Effects of R 56865 on postischemic ventricular function in isolated rat working heart preparations obtained from healthy, diabetic and hypertensive animals

1994 ◽  
Vol 349 (6) ◽  
pp. 619-626 ◽  
Author(s):  
A. J. Pijl ◽  
M. G. C. Hendriks ◽  
K. L. Kam ◽  
M. Paffendorf ◽  
P. A. van Zwieten
1989 ◽  
Vol 256 (2) ◽  
pp. H584-H588 ◽  
Author(s):  
J. M. Brown ◽  
M. A. Grosso ◽  
L. S. Terada ◽  
C. J. Beehler ◽  
K. M. Toth ◽  
...  

Reperfusion with untreated, carbon monoxide-treated, or glutaraldehyde-fixed human erythrocytes (RBC) increased ventricular function and decreased myocardial hydrogen peroxide (H2O2) levels [assessed by H2O2-dependent aminotriazole (AMT) inactivation of myocardial catalase activities] of ischemic, isolated rat hearts. In contrast, reperfusion with RBC that lacked catalase (AMT treated) and/or glutathione (N-ethylmaleimide treated) did not increase ventricular function or decrease myocardial H2O2 levels as much as reperfusion with untreated RBC. By comparison, reperfusion with superoxide dismutase-depleted (diethyldithiocarbamate-treated) or anion channel-inhibited (diisothiocyanodisulfonic acid stilbene-treated) RBC increased ventricular function and decreased myocardial H2O2 levels the same as untreated RBC. The results suggest that catalase and/or glutathione in intact RBC can decrease endogenously generated H2O2 and related reperfusion injury in ischemic, isolated perfused hearts.


2005 ◽  
Vol 100 (3) ◽  
pp. 629-635 ◽  
Author(s):  
Huan Guo ◽  
Shunji Takahashi ◽  
Sungsam Cho ◽  
Tetsuya Hara ◽  
Shiro Tomiyasu ◽  
...  

Pharmacology ◽  
1989 ◽  
Vol 39 (1) ◽  
pp. 11-18 ◽  
Author(s):  
P. Koch ◽  
D. Wilhelm ◽  
B. Wilffert ◽  
T. Peters
Keyword(s):  
R 56865 ◽  

1992 ◽  
Vol 263 (2) ◽  
pp. H333-H340 ◽  
Author(s):  
A. Mitani ◽  
M. J. Shattock

The contribution of Na-activated K channel, the furosemide-sensitive (Na-K-Cl) cotransport, and Na-K pump to extracellular potassium accumulation during global ischemia was investigated using pharmacological blockade of these pathways. R 56865 (a blocker of the Na-activated K channel), furosemide, or ouabain was included in the perfusate before ischemia in the isolated rat heart preparation, and the extracellular K concentration ([K]e) was monitored during 30 min of global ischemia. In control hearts, [K]e showed an early rise (up to 9.0 +/- 0.2 mM from the baseline of 5.9 mM), a fall (to a minimum of 6.7 +/- 0.2 mM), and a late rise (to 14.1 +/- 0.4 mM by the end of ischemia). R 56865 (0.1 and 1 microM) suppressed the early [K]e rise to 50% of the control level. The late rise in [K]e was also significantly suppressed by the higher dose of R 56865. Furosemide (0.1 and 1 mM) reduced the early K accumulation by 35% but did not affect the rise of [K]e during the late ischemic phase. Blockade of Na-K pump by 10 microM ouabain did not increase [K]e during any phase of ischemia and, in fact, 100 microM ouabain profoundly suppressed the early rise in [K]e. We therefore suggest that the Na-activated K channel, the furosemide-sensitive cotransport, and changes in the activity of the Na-K pump may all contribute to extracellular K accumulation during ischemia. However, in addition to these pathways, it seems likely that other pathways for transsarcolemmal K efflux contribute to cellular K loss during ischemia in the isolated rat heart.


Author(s):  
A.S. Dabholkar ◽  
W.W. Carmichael ◽  
K. Berg ◽  
J. Wyman

Intracellular changes in the hepatocytes of isolated rat livers perfused with cyclic heptapeptide toxins are described. The toxins used are 1) -Ala-Leu- β-methyl isoAsp-Arg-ADDA-isoGlu-mdha (M.W. 944) from Microcystis aeruginosa- Lake Akersvatn, Norway; 2) -Ala-Arg-isoAsp-Arg-ADDA-isoGlu-mdha (M.W. 1023) from Oscillatoria agardhii var. - Lake Kolbatnvatn, Norway; 3) -Ala-Arg-isoAsp-Arg-ADDA-isoGlu-dha (M.W. 1009) from Oscillatoria agardhii var. isothrix - Lake Froylandsvatn, Norway. Approximate LD intraperitoneal mouse for the toxins is 50, 500 and 1000 μg/kg respectively.Livers were removed from male Sprague Dawley rats and perfused for 15 min with a blood-free perfusate (50 ml) followed by 60 min with perfusate containing i) 25, 50, or 200 μg of M. aeruginosa toxin ii) 50, 250, 500 or 1000 μg of O. agardhii var. toxin and iii) 1000, 2000, 2500 or 5000 μg of O. agardhii var. isothrix toxin. Control livers were perfused for 75 min with the blood-free perfusate.


2001 ◽  
Vol 120 (5) ◽  
pp. A159-A159
Author(s):  
S RO ◽  
K YAKABI ◽  
T NAKAMURA

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