scholarly journals Potassium-Induced Changes in the Electromechanical and ATPase Activity of Guinea Pig Heart

1976 ◽  
Vol 17 (2) ◽  
pp. 211-221 ◽  
Author(s):  
Kailash PRASAD
Keyword(s):  
Guinea Pig ◽  
Atpase Activity ◽  
Guinea Pig Heart ◽  
Induced Changes

Prostacyclin-thromboxane interactions in the platelet-perfused in vitro heart

1981 ◽  
Vol 241 (1) ◽  
pp. H18-H25
Author(s):  
K. Schror ◽  
P. Kohler ◽  
M. Muller ◽  
B. A. Peskar ◽  
P. Rosen
Keyword(s):  
Arachidonic Acid ◽  
Guinea Pig ◽  
Human Platelets ◽  
Coronary Vascular Resistance ◽  
Guinea Pig Heart ◽  
Vascular Bed ◽  
Bioassay Data ◽  
Induced Changes ◽  
Thromboxane Formation

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.

Ultrastructural and enzymatic development of fetal guinea pig heart

1982 ◽  
Vol 243 (1) ◽  
pp. H87-H93 ◽  
Author(s):  
T. P. Rolph ◽  
C. T. Jones ◽  
D. Parry
Keyword(s):  
Guinea Pig ◽  
Atpase Activity ◽  
Enzyme Activities ◽  
Citric Acid Cycle ◽  
Acid Metabolism ◽  
Fetal Heart ◽  
Glycolytic Enzyme ◽  
Guinea Pig Heart ◽  
Threefold Increase ◽  
Phosphofructokinase Activity

The activities of some enzymes of glycolysis, the citric acid cycle, and amino acid metabolism have been measured in the fetal guinea pig heart over the last third of gestation and correlated with heart ultrastructural development. There is little change in glycolytic enzyme activity except for a two- to threefold increase in phosphofructokinase activity. Mitochondrial content and enzyme activities are low in the early fetal heart, and, although content is similar in the late fetus and adult, enzyme activities increase twofold postnatally, indicating fetal heart mitochondria are incompletely developed. The activities of aspartate and particularly alanine aminotransferase are low in the fetal heart. Over the last third of gestation the myofibrillar content of the fetal myocyte increases twofold to the adult value by term. Associated with this is a fourfold rise in myofibrillar and sarcoplasmic reticulum Ca2+-ATPase activity. Na+-K+-ATPase activity is similar in the late fetal and adult heart but one-third lower in the early fetal heart.

Reserpine-induced changes in cardiac adrenergic receptors

1984 ◽  
Vol 62 (1) ◽  
pp. 23-26 ◽  
Author(s):  
Jamshid Latifpour ◽  
John H. McNeill
Keyword(s):  
Guinea Pig ◽  
Adrenergic Receptors ◽  
Radioligand Binding ◽  
Guinea Pig Heart ◽  
Induced Changes ◽  
Β Adrenergic Receptors

Using radioligand binding techniques, the effect of reserpine pretreatment on ventricular adrenergic receptors from guinea pig was studied. [3H]Prazosin and [3H]dihydroalprenolol were used to label α1- and β-adrenergic receptors, respectively. Administration of 2.5 mg/kg reserpine for 2 days caused a significant increase in the number of β-adrenergic receptors with no effect on their affinity to respective ligands. Similar reserpine pretreatment did not affect either density or affinity of α1-adrenergic receptors for ligands. The results may explain the previous report from our laboratory in which an identical reserpine pretreatment selectively enhanced the inotropic responsiveness of the working guinea pig heart to isoproterenol.

Doxorubicin-induced changes in intracellular Ca2+ transients observed in cardiac myocytes isolated from guinea-pig heart

1994 ◽  
Vol 72 (6) ◽  
pp. 622-631 ◽  
Author(s):  
Jiahua Jiang ◽  
Kyosuke Temma ◽  
Tai Akera
Keyword(s):  
Guinea Pig ◽  
Electrical Field Stimulation ◽  
Electrical Field ◽  
Guinea Pig Heart ◽  
Fura 2 ◽  
Time To Peak ◽  
Doxorubicin Cardiotoxicity ◽  
Intracellular Ca ◽  
Induced Changes ◽  
Cellular Ca

Effects of doxorubicin on intracellular Ca2+ concentrations ([Ca2+]i) were examined using myocytes isolated from guinea-pig heart and loaded with fura 2. Changes in twitch contractions were assessed from the motion of myocytes. Ca2+ transients and contractions were triggered by electrical-field stimulation. Exposure of myocytes to doxorubicin depressed Ca2+ transients and contractions. The time to peak Ca2+ transient was prolonged, and Ca2+ sequestration was delayed. In myocytes treated with doxorubicin, an increase in external CaCl2 concentration from 1.2 to 3.6 mM increased the resting and peak [Ca2+]i and enhanced twitch contraction. In the presence of 3.6 mM CaCl2, isoproterenol failed to enhance Ca2+ transients or contractions of doxorubicin-treated myocytes. Effects of doxorubicin were compared with those of agents known to alter Ca2+ handling by myocytes. Caffeine enhanced the peak and resting [Ca2+]2 and contraction. Verapamil caused a rapid decrease in Ca2+ transients and twitch contractions. The effects of verapamil were reversed by isoproterenol in the presence of 3.6 mM CaCl2. Ryanodine alone and combined with doxorubicin depressed contractions and Ca2+ transients and elevated resting [Ca2+]i. Resting [Ca2+]i was further elevated by an increase in CaCl2 concentration and the addition of isoproterenol. The combination of verapamil and ryanodine inhibited Ca2+ transients and contractions. In the presence of verapamil and ryanodine, an increase in extracellular CaCl2 concentration increased resting and peak [Ca2+]i. Isoproterenol further elevated resting and peak [Ca2+]i and increased twitch contractions. These results indicate that doxorubicin alters cellular Ca2+ handling. The actions of doxorubicin are not mimicked by caffeine, verapamil, ryanodine, or the combination of verapamil and ryanodine. Among these agents, ryanodine produced effects that were closest to those observed with doxorubicin.Key words: doxorubicin cardiotoxicity, intracellular calcium, myocytes, ryanodine, verapamil, caffeine, isoproterenol, fura 2, guinea pig.

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