On the cardioprotective effect of adenosine.

In isovolumically perfused Langendorff heart preparations of guinea pigs adenosine-depending on the experimental protocol-more or less could prevent the hypoxia-induced decrease in myocardial adenosine triphosphate [ATP], creatine phosphate [CP], glycogen and increase in lactate, i.e. showed cardioprotection.

Adenosine receptors mediate both contractile and relaxant effects of adenosine in main pulmonary artery of guinea pigs.

In guinea pig main pulmonary artery precontracted with noradrenaline, adenosine exerted an initial phasic contraction followed by a tonic contraction and a slow relaxation. After selective blockade by 1,3-dipropyl-8-cyclopentylxanthine (DPCPX: 10 nM) of A1 receptors, adenosine only elicited a rapid relaxation. This initial response was characterized by use of adenosine (AR) and its analogues N6-cyclopentyl-adenosine (CPA), R-N6-phenylisopropyladenosine (R-PIA), 2-chloroadenosine (CADO), 5'-N-ethyl-carboxamidoadenosine(NECA), N6-2-(4-aminophenyl) ethyl adenosine (APNEA) and 2-p-((carboxyethyl)-phenethylamino)-5'-carboxamidoadenosine (CGS 21 680).

[Cardioprotective effect of levcromakalim in isolated guinea pig heart preparations].

The aim of present work was to study the cardioprotective effect of the potassium channel opener levcromakalim at a low concentration (0.3 microM) which does not depress heart rate and left ventricular developed pressure. For the determination of the protection against 10 or 20 min duration of hypoxia (95% N2 + 5% CO2) in isovolumically-perfused Langendorff heart preparations of guinea-pigs biochemical parameters (ATP, phosphocreatine, lactate and glycogen) were used.

[Effect of Chinoin-103 on K(+)-activated pNPPase in the rat heart].

Effect of a new beta receptor blocking agent, an aryl oxybutanolamine derivative, the Chinoin--103 on K(+)-activated pNPP-ase activity has been studied. Propranolol and practolol were used as reference substances. It has been established that Chinoin-103 in concentration of 10(-4) M significantly hindered total pNPP-ase activity.

Changes in sarcolemmal adenosine triphosphatase activity and in ouabain sensitivity of rat myocardium in isoproterenol-induced cardiac hypertrophy.

Sodium, potassium-activated adenosine triphosphatase (ATPase) activity and the sensitivity of rat myocardium to ouabain was studied in isoproterenol (IPR)-induced cardiac hypertrophy. IPR in a dose of 5 mg/kg was administered to rats intraperitoneally, once daily, for seven days. Left ventricular trabeculae originating from IPR-treated rats were significantly less sensitive than controls to ouabain-induced positive inotropy.

[Effect of propranolol on ouabain-sensitive Na+,K+-ATPase activity of the rat heat].

Effect of propranolol on activity of basal ATP-ase measured in presence of Mg2+ activator, on that of total ATP-ase determined in presence of Mg2+, Na+, K+ activators and on that of Na+,K+-activated ATP-ase calculated from the difference of the previous two ones has been studied. Propranolol has not considerably influenced basal ATP-ase activity in 10(-7)-10(-4) M concentrations, 30-50% inhibition has been found in 1 X 10(-3)-5 X 10(-3) M concentrations. Effect of propranolol on total ATP-ase activity has been found to be dependent on doses and inhibition has been greater than inhibition experienced in case of basal ATP-ase.

[Effect of Chinoin-103 on Na+, K+-activated adenosine triphosphatase of the rat heart].

Effect of a new beta-blocking agent, a cardioselective aryl oxybutanolamine derivative, the Chinoin-103 on basal and total ATP-aze activities has been studied in total homogenizatum of rat heart. The effect has been compared to previous results of propranolol and to effect of practolol, respectively. It has been established that DL-Chinoin-103-similarly to DL-propranolol but in a little higher concentration--has significantly impeted both basal and total ATP-aze activities.

Study of the factors influencing cardiac growth. III. Digitoxin treatment and thyroxine-induced cardiac hypertrophy in the rat.

Thyroxine (T4) administered to rats in a dose of 1 mg/kg for 12 days induces cardiac hypertrophy. The purpose of the present study was to determine the effect of prophylactic + simultaneous digitoxin treatments on the development of T4-induced cardiac hypertrophy. Digitoxin (1 mg/kg body weight) was given per os, once daily for 6 days prior to T4 administration and continued simultaneously with T4 treatment.

Alterations of contractility and sarcoplasmic reticulum function of rat heart in experimental hypo- and hyperthyroidism.

Myocardial contractility and Ca2+-pump function of sarcoplasmic reticulum (SR) were studied on hearts of untreated, thyroidectomized and thyroxine-treated rats. In hypothyroid rats the contractile force, the maximum velocity of tension development and relaxation significantly decreased (by 73.2%, 68.

Study of the factors influencing cardiac growth. II. Digitoxin treatment and isoproterenol-induced cardiac hypertrophy in the rat.

Isoproterenol (IPR) administered to rats in a dose of 5 mg/kg for 4 days induces cardiac hypertrophy. The purpose of the present study was to determine the effect of prophylactic + simultaneous digitoxin treatment on the development of IPR-induced cardiac hypertrophy. Digitoxin (1 mg/kg body weight) was given per os, once daily for 6 days prior to IPR administration and continued simultaneously with IPR treatment.

Study of the factors influencing cardiac growth. I. Comparison of cardiomegaly induced by isoproterenol in euthyroid and thyroidectomized rats.

The purpose of the present work was to study the cardiac growth-stimulating effect of IPR in hypothyroid animals, in which the in vitro sensitivity of the myocardium to beta-adrenergic agonists is significantly decreased. To determine the degree of myocardial enlargement, wet and dry ventricle weight and myocardial RNA, DNA and protein were measured. IPR administered to euthyroid rats in a dosage of 5 mg/kg/day for 4 days induced cardiomegaly.

Comparison of ATPase activity of cardiac myosins from different species.

Ca2+--ATPase activity of myosins prepared from hearts with different shortening speeds was measured in order to determine whether an alteration in hydrolitic activity or in the affinity of myosin for its substrate, or both, may be responsible for the species differences in Ca2+--ATPase. The KM values of ATP for cardiac myosins from rat, guinea-pig and rabbit did not differ significantly, whereas the Vmax decreased in the following order: rat greater than guinea pig greater than rabbit. These facts lead us to assume that, in spite of a great similarity of the active centres of the these myosins, the catalytic sites may not be identical.

Comparison of ATPase activity of cardiac sarcoplasmic reticulum fraction from rat and dog.

The purpose of the present study was to compare the ATPase activities of cardiac SR in two species in which the different intrinsic myocardial contractility can only partially be explained by the different properties of cardiac myosins. In cardiac SR isolated from rat heart, the total ATPase activity was 1512.5 +/- 23.

ATPase activity of sulfhydryl-modified cardiac myosin from normal and isoproterenol-treated rats.

The possible role of sulfhydryl groups in the adaptation of cardiac myosin to work overload has been examined. The functional integrity of sulfhydryl groups was evaluated by measurement of Ca2+- and K+-(EDTA)-ATPase activities of myosins following sulfhydryl modification. No activation of Ca2+-ATPase of normal rat cardiac myosin was observed after pMB or NEM pretreatment.

Thyroxine-induced cardiomegaly: assessment of nucleic acid, protein content and myosin ATPase of rat heart.

1 mg/kg L-thyroxine was administered to rats for 14 days to evaluate the potential of the hyperthyroid state to induce heart hypertrophy and its effect on myosin adenosine-triphosphatase (ATPase) activity. Evidence of hyperthyroidism such as weight loss, elevation of rectal temperature, increased heart rate and oxygen consumption, was observed in all treated rats. Cardiac enlargement was determined by comparison of wet and dry ventricle weights, myocardial RNA, DNA and protein content.

Studies on the superprecipitation of actomyosin in isoproterenol-induced cardiac hypertrophy.

Superprecipitation of normal and hypertrophic cardiac actomyosin--made from individually purified cardiac myosin and skeletal F-actin-, compared with that of synthetic skeletal actomyosin was investigated. A proportional relationship was found between the extent maximum of superprecipitation (Emax) and the concentration of actomyosin complex in the range of 0.1-0.

Studies on adenosine triphosphatase activity of rat cardiac myosin in isoproterenol-induced cardiac hypertrophy.

Ca2+- and K+ -activated ATPase activity of cardiac myosin from normal and hypertrophied rat hearts was investigated. Cardiac hypertrophy was induced by isoproterenol treatment. A nearly 40% increase in heart mass was seen after seven consecutive days of isoproterenol injection (5 mg/kg) as determined by either heart weight expressed as per cent of body weight or by dry heart weight and total protein content.

Immunofluorescent and migration inhibition studies in rats with experimental myocardial infarction.

The appearance of circulating anti-heart antibodies and myocardium-bound antibodies was demonstrated after experimental myocardial infarction induced by coronary ligation or high doses of isoproterenol in rats. Rat heart homogenate and mitochondria at 500 microgram/ml protein level inhibited the migration of leucocytes obtained from rats following myocardial infarction. The immunological consequences were similar in infarctions induced by coronary ligation or isoproterenol treatment.

Prevention of isoproterenol-induced cardiac hypertrophy by beta-blocking agents in the rat.

The effect of the beta-blocking agents propranolol and oxprenolol on isoproterenol-induced cardiac hypertrophy has been investigated in the rat. To evaluate the degree of inhibition biochemical parameters related to cardiomegaly were measured. When given alone in the dose range used for protection, the beta-blocking agents did not cause any significant change in total myocardial RNA, DNA and protein.