Effect of ouabain on potassium exchange in hypothermic mammalian heart

1962 ◽  
Vol 203 (5) ◽  
pp. 834-838
Author(s):  
Sidney S. Schreiber ◽  
Murray Oratz ◽  
Marcus A. Rothschild

Potassium exchange was studied in the intact working hypothermic guinea pig heart in vitro with K42. As at 37 C, buildup and washout experiments demonstrated two compartments of K exchange, but these behaved differently with reductions in temperature to 20 C. The rate of K exchange of the "fast" compartment decreased with lowered temperatures, whereas the rate of "slow" compartment exchange either remained unaffected or increased slightly. Ouabain had no apparent effect on the fast compartment K exchange. Toxic levels of ouabain, which inhibited entrance of K into the slowly exchanging phase at 37 C, showed a minimal effect on this compartment at 20 C. The decreased ouabain inhibition at 20 C was paralleled by a concomitant decrease in toxicity (contracture and ventricular fibrillation). It was postulated that intracellular cardiac K exchange involved two separate processes which responded differently to low temperatures. Ouabain action was indicated to be specifically on that process which was insensitive to cold temperatures.

1961 ◽  
Vol 200 (5) ◽  
pp. 1055-1062 ◽  
Author(s):  
Sidney S. Schreiber ◽  
Murray Oratz ◽  
Marcus A. Rothschild

The effect of the digitalis glycoside, ouabain, on potassium exchange in the guinea pig heart in vitro was studied with the aid of K42. With modified Ringer's solution as a perfusate at 38 C, K was found to exchange at two rates in both washout and buildup studies. In vivo equilibration studies also suggested more than one rate of exchange. Ouabain, in vitro, effected inhibition of entrance of K into the slowly exchanging compartment, but did not affect influx into the fast compartment or efflux from the fast or slow compartments. The ouabain inhibition was seen at Ringer's K concentrations of 3.8–4.3 mEq/liter was equivocal at K concentrations of 5.0–5.5 mEq/ liter and absent at K concentrations of 7.0–7.5 mEq/liter. It was postulated that ouabain inhibition was directed toward the slowly exchanging fraction of intracellular potassium.


2012 ◽  
Vol 7 (3) ◽  
Author(s):  
A.M. Mujibul Haq ◽  
Md. Mahbubul Huque ◽  
Shah Abdur Rahman Chaudhury ◽  
Mohammad Nurul Haque

1974 ◽  
Vol 52 (3) ◽  
pp. 602-612 ◽  
Author(s):  
Minh-Hau Nguyen ◽  
L. Gailis

Guinea-pig hearts were perfused at constant pressure with Krehs–Henseleit bicarbonate buffer equilibrated with 95% O2 – 5% CO2. Acetaldehyde at 1 and 5 mM increased coronary flow, oxygen consumption, and heart rate. At 0.2 mM, it increased coronary flow and oxygen consumption only. In the rapidly paced heart, 1 mM acetaldehyde increased coronary flow, but not heart rate or oxygen consumption. Acetaldehyde increased coronary flow and oxygen consumption of the potassium-arrested heart. Acetaldehyde increased all parameters of the hypoxic heart (25% O2 gas phase), but the anoxic heart was not affected (coronary flow was already maximal).Reserpine (in vivo) and catecholamine β blockers (dichloroisoproterenol and propranolol) (in vitro) blocked the heart rate increases and moderated the rise in oxygen consumption. Dichloroisoproterenol plus phentolamine blocked the increases of both heart rate and oxygen consumption. None of the compounds affected the increase of coronary flow produced by acetaldehyde. Epinephrine, norepinephrine, and tyramine increased the heart rate and oxygen consumption, but not the coronary flow. Theophylline increased all three parameters. Neither tranylcypromine nor atropine modified the acetaldehyde effect. We conclude that the increase in heart rate is mediated by catecholamine β receptors. The increase in coronary flow is independent of the increase in heart rate or oxygen consumption and is not mediated by catecholamines.


2003 ◽  
Vol 14 (6) ◽  
pp. 621-631 ◽  
Author(s):  
Mark Warren ◽  
Prabal K. Guha ◽  
Omer Berenfeld ◽  
Alexey Zaitsev ◽  
Justus M.B. Anumonwo ◽  
...  

1981 ◽  
Vol 241 (1) ◽  
pp. H18-H25
Author(s):  
K. Schror ◽  
P. Kohler ◽  
M. Muller ◽  
B. A. Peskar ◽  
P. Rosen

A preparation of an isolated platelet-perfused guinea pig heart is described, which was utilized to study prostacyclin-thromboxane interrelationships. Infusion of washed human platelets (4 X 10(8)/min) through the coronary vascular bed stimulated the vascular PGI2 production from 114 +/- 27 to 350 +/- 30 pg/ml (P less than 0.01) and was associated with a significant increase in platelet cAMP from 1.2 +/- 0.4 to 2.6 +/- 0.9 pmol/10(8) platelets (P less than 0.05). Administration of arachidonic acid (AA) (45 micrograms) to the system led to a further increase (eight- to ninefold) of PGI2 and yielded marked thromboxane formation (20-25 ng/ml). Treatment of the hearts with aspirin (1 mM) prevented the PGI2 formation and AA-induced increase in platelet cAMP. Treatment of platelets with aspirin prevented thromboxane formation but did not influence AA-induced changes in platelet cAMP and vascular PGI2 production. Bioassay data of PGI2 and rabbit aortic contracting substance gave results comparable to radioimmunoassay of 6-keto-PGF1 alpha and thromboxane B2. AA always decreased the coronary vascular resistance whether thromboxanes were formed or not.


1992 ◽  
Vol 220 (2-3) ◽  
pp. 213-236 ◽  
Author(s):  
Michael Gwilt ◽  
Christopher G. Henderson ◽  
Jonathon Orme ◽  
Janet D. Rourke

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