Changes in heart rhythm variability were studied in male and female mature and 5-6-week-old rats under conditions of 7-day administration of β1-adrenoreceptor blocker atenolol (2.5 mg/kg) and α1-adrenoreceptor agonist phenylephrine (0.3 mg/kg). Atenolol administration to mature rats was followed by a slight deceleration of cardiac rhythm, a tendency to heart rate variability decrease in the HF range, and moderate increase in centralization of regulation. In 6-week-old rats, increased variability of cardiointervals and significant increase of centralization of the heart rhythm regulation due to an increase in the power of low-frequency waves (specifically VLF) were observed. In both mature and young rats, changes of heart rate frequency and variability in response to atenolol administration were more pronounced in females. Phenylephrine administration was followed by a significant heart rate deceleration, increase in cardiointerval variability and centralization of heart rate regulation in mature rats and by a decrease in heart rate variability in all frequency ranges in 6-week-old rats. In mature rats, changes in heart rate frequency and variability produced by phenylephrine administration were more pronounced in males; in young rats, the most strained heart rhythm developed in females.
We studied the effect of phenotropil (25 mg/kg intraperitoneally, 5 days) on the immune and psychoemotional state of Wistar rats with LPS-induced immune stress. Hyperactivity of the immune system in animals after treatment with Pseudomonas aeruginosa LPS (100 μg/kg intraperitoneally, 3 days) manifested in a significant increase in the delayed-type hypersensitivity index, antibody titer in the reaction of passive hemagglutination, and phagocytic activity of peripheral blood neutrophils. Locomotor, orientation, and exploratory activities were reduced, while anxiety increased in animals with immune stress. Phenotropil exhibited the psychoimmunomodulatory effect under these conditions, which manifested in prevention of anxiety and fear response, increase in horizontal locomotion and exploratory behavior, and improvement of immunoreactivity.
We studied pathways of apoptosis regulation during experimental hepatopathy caused by treatment with antitubercular drugs and involvement of some hepatoprotectors and immunomodulators in the regulation of hepatocyte apoptosis induced by antitubercular drugs. The intensity of apoptosis and expression of apoptosis-associated molecules were evaluated. It was shown that antitubercular drugs induce apoptosis in hepatocytes by triggering external signaling pathway and p53-dependent signaling pathway and simultaneously reducing the level of anti-apoptotic Bcl-2 protein. Runihol, remaxol, and cycloferon reduced degenerative effects in the liver, though the level of apoptosis remained high. Ademetionine in tablets and reamberin improved the microstructure of the liver by inhibiting both apoptotic pathways induced by the antitubercular drugs; in other words, they have distinct hepatoprotective and apoptosis-protective effects, which is especially important at the late stages of ontogeny.
The aim of this study was to identify the involvement of interferon-alpha (IA) in controlling apoptosis of cells of the hypothalamo-hypophyseal-adrenocortical system (HHACS) in young and aged mice in conditions of hyperoxia. Oxidative stress led to increases in the numbers of cells synthesizing the proapoptotic protein c-fos in the paraventricular nucleus in mice of both age groups. However, the protective actions of IA in stress were more marked at the earlier stage of apoptosis in young mice. Thus, the level of involvement of IA in controlling programmed cell death of hypothalamic cells depends on the age of the animals. In the fascicular zone of the adrenals in young mice, the number of dying cells was significantly greater after administration of IA, but remained at the control level in conditions of hyperoxia alone and in combination with IA. The proportion of apoptotic cells in the adrenals of aged mice was no different from that in young mice and did not change in response to any of the treatments used.
Single injection of muscarinic cholinoceptor blocker atropine (1 mg/kg) to outbred male rats reduced β-adrenergic responsiveness of erythrocytes (by 2.2 times) and the content of epinephrine granules on erythrocytes (by 1.5 times), significantly increased HR and rigidity of the heart rhythm, and manifold decreased the power of all spectral components of heart rhythm variability. Stimulation of the central neurotransmitter systems increased β-adrenergic responsiveness of erythrocytes (by 15-26%), decreased the number of epinephrine granules on erythrocytes (by 25-40%), and increased HR and cardiac rhythm intensity. These changes were most pronounced after stimulation of the serotoninergic system. Administration of atropine against the background of activation of central neurotransmitter systems did not decrease β-adrenergic responsiveness of erythrocytes (this parameter remained at a stably high level and even increased during stimulation of the dopaminergic system), but decreased the number of epinephrine granules on erythrocytes, increased HR, and dramatically decreased the power of all components of heart rhythm variability spectrum. The response to atropine was maximum against the background of noradrenergic system activation and less pronounced during stimulation of the serotoninergic system. Thus, substances that are complementary to cholinergic receptors modulated adrenergic effect on the properties of red blood cells, which, in turn, can modulate the adrenergic influences on the heart rhythm via the humoral channel of regulation. Stimulation of central neurotransmitter systems that potentiates the growth of visceral adrenergic responsiveness weakens the cholinergic modulation of the adrenergic influences, especially with respect to erythrocyte responsiveness. Hence, changes in the neurotransmitter metabolism in the body can lead to coupled modulation of reception and reactivity to adrenergic- and choline-like regulatory factors at the level of erythrocyte membranes, which can be important for regulation of heart rhythm.
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