysfunction induced by the initial positive portion. Photocell mechanograms and intracellular microelectrodes monitored extrasystoles and depolarization-induced arrhythmias. Rectifying or truncating biphasic waveforms did not alter the excitation threshold. However, shock intensities producing specific postshock arrhythmias or a specific severity of postshock prolonged depolarization differed significantly when biphasic waveforms were truncated or rectified. The voltage gradient producing a specific dysfunction was 12-14% lower for the truncated version than for the biphasic; that for the rectified version was 17-27% lower than for the biphasic version (although both contained the same energy). Safety factor, the ratio between shock intensity producing specific dysfunction and that producing excitation, was determined for each waveform. Biphasic waveforms had larger safety factors than truncated or rectified waveforms. Since safety factor, as measured in cultured myocardial cells, closely corresponds with in situ defibrillating effectiveness (14), the significantly higher safety factors of biphasic waveforms suggest that carefully shaped biphasic waveforms might improve the efficacy and safety of cardiac defibrillation procedures.


2003 ◽  
Vol 442 (4) ◽  
pp. 356-363 ◽  
Author(s):  
Keiko Mashimo ◽  
Shigeru Sato ◽  
Youkichi Ohno

1967 ◽  
Vol 158 (4) ◽  
pp. 501-507 ◽  
Author(s):  
Ruth E. Rumery ◽  
William O. Rieke

1998 ◽  
Vol 11 (2) ◽  
pp. 317
Author(s):  
Ock Kyu Park ◽  
Jae Min Oh ◽  
Jeong Joong Kim ◽  
Min Kyu Choi ◽  
Seung Taeck Park ◽  
...  

1994 ◽  
Vol 267 (5) ◽  
pp. H1948-H1954 ◽  
Author(s):  
E. Hashimoto ◽  
T. Ogita ◽  
T. Nakaoka ◽  
R. Matsuoka ◽  
A. Takao ◽  
...  

Vascular endothelial growth factor (VEGF or vascular permeability factor), a direct-acting, endothelial cell-specific mitogen, has been suggested to be involved in development and maintenance of vasculatures in tumor neovascularization and in normal tissues. To investigate possible roles of VEGF in ischemic hearts, we studied induction of VEGF mRNA by ischemia and hypoxia using coronary artery-ligated hearts in vivo and perfused hearts and cultured myocardial cells in vitro. VEGF mRNA was potently induced by ischemia in the heart in vivo. In perfused hearts, maximum expression was rapidly induced (within 30 min) by transient reversible ischemia (5–10 min of ischemia) and lasted at least 3 h. Induction was also caused by hypoxia, which was confirmed in perfused hearts and cultured myocardial cells. These results suggest that induction of VEGF mRNA is upregulated by oxygen deprivation in the heart and that not only infarction but also chronic ischemia in the clinical setting could induce VEGF as a potent angiogenesis factor to stimulate coronary collateral formation.


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