Biomedical subjects
Publications and source records attributed to N Z Kliueva.
After a 10-minute incubation, both the parathyroid hypertensive factor (PHF) and parathyroid hormone (PTH) reduced myocardial contractility and accelerated myocardial relaxation. Effects of the PTH and PHF on myocardial inotropic characteristics were of opposite directions.
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The effects of low (8.0 mg/l) and normal (80 mg/l) Ca2+ water diets on systolic blood pressure (SBP) and hypertensive plasma activity were studied. At the end of the 16-week experimental period SBP in the low-Ca2+ group of animals was higher than in the control group after the water treatment: 161 sigma 9 and 120 +/- 4 mm Hg respectively. Significant hypertensive plasma activity of the Ca(2+)-deficient rats was noted in all cases. WKY plasma of the rats of normal-Ca2+ group had no significant effect on SBP. Water correction according to the physiologically recommended levels of calcium can prevent the development of arterial hypertension and occurrence of hypertensive plasma activity.
The arterial pressure was significantly higher in the calcium-deficient group of rats as compared with the normal rats: 150 +/- 7 and 116 +/- 2 mm Hg, resp. The first group of animals had a hypertensive factor in the blood. The hypertensive activity of the calcium-deficient animals was associated with no known pressor agents and was rather similar to Pang's hypertensive factor. The latter was also found in some patients with essential hypertension.
The technique of differentiation of the envelope of total activity of the diaphragm motoneurons in anesthetized cats revealed that augmentation of the chemostimulus induced a linear growth of the latetinspiration inhibition which increased after bilateral vagotomy. Duration of the postinspiration phase does not depend on the level of activation of the chemoreceptors and lung stretch receptors. Vagotomy induces a discrete elongation of the postinspiration phase due, apparently, to effects from the structures of rostral pons.
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Contemporary ideas of the mechanism of respiratory rhythmogenesis are considered. A mathematical model of these mechanisms is described as well as the results of its study underlying a proposed scheme of neuronal network which is able to maintain a regular alternation of respiratory phases within the wide range of physiological states. Three neuronal pools constitute the basis of the proposed network: the inspiratory neurons I alpha and I beta (the former excite the latter) and the added pool of expiratory neurons Ee which can be excited by the I beta neurons and inhibits the I alpha neurons. Presence of the Ee pool enables to obtain stable expiratory inhibition of the I alpha neurons. The model takes into consideration the proexpiratory effect of the lungs' stretch receptors as well as the proinspiratory action of the irritant receptors.
In experiments on anesthetized cats, switch on of additional inelastic respiration resistance (resistive load) produced, apart from slowing of the respiratory flows, an increase in the activity of motoneurons and inspiratory intrathoracic pressure. Bilateral vagotomy resulted in disappearance of resistive load-induced elevation of the phrenic nerve activity, but did not abolish the growth of the inspiratory effort. Analysis of the evidence obtained indicates that activation of phrenic motoneurons associated with increased respiration resistance is underlain by prolongation of the inspiratory phase that is consequent on relaxation of the inspiratory inhibition. It is suggested that, in addition to the mechanism depicted, the compensatory reaction to the resistive load involves, apart from diaphragm participation, other inspiratory muscles as well as enhanced contractions of respiratory muscles provided by the properties of muscular fiber.
The resistant load (an increased aerodynamic resistance to the gas flow) augmented both the intrathoracic pressure (ITP) and activity of the diaphragm neurons (ADN) in anesthetized cats. The increase in these parameters after alteration of CO2 tension in the alveolar gas (PACO2) by 1 mm Hg was also augmented whereas the increase of respiratory volumes (VT) was reduced. After bilateral vagotomy the inspiratory resistant load somewhat inhibited the ADN, still more so at increasing PACO2, whereas the ITP absolute values and its increase grew up. The analysis of ITP and ADN relationships suggests a significant part of intercostal and auxiliary muscles in the inspiratory increase occurring on resistant load. This becomes clearer after shunting the afferent system of lungs.
In anesthetized cats, an increase in inspiratory resistance in conditions of growing hypercapnia entailed elongation of inspiration and of the whole respiratory cycle, as well as decrease of the volume threshold for cessation of inspiration. The latter occurred after bilateral vagotomy too, whereas no significant changes of the temporal parameters followed the increase in the resistance. The temporal rearrangements of the respiratory cycle seem to be due to the vagal effects, while the extravagal influences, probably the reflexes from the stretch receptors of intercostal muscles, are responsible for changes of the volume component in the relations characterizing the mechanism of cessation of inspiration.
In anesthetized cats and in healthy humans, lung ventilation, activity of diaphragmal motoneurons and intercostal muscles, shift of the intrathoracic pressure, inspiratory occlusional pressure, and maximal rate of the initial increase in inspiratory pressure, were studied. Depending on conditions of the respiratory system functioning, any one from among the above parameters can reflect the efferent output of the respiratory center. Each of them, however, has limitations of its own.
In cat+s, increased resistance against breathing at the background of hyperventilation with a hypercapnic mixture reduces the 1-min ventilation. However, the bioelectric activity of the diaphragmatic nerve becomes augmented, thus indicating an increase in the respiratory center inspiratory activity. Vagotomy was followed by a decreased ventilatory response to CO2. Suppression of ventilation and augmentation of the diaphragmatic nerve activity during additional resistance against breathing in vagotomized animals were preserved on account of a considerably greater activity of the respiratory center. The data obtained suggest that, in conditions of combination of increased resistance against breathing with hypercapnia, the lungs afferent system fulfills an optimization of activity of the ventilatory apparatus.
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In anesthesized cats inspiratory activity of the respiratory center at first increased and then decreased with increases in total pressure of the nitrogen-oxygen atmosphere to 7, 11, and 21 atm (at normal PO2). The effort made by respiratory muscles increased gradually. These changes were augmented by hypercapnia. Possible role of nitrogen anesthesia and compensatory reactions to the increased breathing resistance in the department of the above changes is discussed.
The effect of altered gas density on the respiratory function was investigated in relation to the velocity of gas flows in airways. In the normal man breathing of normoxic He-O2 (with a density of 0,34 as compared to air) slightly decreased and inhalation of SF6-O2 (with a density of 4.2) significantly increased the metabolic rate of 1 1 ventilation. These effects were distinct when inspiratory flows reached threshold values. In anesthesized cats, He-O2 breathing reduced inspiratory activity upon forced respiration, and SF6-O2 breathing increased it upon quiet respiration. These findings can be used to predict limiting densities of respiratory mixtures for a normal man performing physical work of a certain load undersea.