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D Susić

Publications and source records attributed to D Susić.

48 records · Page 3Linked to original sources
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Ouabain arrhythmogenicity in hypertrophied right and left ventricle of the rat.

Susceptibility to the arrhythmogenic action of ouabain was tested in rats with right ventricular hypertrophy, due to experimental chronic hypoxic pulmonary hypertension, and in spontaneously hypertensive (SH) rats with left ventricular hypertrophy. As parameters of arrhythmogenicity the time-duration of infusion of a solution of ouabain (1 g/100 ml), at a rate of 0.7 mg/kg per minute, was measured until the appearance on the ECG of the first premature ventricular contraction, ventricular tachycardia and cardiac arrest. All three effects of digitalis toxicity (premature ventricular contraction, ventricular tachycardia and cardiac arrest) appeared significantly earlier both in rats with right ventricular hypertrophy, due to chronic experimental hypoxic pulmonary hypertension, and in SH rats with hypertrophy of the left ventricle, as compared to the infusion time of the same solution of ouabain needed to elicit the mentioned toxic effects in control rats without ventricular hypertrophy.

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Isometric relaxation of hypertrophied right ventricle in rats.

In rats with experimental hypertrophy of the right ventricle due to chronic increase in pressure load -dP/dTmax, a parameter of isometric relaxation, is significantly reduced at a stage of impairment of myocardial function at which the parameter of isometric contractility still remains unaffected.

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Effects of SQ 14.225, an orally active inhibitor of angiotensin-converting enzyme, on hypoxic pulmonary hypertension and right ventricular hypertrophy in rats.

Treatment with SQ 14.225, an inhibitor of the enzyme converting angiotensin I to angiotensin II and lowering of plasma renin activity by dietary salt overload, significantly decreased hypertrophy of the right ventricle in chronically hypoxic rats. The smaller degree of right ventricular hypertrophy registered in hypoxic rats with suppressed activity of the renin-angiotensin system was proportional to the decrease in hypoxic pulmonary hypertension noted in these animals. Lowering of pulmonary hypertension in chronically hypoxic rats by suppression of the renin-angiotensin system is consistent with the idea that angiotensin II may be involved in eliciting hypoxic pulmonary vasoconstriction. Inhibition of converting enzyme also lowered the systemic arterial pressure in hypoxic rats, but this finding could not be taken as evidence for the role of the renin-angiotensin system in homeostatic control of blood pressure in normal animals, since the plasma-renin activity in hypoxic rats is increased and the blood pressure higher than in rats kept under normoxic conditions.

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Separate and combined use of verapamil, aspirin and captopril in experimental chronic pulmonary hypertension.

In Wistar rats, rendered pulmonary hypertensive by chronic confinement in normobaric "hypoxic cages", impairment of transmembrane transport of calcium by Verapamil and blockage of the action of Angiotensin I converting enzyme by Captopril when applied simultaneously did not show an additive effect in reducing the rise of pulmonary artery pressure and decreasing the augmentation of right ventricular mass. Similarly, the action of Verapamil together with decrease of prostaglandin synthetase activity by Aspirin showed no additive effect. Although in this way the results of the present study failed to give substantial support to the idea of the existence of several mediators of hypoxic pulmonary vasoconstriction, they by no means deny this possibility.

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Plasma renin activity and hypertrophy of the right ventricle in hypoxic rats.

A NaCl load in chronically hypoxic rats abolished the increase in plasma renin activity occurring in rats exposed to hypoxia of the same degree and duration but with normal NaCl intake. The parallel reduction in hypoxic hypertrophy of the right ventricle in NaCl-loaded rats could be considered as indirect evidence supporting the view that renin may be involved in the development of heart hypertrophy.

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Hypotensive effect of heparin on experimental chronic pulmonary hypertension in rats.

Daily heparin injections (300 mg s.c.) during four weeks of hypoxic exposure resulted in a smaller rise in pulmonary artery pressure as compared with otherwise nontreated rats exposed to the same regimen of hypoxia. Heparin treatment did not significantly affect the systemic arterial pressure of the hypoxic rats. In spite of the different pressure load of the right ventricle after hypoxia in treated and control rats, there was no difference in parameters indicative of the degree of right ventricular hypertrophy between these two groups of hypoxic rats. This finding suggests that the difference in pressure load between the two groups of hypoxic rats occurred late in the course of hypoxic exposure.

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