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Biomedical subjects

A P Kallikorm

Publications and source records attributed to A P Kallikorm.

At least 19 recordsLinked to original sources
PubMed1991

Thyroid control over membrane processes in rat heart.

We have studied the effects of hypo- and hyperthyroidism on sarcolemmal (SL) and sarcoplasmic reticular (SR) ion transport processes and mitochondrial energy production in rat heart. The following conclusions were derived. 1) Compared with euthyroid state, hyperthyroidism led to increased SR Ca(2+)-accumulation. In SL, the activities of Ca(2+)-stimulated adenosine triphosphatase (ATPase), ATP-dependent Ca2+ pumping, and Na(+)-Ca2+ exchanger were not affected; but ouabain-sensitive Na(+)-K(+)-ATPase activity was enhanced. 2) Hypothyroidism resulted in depressed activities of Ca2+ pumps both in SL and SR. In SL, the Na(+)-K(+)-ATPase activity was decreased, but Na(+)-Ca2+ exchange was unaltered. 3) Thus slower relaxation of the hypothyroid myocardium may be attributed to depressed functioning of Ca2+ pumps in SR and SL, whereas faster relaxation of the hyperthyroid heart may be based on increased Ca(2+)-pumping activity of SR. 4) Hyperthyroidism and hypothyroidism, respectively, led to enhanced and decreased rates of mitochondrial phosphocreatine synthesis. The thyroid state appears to control the functional coupling between mitochondrial creatine kinase and ATP-ADP translocase: the energy of oxidative phosphorylation was transformed into phosphocreatine more effectively in mitochondria from hypothyroid hearts than in those from hyperthyroid hearts.

Adenosine Triphosphatases↗
PubMed1990

Modulation of stimulation frequency responses and calcium dependency of functional parameters in hyperthyroid rat ventricular papillary muscles.

The effects of stimulation frequency (0.2-1.5 Hz) and extracellular calcium concentration ([Ca2+]o) (0.6-15.0 mM) on the contractile function of thin papillary muscles of euthyroid and hyperthyroid rats were studied. Hyperthyroidism led to a decrease in developed tension (DT) and time to peak tension (TPT), but it exhibited no influence on the maximal rates of contraction (+dT/dt) and relaxation (-dT/dt). Also, the mean rates of contraction were similar in euthyroid and hyperthyroid muscle groups. The increase in stimulation frequency brought about a marked decrease in DT, +dT/dt, and -dT/dt of euthyroid papillary muscles at lower frequencies in comparison to papillary muscles in the hyperthyroid group. At stimulation frequencies above 1.0 Hz, the absolute and relative levels of DT and -dT/dt of hyperthyroid myocardium were elevated over euthyroid preparations. At the same time, TPT was unchanged in any of the muscle groups. Hyperthyroidism modulated the relationships between contractile parameters and [Ca2+]o. At a [Ca2+]o of 1.0-4.0 mM, the DT of hyperthyroid papillary muscles was lower than in euthyroid muscle. At 4.0 and 8.0 mM of [Ca2+]o, the equal values of maximal DT were registered for euthyroid and hyperthyroid papillary muscles, respectively. An increase in the [Ca2+]o in the range of 1.0-15.0 mM was accompanied by an increase in TPT of both muscle groups, but to a greater extent in hyperthyroid myocardium. In conclusion, the myocardium of hyperthyroid rat appeared to exhibit decreased sensitivity to calcium as well as to the negative inotropic effect of enhanced stimulation frequency. Alterations of the processes of transsarcolemmal movement and intracellular recycling of Ca2 may be implicated.

Animals↗
PubMed1990

[Synthesis of phosphocreatine in heart mitochondria of rats with hyperthyroidism].

The mechanisms of the phosphocreatine/creatine ratio decrease in female Wistar rats with hyperthyroidism were studied. L-Thyroxin was injected to animals in doses of 50 and 100 micrograms/100 g of body weight, daily for 1 and 2 weeks. Oxidative phosphorylation and the rate of phosphocreatine synthesis were studied in isolated rat heart mitochondria. It was found that hyperthyroidism caused an increase in the ADP-activated mitochondrial respiration, whereas the coupling between electron transport and ADP phosphorylated remained at a constant level. Besides oxidative phosphorylation, activation, hyperthyroidism increased the rate of phosphocreatine synthesis at high values of the phosphocreatine/oxygen ratio. Thus, hyperthyroidism is unaccompanied by and significant changes in the coupling of mitochondrial creatine kinase with oxidative phosphorylation.

Adenosine Diphosphate↗
PubMed1989

[Characteristics of the frequency dependence of the contraction force in the hyperthyroid rat myocardium].

We have studied the effect of increased contraction frequency (from 0.2 to 1.5 Hz) on developed tension (delta T) in thin papillary muscles of eu- and hyperthyroid rats. The results show that while increasing the contraction frequency, the delta T of euthyroid papillary muscles decreased at lower frequencies than in hyperthyroid group. Also, at the contraction frequencies above 1.0 Hz the absolute and relative levels of delta T of hyperthyroid myocardium were less decreased than in euthyroid preparations. In conclusion, the myocardium of hyperthyroid rat is characterized by a decreased sensitivity to negative inotropic effect of enhanced contraction frequency. In is probably due to the acceleration of the processes of intracellular Ca2+ recycling during diastole under the influence of hyperthyroidism.

Animals↗
PubMed1987

[Energy-related disorders of myocardial contractility in calcium overload of the cardiomyocytes].

Langendorff perfusion of euthyroid rat heart with 10 mM phosphocreatine (PCr) in Krebs-Henseleit solution in conditions of Ca2+-paradox significantly potentiated the development of contracture and produced a 4-fold increase in perfusion pressure as compared to heart contractility in PCr-free, but otherwise similar conditions. Similarly, in case of hyperthyroid myocardium, addition of PCr into hypoxic perfusate (glucose omitted) in the presence of supranormal extracellular Ca2+ (5.0 mM) irreversibly inhibited the restitution of resting tension and developed tension during aerobic reperfusion. In the same conditions, PCr did not modulate contractility of euthyroid myocardium. These results are consistent with Ruigrok's hypothesis (1978) that intracellular Ca2+ redistribution is energy-dependent, provided PCr can penetrate into cardiomyocytes and stimulate ATP-dependent accumulation of Ca2+ in mitochondria, leading to an impairment of energy production. It is concluded that PCr exerts its cardioprotective effect only in case of a reversible (acute) phase of ischemia.

Animals↗
PubMed1985

Hormone regulation of cardiac energy metabolism. I. Creatine transport across cell membranes of euthyroid and hyperthyroid rat heart.

Hyperthyroid rat heart was studied with the purpose of identifying the mechanism for the significant decrease in total creatine (free creatine plus phosphocreatine) observed in this pathology and its consequences on heart function. Administration of L-thyroxine in doses of 50-100 micrograms/100 g of body weight during a week resulted in a reversible decrease of the total creatine by 40-50%. Simultaneously, remarkable changes in the creatine transport system across the cardiac cell membranes were observed: both the maximal rate of its active uptake and its passive movement along its concentration gradient were enhanced. In euthyroid hearts, the parameters of creatine uptake (Km approximately or equal to 0.05 mM, Vmax = 20 nmole/min/g dry weight) were similar to those for skeletal muscle and the passive movement of creatine was negligible. In hyperthyroid hearts the latter rate was enhanced to 0.4 mumole min/g dry weight, this showing reversible damages in the cell membrane structure induced by L-thyroxine. This conclusion is consistent with observed penetration of colloidal lanthanum into the cells of hyperthyroid hearts. Perfusion of hyperthyroid rat hearts with 50 mM creatine significantly restored creatine content in the cells, Hyperthyroid hearts with decreased creatine content were found to develop ischemic contracture more rapidly and in higher extent than the euthyroid hearts. Increased sensitivity to ischemic damage may be related to decreased efficiency of energy channeling via phosphocreatine pathway.

Animals↗
PubMed1981

[Dynamics of the insulin, somatotropic hormone, glucose and free fatty acid content in the blood during a direct myocardial revascularization operation under neuroleptanalgesia].

The dynamics of the content of insulin, somatotropic hormone, glucose and the free fatty acids were studied in 32 male patients with ischaemic heart disease subjected to direct revascularization on the myocardium under neuroleptanalgesia and artificial circulation with moderate hypothermia and haemodilution. It is established that during operations on the coronaries under these conditions insulin secretion is not depressed, despite stable increase of the somatotropic hormone in the blood. High concentrations of glucose and insulin in the blood prevent the rise of the free fatty acids.

Blood Glucose↗
PubMedDate not supplied

[Characteristics of the sensitivity of the pancreatic beta cells to arginine and glucose in patients with type-2 diabetes mellitus].

The sensitivity of pancreatic beta-cells to i. v. injection of glucose and arginine was determined in patients with insulin-independent diabetes mellitus (IIDM) of various duration and with different therapeutic response to sugar lowering drugs (SLD). In a group of healthy persons who were examined in a similar way, a peak rise of insulin was observed after injection of glucose and arginine. A peak rise of insulin after glucose administration was absent in patients managed with SLD, whereas an insulin level during the arginine test reached 302 +/- 12.7 pmol/l. In most of the patients showing resistance to SLD, who received insulin therapy after examination, a maximum insulin level value was 106 +/- 12.1 pmol/l only. Thus the arginine test can be used to state SLD therapy inefficacy and for substantiation of insulin therapy.

Adult↗
PubMedDate not supplied

[Functional study of the hypophyseal-thyroid and adrenal systems in physiological pregnancy and late toxicosis].

A comprehensive study was conducted in 30 healthy nonpregnant women, 115 healthy pregnant women and in 38 pregnant women with late toxicosis as well as in 25 healthy infants and 29 infants born to mothers with late toxicosis. A radioimmunoassay was used to measure serum thyrotropin (TSH), somatotropin (STH), adrenocorticotropin (ACTH), thyroxine (T4), triiodothyronine (T3), cortisol (CORT) and aldosterone (ALDO) levels. A catecholamine (CA) level was determined dy fluorimetry. Elevated ACTH, TSH, CORT and ALDO levels were noted in normal pregnancy. The above data indicated that the pituitary-thyroid and pituitary-adrenal systems of pregnant women formed adaptive reactions to the body demand for hormones. The reduction of ACTH and T3 levels and rise of CORT, ALDO, T4 levels and the serum protein thyroxine-binding capacity were noted in the pregnant women with late toxicosis. These hormonal differences may be indicative of a decrease in the reserves of women with late toxicosis. It is concluded that the pituitary-thyroid and pituitary-adrenal systems in newborns are capable of maintaining homeostasis by the moment of birth.

Adolescent↗