The Effects of the NMR Shift-reagents Dy(PPP)2, Dy(TTHA) and Tm(DOTP) on Developed Pressure in Isolated Perfused Rat Hearts. The Role of Shift-reagent Calcium Complexes

2001 ◽  
Vol 33 (11) ◽  
pp. 1945-1956 ◽  
Author(s):  
Balázs Gaszner ◽  
Tamás Simor ◽  
Gábor Hild ◽  
Gabriel A. Elgavish
Keyword(s):  
Shift Reagent ◽  
Rat Hearts ◽  
Perfused Rat Hearts ◽  
Calcium Complexes ◽  
Shift Reagents ◽  
Developed Pressure ◽  
Isolated Perfused Rat Hearts

The protective role of neocuproine against cardiac damage in isolated perfused rat hearts

1990 ◽  
Vol 8 (2) ◽  
pp. 133-143 ◽  
Author(s):  
Yori J. Appelbaum ◽  
Jeffrey Kuvin ◽  
Joseph B. Borman ◽  
Gideon Uretzky ◽  
Mordechai Chevion
Keyword(s):  
Protective Role ◽  
Cardiac Damage ◽  
Rat Hearts ◽  
Perfused Rat Hearts ◽  
Isolated Perfused Rat Hearts

Catecholamines and preconditioning: studies of contraction and function in isolated rat hearts

1999 ◽  
Vol 277 (1) ◽  
pp. H136-H143 ◽  
Author(s):  
David J. Hearse ◽  
Fiona J. Sutherland
Keyword(s):  
Ischemic Preconditioning ◽  
Untreated Control ◽  
Vehicle Control ◽  
Left Ventricular ◽  
Rat Hearts ◽  
Perfused Rat Hearts ◽  
Developed Pressure ◽  
And Function ◽  
Postischemic Recovery ◽  
Isolated Perfused Rat Hearts

The aims of this study were to determine whether 1) like ischemic preconditioning, transient exposure to norepinephrine before ischemia exacerbates contracture during ischemia and 2) protection afforded by norepinephrine is stereospecific (receptor mediated). Isolated perfused rat hearts were randomized into five groups ( n = 6/group): 1) ischemic preconditioning (3 min of ischemia + 3 min of reperfusion + 5 min of ischemia + 5 min of reperfusion), 2) untreated control, 3) vehicle control (ascorbic acid), 4) substitution of preconditioning ischemia by perfusion with d-norepinephrine, and 5) substitution of preconditioning ischemia by perfusion with l-norepinephrine. This was followed by 40 min of zero-flow ischemia and 50 min of reperfusion. Ischemic preconditioning and l-norepinephrine exacerbated contracture (time to 50% contracture = 9.2 ± 1.1 and 9.0 ± 1.1 vs. 13.3 ± 0.3, 12.4 ± 0.5, and 13.2 ± 0.4 min for untreated control, vehicle control, and d-norepinephrine, respectively, P < 0.05). Postischemic left ventricular developed pressure was poor in untreated control (23.0 ± 2.2%), vehicle control (26.9 ± 2.3%), and d-norepinephrine (19.8 ± 2.8%) groups but good in preconditioned (52.4 ± 5.1%) and l-norepinephrine (52.5 ± 1.1%) groups ( P < 0.05). Thus norepinephrine preconditioning, like ischemic preconditioning, causes a paradoxical exacerbation of contracture coupled with enhanced postischemic recovery; both effects are stereospecific.

23Na NMR shift reagents enhance cardiac staircase effect in isolated perfused rat hearts

1999 ◽  
Vol 12 (5) ◽  
pp. 267-274 ◽  
Author(s):  
Tamás Simor ◽  
Tamás Lóránd ◽  
Áron Szöllösy ◽  
Balázs Gaszner ◽  
Stanley B. Digerness ◽  
...  
Keyword(s):  
Rat Hearts ◽  
Staircase Effect ◽  
Perfused Rat Hearts ◽  
Shift Reagents ◽  
23Na Nmr ◽  
Isolated Perfused Rat Hearts

Thermodynamic limitation for Ca2+ handling contributes to decreased contractile reserve in rat hearts

1998 ◽  
Vol 275 (6) ◽  
pp. H2064-H2071 ◽  
Author(s):  
Rong Tian ◽  
Jessica M. Halow ◽  
Markus Meyer ◽  
Wolfgang H. Dillmann ◽  
Vincent M. Figueredo ◽  
...  
Keyword(s):  
Atp Hydrolysis ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Contractile Reserve ◽  
Rat Hearts ◽  
Intracellular Ca ◽  
Perfused Rat Hearts ◽  
Thermodynamic Driving Force ◽  
Developed Pressure ◽  
Isolated Perfused Rat Hearts

The free energy release from ATP hydrolysis (‖ΔG∼p‖) is decreased by inhibiting the creatine kinase (CK) reaction, which may limit the thermodynamic driving force for the sarcoplasmic reticulum (SR) Ca2+ pumps and thereby cause a decrease in contractile reserve. To determine whether a decrease in ‖ΔG∼p‖ results in decreased contractile reserve by impairing Ca2+ handling, we measured left ventricular pressure and cytosolic Ca2+concentration ([Ca2+]c; by indo 1 fluorescence) in isolated perfused rat hearts, with >95% inhibition of CK with 90 μmol iodoacetamide. Iodoacetamide did not directly alter SR Ca2+-ATPase activity, baseline left ventricular developed pressure, or baseline [Ca2+]c. When perfusate Ca2+ concentration was increased from 1.2 to 3.3 mM, LV developed pressure increased from 67 ± 6 to 119 ± 8 mmHg in control hearts ( P < 0.05) but did not significantly increase in CK-inhibited hearts. Similarly, the amplitude of the [Ca2+]ctransient increased from 548 ± 54 to 852 ± 140 nM in control hearts ( P < 0.05) but did not significantly increase in CK-inhibited hearts. We conclude that decreased ‖ΔG∼p‖ limits intracellular Ca2+ handling and thereby limits contractile reserve.

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