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Biomedical subjects

K Greeff

Publications and source records attributed to K Greeff.

At least 55 records · Page 3Linked to original sources
PubMed1976

Increase in the (Na+ + K+)-ATPase activity in heart muscle after chronic treatment with digitoxin or potassium deficient diet.

In guinea pigs, administration of digitoxin (0.3 mg/kg s.c. for 7-24 days) causes an increase in activity of the (Na+ + K+)-ATPase of the heart. The plasma K+ level and the K+ content of the heart muscle of these animals remains unchanged and there is no significant alteration in the digitoxin toxicity compared to controls. In guinea pigs with potassium deficiency produced by a potassium deficient diet for 12 days, there is a related increase of the (Na+ + K+)-ATPase. The plasma K+ level of these animals is diminished while the K+ content in the heart muscle remains unchanged the toxicity of digitoxin is enhanced. In both test groups the increase in the (Na+ + K+)-ATPase activity is limited to enzymes from heart muscle, those from brain or kidney remaining unaffected. This increase in activity seems to be the result of an adaptive enzyme induction.

Adenosine Triphosphatases↗
PubMed1975

[Cardiac side-effects of bencyclan].

Bencyclan (Fludilat), used therapeutically as a vasodilator drug, exerts a distinct negative inotropic and chronotropic action on myocardium, in contrast to papaverine. It prolongs the functional refractory period in the isolated heart preparation. In isolated myocardial mitochondria it decreases the velocity of oxidative phosphorylation and the rate of calcium uptake. These results indicate that heart function should be checked if bencyclan is applied at high dosage, especially if other cardio-depressive substances such as narcotics, antidepressive and antiarrhythmic agents as well as beta-adrenergic blockers are used at the same time. On the other hand, the results suggest that bencyclan should be tested for possible use in the treatment of ischaemic heart disease as well as ventricular and supraventricular tachycardia.

Adrenergic beta-Antagonists↗
PubMed1975

Calcium uptake and storage in isolated heart mitochondria influenced by sodium and potassium ions.

With rising concentrations of KCl the rate of Ca2+ uptake was moderately increased by 37 percent. NaCl induced a strong decrease of the rate of Ca2+ uptake from 498 to 194 nmoles of Ca2+ per sec-gm of protein (0-100 mM NAaCl). Elevating the K+/Na+ quotient from 0.1 to 15.7, we found a concomitant alteration of the rate of Ca2+ uptake which is mediated exclusively by sodium ions. These data indicate that with lowering of the K+/Na+ gradient there is a marked diminution of the mitochondrial rate of Ca2+ uptake and Ca storage. Our findings may contribute to answering how Na+-K+ exchange at the cell membrane may influence intracellular Ca2+ binding and Ca2+ turnover.

Animals↗
PubMed1975

[Animal experiments on the effect of triamterene and amiloride on heart and circulation and the toxicity of digoxin (author's transl)].

1. In anesthetized cats 2,4,7-triamino-6-phenyl-pteridine (triamterene) (5 mg/kg i.v.) causes a short-lasting increase in blood pressure, a decrease in heart rate, whereas the contractility (see article) remains unchanged. N-Amidino-3,5-diamino-6-chloropyrazinecarboxamide (amiloride) (5 mg/kg i.v.) causes a fall of blood pressure, an increase in heart rate, and an increase in contractility. 2. In cats the i.v. toxicity of digoxin is diminished by pretreatment with triamterene or amiloride; the arrhythmias and the cardiac arrest are significantly delayed in the course of an infusion of digoxin. In guinea-pigs a pretreatment with triamterene only delays the arrhythmias but not the lethal effect of digoxin or g-strophanthin. 3. In the isolated atria of the guinea-pig triamterene and amiloride (5 mug or 50 mug/ml) lowers the rate of contraction and prolongs the functional refractory period. The force of contraction is increased by triamterene and diminished by amiloride.

Amiloride↗