[Distant compression fracture in a child with dysplastic changes in the spine].
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Biomedical subjects
Publications and source records attributed to V V Suchkov.
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Blood flow through the cortex and medulla of the rat and rabbit kidney was measured with the hydrogen wash-out technique. Stimulation of the midbrain RF caused vasoconstriction both in cortex and medulla. This constriction was abolished by kidney denervation and became stronger under conditions of stabilized arterial blood pressure. The data obtained suggest that both the cortical blood flow and the medullary one are continuously controlled by extrarenal neural influences. These influences are reduced when renal perfusion pressure rises and are modulated by the intrarenal autoregulator mechanisms.
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An experimental study in 12 anesthesized rabbits has demonstrated, by means of the hydrogen clearance test, that carotid sinus baroreceptors participate in the control of both the cortical (CF) and the medullary (MF) renal flow. The direction and magnitude of CF and MF changes in case of sinocarotid reflexes are determined by the relationships between extrarenal nervous effects, systemic blood pressure (BP) and self-regulative response of the cortex and the medulla. Arterial hypotension during depressor sinocarotid reflexes is accompanied by decreased CF and MF, while blood pressure stabilization increases CF and MF in these conditions. Arterial hypertension associated with pressor sinocarotid reflexes is accompanied by decreased CF, whereas MF changes may take different directions depending on the severity of hypertension. In a denervated kidney, sinocarotid reflexes cause CF and MF changes of the same direction as changes in BP, which are, however, less pronounced due to self-regulative intrarenal mechanisms being switched on. Simultaneous denervation of the kidney and BP stabilization can prevent completely CF and MF changes associated with sinocarotid reflexes.
Experiments on 52 Wistar rats were made to induce hemorrhagic shock by exemption of 40% blood from the jugular vein, which was followed by intravenous injection of either physiological solution or naloxone in doses of 0.4 and 1 mg/kg. Naloxone in a dose of 1 mg/kg was found to improve the animals' status as compared with the control (injection of physiological solution). On the contrary, injection of naloxone in a dose of 0.4 mg/kg led to the deterioration of the animals' status. Based on these data it is suggested that different opiate receptors play an inconclusive role in the development and progress of hemorrhagic shock induced by acute hemorrhage.
Naloxone or physiological solution were injected in different doses to 11 baboons (Papio hamadryas) weighing 7-8 kg after bloodletting in a volume of 40% of the total amount of the blood. Naloxone effectively raised (in all the doses) the arterial blood pressure which dropped after bloodletting. The action of naloxone injected in small doses was more pronounced and had unique time parameters. Besides, the respiratory rate was also increased. Injection of nalorphine in a dose of 1 mg/kg produced a similar but a more demonstrable action as compared with naloxone in a dose of 1 mg/kg. A conclusion is made about the possibility of using the antagonists of opioid peptides on a clinical basis for the treatment of shock conditions. An assumption of an inconclusive role played by the subtypes of opiate receptors in the formation of shock conditions is also confirmed.
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It has been found that neuropeptide leienkephalin and tyrosine occupying an N-end position in the peptide chain of leienkephalin are activators of the contractile activity of lymphatic microvessels of the mesentery. It is being attempted to obtain an even more active leienkephalin analogue by increasing the tyrosine content in its peptide chain.
This study showed that arterial blood pressure of chemically sympathectomized rats (SR) was decreased, whereas heart rate was increased relative to controls. The cardiac output in SR was higher than that in intact animals (by 36% under urethane anaesthesia and by 80% without anaesthesia). The total peripheral resistance of SR was 1.7 times less than normal, although the magnitude of the structural component of resistance was increased. The half-time clearance of 133Xe from skeletal muscle during motor nerve stimulation was greater in SR than in intact rats by a factor of 2. It is concluded that the number of small resistance vessels in SR is low, while the lumen of individual vessels is greater than in controls, thus giving rise to an insufficient "vasodilator reserve".
The effect of bradykinin on microcirculation was studied in vivo on the rat mesentery. Bradykinin (0.01--10 micrograms) caused three types of reactions of arterioles and venules (constriction, dilatation, no changes in the diameter) in relation to the dose used. Preliminary application of noradrenaline changed the sensitivity of microvessels to bradykinin towards the increased frequency of dilatation. The increased permeability by red cells in postcapillaries and in venules arose in the areas of the greatest stretch (sites of confluences and ridges of vessels wavy in outline) and was accompanied by deformation and shortening of venules. It was disclosed that bradykinin exerted a pronounced pain effect that promoted awakening of the animals from anesthesia.
Desympathized rats developed a lower arterial pressure, a higher heart rate and a greater one--minute blood volume heart output as compared to intact rats. The total peripheral resistance in the major circulation of desympathized rats is by 1.7 times lesser although their structural component of the resistance is higher. The latter finding seems to be due to a reduce density of vessels per unit of tissue volume. The time of half--washing of Xe33 out of intramuscular depot in working hyperemia during motor nerve stimulation is nearly twofold in desympathized rats. The humber of small resistance vessels seems to be lessened per unit of tissue volume in desympathized animals whereas the lumen of separate vessels in them is larger than in normal animals. This accounts for considerable reduction of the range of vasomotor vascular regulation in desympathized animals.
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It was shown on 36 nonanesthetized rats by polarography from H2 elimination and PO2 recording that cortical and medullary circulation in the kidneys undergoes continuous fluctuations. A definite relation of these fluctuations with circulatory changes in the cerebral limbicoreticular structures was noted. In electric stimulation of the reticular formation and the hypothalamus on the background of arterial hypertension the cortical circulation decreased by 88.5% while the medullary circulation increased by 82.8%. In hypertension of over 180--235 mm Hg, the blood flow both in the cortical and in the medullary substance ceased practically. Chronic disturbance in the blood supply to the brain led to arterial hypertension and short-lived (10--20 days) increase of the blood plasma renin activity to 417.8% and its subsequent normalization by the 65th day. At the same time, renal blood flow dropped progressively and the reaction of the renal vessels to hypercapnic load became less manifest, which testified to changes in their reactive-structural characteristics. Summarizing the results obtained and the data of other investigators, the author concludes that neurogenous disorders of renal blood flow hold one of the key positions in the formation of arterial hypertension of different etiology.
The blood antidiuretic activity was studied in patients with hypertensive disease in a period between crises and during a hypertensive crisis. The antidiuretic activity of blood was found to be higher in patients who had crises than in those with no history of crises. Blood antidiuretic activity diminishes during a hypertensive crisis, which is evidently due to the inhibiting effect on the hypothalamus of the receptors of the cardiovascular system. Similar results were obtained in experiments in elevation of arterial pressure induced by electric stimulation of the hypothalamic nuclei. It is concluded that the antidiuretic hormone plays a pathogenetic role in hypertensive disease which is marked by the development of crises.
The cerebral volume blood flow was measured in acute canine experiments in three major arteries of the brain using an electromagnetic flowmeter. Paroxysms of ventricular tachycardia caused by electric stimulation of the heart resulted in varying degrees of reduction of the cerebral blood flow and arterial pressure that was most significant with cardiac contractions rate exceeding 240/min. Bradycardia with the contractions rate below 60/min also caused a reduction of the cerebral blood flow and arterial pressure. A parabolic correlation was revealed between the changes in the heart contractions rate and the amount of decrease of the cerebral blood flow and arterial pressure. Grouped ventricular extrasystoles resulted in a brief sharp fall of the cerebral blood flow...
The methods of determining the maximum permissible and functionally justifiable (upper and lower) limits of arterial pressure fluctuations limiting the zones of individual "comfort" "caution" and "alarm" for every patient are described. The mathematical method of the least squares was used for long-term control of the maintenance of arterial pressure within the limits individually pre-set for those treated on an out-patient basis. The above methods permit to decrease the duration of therapy with a minimal drug expenditure and to ensure a mass control of the efficacy of hypotensive therapy.
The local cerebral blood flow and oxygen tension in the brain cortex, the reticular formation of the mesencephalon and the posterior hypothalamus were studied in chronic experiments in non-anesthetized rabbits with experimentally induced myocardial infarction. During the initial hours after the occlusion of the coronary artery a distinct reduction of the blood flow and oxygen tension was noted in the mentioned structures of the brain, against the background of an arterial pressure fall; in the subsequent days a varying dynamics of the re-establishment of the cerebral blood flow and arterial pressure was observed. It is suggested that in myocardial infarction not only the general hemodynamics undergoes certain changes, but the reserves of the autoregulation mechanisms of the cerebral blood flow get sharply reduced, resulting in brain tissue hypoxia and disorders in the regulation of cardiac activity and the peripheral vascular tone.