Search

Background: Malnutrition is a critical concern in ICU settings. It is associated with increased morbidity and mortality, yet its prevalence and impact on clinical outcomes in patients with stroke and traumatic brain injury (TBI) remain underexplored., Objective: To evaluate the prevalence and impact of malnutrition risk on clinical outcomes in ICU patients with TBI, ischemic stroke, and hemorrhagic stroke, and to identify key risk factors associated with malnutrition risk., Methods: This retrospective cohort study utilized electronic health records encompassing ICU admissions from 2017 to 2023. Patients with either stroke or TBI were included, with malnutrition risk assessed using the prognostic nutritional index. Data were extracted and analyzed to determine patient characteristics, clinical and laboratory parameters, and outcomes., Results: This study included 1352 patients (267 TBI, 825 ischemic stroke, and 260 hemorrhagic stroke patients, >30% with pneumonia at admission). Severe malnutrition risk at admission was observed in over 60% of patients. Stroke patients, particularly those with hemorrhagic stroke, exhibited a higher risk of malnutrition compared to TBI patients. Malnutrition risk was associated with significantly higher hospital mortality and increased need for mechanical ventilation. Predictive factors for malnutrition risk included advanced age, higher SOFA scores, lower FOUR and GCS scores, and the presence of pneumonia at admission., Conclusions: Risk of malnutrition is highly prevalent among ICU patients with TBI, ischemic, and hemorrhagic stroke, significantly impacting mortality and other clinical outcomes. Identifying and managing malnutrition early in the ICU setting is crucial for improving patient outcomes. Further prospective, multicenter studies are needed to validate these findings and develop effective interventions.

The problem of chronic critical illness therapy is relevant all over the world. Revealing the metabolic function in patients in chronic critical condition is an important link in the development of adequate treatment and rehabilitation tactics. The aim - identification of metabolic features in chronic critical patients after brain injury in the first 3 days from the moment of admission to the rehabilitation center. Material and methods . Single-center observational study included a group of 25 patients with chronic critical illness, aged 38.7±14.0 years with body mass index 20.8± 4.3 kg/m 2 (min 14.5; max 29.7), who were on independent breathing through a tracheostomy tube, and who have pronounced neurological disorders in the form of depression of minimally conscious state, FOUR scale from 12 to 16 points, as well as bedsores 1-2 stage and polysegmental pneumonia. The patients underwent indirect calorimetry and analysis of biochemical parameters of protein, carbohydrate, fat and mineral metabolism, as well as the level of nitrogen excretion with urine. Results and discussion . The data obtained indicate that chronic critical ill patients with the consequences of traumatic brain injury had pronounced metabolic disorders, mainly of a protein component. Total protein level decreased up to 61.0±9.4 g/l (min 39.1; max 83.1), albumin up to 30.2±6.0 g/l (min 17.4; max 37.8), prealbumin up to 0.13± 0.06 g/l (min 0.04; max 0.23) and transferrin up to 147.7±37.7 mg/dl (min 84.0; max 209.0). The patients' requirement in protein was 106.4±38.5 g/day (min 57.1; max 160.5) or 1.55±0.46 g/kg/day (min 0.75; max 2.22). The level of resting energy expenditure measured by indirect calorimetry was 1549.1±421.8 kcal/day (min 673.0; max 2430.0) or in terms of body weight 24.8±7.6 kcal/kg/day (min 12.4; max 45.8). Conclusion . The data obtained indicate a continuing catabolic phase in patients more than 30 days after the primary injury, which led to their chronic critical condition., Competing Interests: The authors declare no overt and potential conflict of interest related to the publication of this article., (Copyright© GEOTAR-Media Publishing Group.)

Background: Mouse models of allergic asthma play a crucial role in exploring of asthma pathogenesis and testing of novel anti-inflammatory drugs. Widely used acute asthma models usually developed with adjuvant (aluminum hydroxide (alum)) do not reproduce one of the main asthma feature - airway remodeling while chronic asthma model mimic the pathophysiology of human disease. Moreover, the use of alum causes distress in experimental animals and impedes the test of adjuvant-containing drugs. In this study, we aimed to develop a chronic adjuvant-free asthma model with pronounced asthmatic phenotype., Methods: Female BALB/c mice were divided into 3 groups. The first group was sensitized with intraperitoneal injections of ovalbumin (OVA) emulsified in aluminum hydroxide on days 0, 14, 28 followed by two stages of intranasally challenge with OVA on days 41-43 and 62-64. The second group was subcutaneously sensitized with the same dose of OVA without adjuvant and challenged on the same days. The third group (negative control) included mice which did not received any kind of treatment (i.e. sensitization and challenge). Serum levels of OVA-specific IgE, IgG2a and IgG1 antibodies were detected by ELISA. Airway hyper-responsiveness was measured by non-invasive plethysmography on days 44 and 65. Bronchoalveolar lavage fluids (BALF) sampled in all groups on days 45 and 66 were analyzed by light microscopy. The left lung was removed for histological analysis. The IL-4 and IFNγ mRNA expression in BALF cells was evaluated by RT-PCR., Results: The OVA-specific IgE antibody response was two-fold increased in mice from adjuvant-free group compared to the adjuvant group that reflects reorientation of immune response towards Th2 phenotype. At the same time, the level of OVA-specific IgG1 and IgG2a antibodies was increased in the adjuvant group. Airway hyperresponsiveness to methacholine in mice of both experimental groups was two-fold higher than in control. Analysis of cell composition in BAL has shown a significant increase in eosinophil count in both experimental groups that indicate the development of allergic inflammation. Lung histology revealed airway remodeling in both experimental groups including goblet cell hyperplasia/metaplasia, thickening of airway walls, collagen deposition in the wall of distal airways. Additionally, the tendency to develop hypertrophy of bronchial smooth muscle layer was observed. Study of gene expression in BAL cells revealed the increase of IL-4 level in both adjuvant and adjuvant-free groups while IFNγ expression in both experimental groups was similar to control group., Conclusion: We have developed a chronic adjuvant-free mouse asthma model which possesses all necessary features of the disease including airway remodeling and is more suitable for pre-clinical evaluation of novel therapeutic approaches including adjuvant-containing drugs., (Copyright © 2019 Elsevier B.V. All rights reserved.)

Using a TV device for studying microcirculation (×40), we analyzed the density of the whole microvascular network and the density of arterioles in the pia mater of the sensorimotor cortex in SHR rats of different ages (3-4 and 12 months) after intracerebral transplantation of human mesenchymal stem cells. We found that the density of pial microvascular network in SHR rats receiving transplantation of human mesenchymal stem cells increased to a level observed in young Wistar-Kyoto rats.

Using a TV device to study brain microcirculation, we found that after a course of vascular peptide bioregulator the density of microvascular network of pia matter of old hypertensive rats (12 months) sensomotor cortex increased about 1,7 times compared to intact old rates SHR. This perfusion in the tissue of the cerebral cortex and the degree of blood oxygen saturation in the microvasculature of this tissue region raised.

Using a TV unit for microcirculation studies, we studied the density of the entire microvascular network and its arterial compartment in the pia mater of the sensorimotor cortex in intact young and aged rats (2-3 and 22-24 months) and aged rats after a course of vascular peptide bioregulator Slavinorm. The experiments showed that the density of microvascular network in intact animals decreased by 1.6 times with aging. Treatment with the peptide bioregulator 2.5-fold increased the density of the microvascular network in aged rats in comparison with intact animals of the same age, the density of the arterial compartment of the microvascular network in the pia mater increased by 2.8 times.

Using a TV device to study brain microcirculation, we found that after a course of vascular peptide bioregulator the density of microvascular network of pia matter of old rats (22-24 months) sensomotor cortex increased about 2,5-2,8 times compared to control old rates; and noradrenaline-induced constriction reactions and acetylcholine-induced dilative reactions of the pial arterioles increased significantly. This perfusion in the tissue of the cerebral cortex is not increased, but the degree of blood oxygen saturation in the microvasculature of this tissue region raised.

We studied the density and structure of the microvascular network of the pia mater, the blood flow rate and oxygen saturation in the sensorimotor cortex of young spontaneously hypertensive rats (SHR). The density of the microvascular network in hypertensive animals was by ~1.4 times lower than in normotensive Wistar-Kyoto rats (control) and arteriolar bed density was lower by ~1.9 times. The blood flow rate in tissue and oxygen saturation in the sensorimotor cortex in SHR rats were significantly lower than in control animals.

The results of the experimental studies reveal the decrease of vascular rigidity with the increase of systemic error of the arterial pressure values estimated via implication of transfer functions following haemorrhage modeling in rats. Compensation of the circulating blood volume by means of dextran infusion resulted in restoration of both vascular rigidity and systemic error of estimated arterial pressure. The results can be put into medical practice as an approach for testing of non-invasive methods in cardiovascular research.

We studied the density of the microvascular network in the pia mater, the tissue perfusion and saturation of the oxygen of sensorimotor cortex of hypertensive rats of different ages. Our investigations shown that the microvascular density in the pia mater was not only decreased, but also was increased. The perfusion of sensorimotor cortex was reduced and tissue saturation was enlarged. By the age of 12 months orienting-exploratory rats behavior became worse significantly in all major indicators of the test «open field».

Using a TV device to study microcirculation in brain we found that intracerebral transplantation of mesenchymal stem cells to 12-months old rats led to a significant increase (circa 1,5-fold times) of microvascular density in pia tissue and to increased constriction reactions of pia arterioles in response to noradrenalin application on a brain surface. Both microvascular density and pia arterioles reactivity was completely preserved in aging until 22-24 months.

Male Wistar-Kyoto rats, aged 22-24 months, were intracerebrally transplanted syngeneic mesenchymal stem cells (MSC). Cognitive functions of these animals were tested in 3 weeks. The density of microvascular bed, the tissue blood flow, saturation of mixed blood in cortex microvessels were measured under the standard conditions, under the impact of noradrenaline and in the context of global ischemia. The control groups consisted of rats aged 2-3 months and 22-24 months. MSC transplantation have a positive impact on the microcirculation in brain cortex of old animals: reduction of vascular density was prevented, level of saturation in the blood vessels was increased, which enabled animals to endure easier extreme impacts, but did not correct age-related deterioration of cognitive functions.

Using a TV device for studying microcirculation (×160), we analyzed the responses of arterioles in the pia mater of the sensorimotor cortex in young (2-3 months) and old (22-24 months) rats after local application of a vasoconstrictor (norepinephrine, 10(-6) M) or vasodilator (acetylcholine, 10(-6) M). The responses of the arterioles were evaluated by changes in their diameter and by the number of responding vessels in the field of view. The constrictor responses of the pial arteries to norepinephrine did not significantly differ in intact young and old rats. The number and degree of dilatory responses to acetylcholine in old rats were lower than in young animals by 14 and 30%, respectively. Intracerebral transplantation of mesenchymal stem cells to old rats had practically no effect on reactivity of pial arterioles to acetylcholine, while the number of constricted vessels in response to norepinephrine increased by ~20%.

A highly sensitive test system, based on the method of immuno-PCR, was developed for the detection of two staphylococcal toxins: enterotoxin A (SEA) and toxic shock syndrome toxin (TSST). A key element of the developed systems was obtaining supramolecular complexes of bisbiotinylated oligodeoxynucleotides and streptavidin, which were used as DNA tags. Specificity studies showed no cross-reactivity when determining SEA and TSST. The sensitivity of detection of these toxins in the culture supernatants S. aureus was not less than 10 pg/mL.

Using a television-based vital microscopy method and immunohystochemical analysis, we have assessed the effect of intracerebral transplantation of syngeneic mesenchymal stem cells (MSC) on the brain cortex structure and the microcirculation in the pia mater of old rats. Using "open field" system, we have studied the effect of MSC transplantation on position-finding and discovery behavior of older animals. We have found that density of microvascular network of the pia mater increased ca. 1.9-fold in MSC recipients, compared to age-matched intact animals. Density of the arteriolar area of microvascular network of the pia mater increased ca. 2-fold. Reactivity of the newly formed arterioles was nearly equal to that of native microvessels. Intracerebral transplantation procedure itself was traumatic for brain cortex of rats, but it had no effect on the microcirculation in the contralateral hemisphere. Intracerebral transplantation of MSC did not improve locomotor behavi- or and emotional stage of old rats, did not increase their position-finding and discovery activity.

Male Wistar-Kyoto rats aged 22-24 months were intracerebrally transplanted with syngenic bone marrow mesenchymal stem cells (BM MSC) established from the donor aged 3-4 months and 20-22 months, respectively. Using a TV device to study microcirculation in vivo, we have established that transplantation of BM MSC from young donors increased a density of the microvascular network in the pia mater of the sensorimotor cortex in old rats approximately 1.9-fold, comparing to age-matched controls, while a density of the arteriolar compartment increased approximately 2.1-fold. Transplantation of BM MSC from old donors did not lead to the significant increase in the density of the microvascular network in the pia mater, while a density of the arteriolar compartment increased approximately 1.5-fold.

We studied the effect of intracerebral transplantation of bone marrow mesenchymal stem cells on microcirculation (density of microvascular network and reactivity of arterioles) in the pia mater of 2-3-month-old rats. It was found that after transplantation of mesenchymal stem cells, the density of pial microcirculatory network in the contralateral hemisphere significantly increased (by 1.7 times; p<0.05) in comparison with both intact animals and controls. The number of arterioles in the studied area increased most markedly (by ≈2.5 times; p<0.05) in comparison with other groups. Intracerebral transplantation of mesenchymal stem cells or conditioned culture medium (α-MEM) had no effect on reactivity of pial arterioles.

Using a TV device for studying microcirculation (×40), we studied the density of the whole microvascular network and arteriolar its compartment in the pia mater of the sensorimotor cortex in rats of different age (2-3, 12, and 24 months) after intracerebral transplantation of mesenchymal stem cells or nutrient medium (control). The density of the microvascular network in the pia mater remained practically unchanged until 1 year, but then decreased by 1.8 times with adding (up to 2 years). MSC transplantation 1.5-1.8-fold increased the density of the pial microvessels in animals of all age groups in comparison with intact and control rats; the density of the arteriolar compartment increased by 2.1-2.4 times. Intracerebral injection of MSC to 1-year-old animals prevented pathological decrease in the density of microvascular network during the next year of life.

We studied the density of whole microvascular network and separately the density of arterioles in the pia mater of sensorimotor cortex of rats of different ages. Also pial arteriolar reactivity on exposure to norepinephrine or acetylcholine chloride was evaluated. The microvascular density and the arteriolar reactivity in the pia mater were not significantly changed before the age of 12 months. In the age of 22-24 months the density of whole microvascular network decreased 1,7 times at the mean and the density of arterioles decreased 1,2 times. There were no significant changes of pia arterioles constriction during the animals life but dilatation was noticeably worse in senility. Orientation and exploratory behavior got worse to the age of 22-24 months: the number of behavioral acts in the "open field" test decreased 1,5-2,3 times in comparison with young animals.

Male Wistar-Kyoto rats (12 and 22-24 months old) were intracerebrally transplantated with syngeneic mesenchymal stem cells (MSC). Three weeks or one year later, orientation and exploratory behavior of the same animals (not 2 years old) was assessed using an «open field» test. Older rats (22-24 months old) were inhibited in the basic behavioral acts in comparison to younger animals (2-3 months old). Transplantation of MSC did not cause improvement of an orientation and exploratory behavior of aged rats. Morphological and immunohistochemical analysis suggests intracerebral MSC transplantation led to the injury of the cortex of the ipsilateral hemisphere.

We studied the effect of intracerebral transplantation of mesenchymal stem cells on the density of pial arterioles in rat brain cortex. It was shown that intracerebral transplantation although causes damage to about half the area of the ipsilateral pia mater, does not change the density of the microvascular network neither in border region of the injured tissue, nor in the contralateral hemisphere. Intracerebral transplantation of mesenchymal stem cells promoted arteriogenesis in the pia mater of the contralateral hemisphere: density of arterioles in this area was significantly (by about 2.5 times higher) than in other experimental animals.

Using a TV installation for studying the microcirculation (with 30-160-fold magnification), the density of microvascular network in the pia matter of the rat brain sensomotor cortex was determined after intracerebral transplantation of mesenchymal stem cells (MSC) or (as control) of the MSC cultivation nutrition medium, or of saline. The results have shown that intracerebral transplantation does not change density of microvascular network in the pia mater of the ipsilateral hemisphere. Transplantation of the MSC led to a 1.8-fold increase of density of the pia matter of the contralateral hemisphere as compared with control animals; the number of arterioles in the same zone was 2.5-fold higher than in intact rats.

In experiments on rats, changes in blood pressure and cardiac output in response to antiorthostatic (head-down) tilt 15° and 45° were examined under conditions of decreased arterial tone induced by sodium nitroprusside. The decrease in initial systemic blood pressure to 90 mm Hg attenuated the pressor responses to antiorthostasis, while further drop in blood pressure to 70-60 mm Hg provoked depressor responses in half cases. No blood pressure responses to antiorthostasis were observed when blood pressure dropped to 50 mm Hg. Correlation analysis confirmed the existence of a direct dependence of pressor responses to orthostasis on the initial blood pressure.

The NO-dependent mechanism of system hemodynamics reactions comprising increased system blood flow (cardiac output) and blood pressure to head-down tilting at 6, 12 and 18 degrees was studied in anaesthetized rats. Tilting of the rats with inhibited NO synthesis was shown to aggravate hypertension and elevate total peripheral resistance (TPR). Therefore, it can be concluded that NO-dependent vasodilation is involved in regulation of the arterial tone during tilting.

Increased pressor response to the infusion of alpha1-adrenoceptor agonist phenylephrine was observed in conditions of inhibited NO synthesis: the mean blood pressure increased from 33.7 to 41.1% and the total peripheral resistance increased from 6.8 to 22.0%. The effect of vasodilation induced by NO secretion in the vascular endothelium after the stimulation by alpha1-adrenoceptors on the degree of pressor changes and changes in the total peripheral resistance is proposed.

Blockade of NO synthesis in most narcotized rats was followed by an increase in depressor effects (by 45%) and decrease in total peripheral resistance (by 63%) upon treatment with isopropyl norepinephrine (isoproterenol). Our results indicate that NO secretion in the endothelium modulates the systemic hemodynamic response to beta(2)-adrenoceptor stimulation.

Blockade of NO synthesis in narcotized rats potentiated pressor effects of phenylephrine by 55% and increased total peripheral resistance by 153%. Vasodilation caused by enhanced NO secretion modulated pressor shifts evoked by stimulation of alpha(1)-adrenoceptors with phenylephrine.

Anastomotic leakage due to loosening of sutures is the frequent cause of lethality. To prevent such complication, a sleeve-type esophago-enteric and esophagogastric anastomosis was used. Its design eliminates the major cause of failure--the basic sutures running through the soft muscular wall of the esophagus. The new anastomosis was used in ca. 42 patients: Lewis operation (24), proximal resection of the stomach and distal thoracic part of the esophagus and adjuvant intrapleural esophagoplasty with the distal end of the stomach (8), gastrectomy with resection of the distal thoracic part of the esophagus and concomitant intrapleural esophagoplasty with small intestine (S.S.Yudin) (10). Postoperative complications were reported in 18 patients (42.9%); lethality--11.9%. No leaking esophageal anastomosis was registered.

The aim was to describe endothelium-dependent reactions of system hemodynamics to the reduction in system blood circulation (cardiac output) by orthostatic positioning of anesthetized rats. Head rise at 15, 30 and 45 degrees and NO synthesis depression increased the hypotensive reaction to orthostasis by 32, 60 and 71%, respectively, as compared with values prior to the block. This allows the conclusion concerning the recruitment of an NO-dependent vasodilative mechanism in vascular control. It was shown that NO modulated the arterial system reactivity to orthostasis the magnitude of which depended on baseline blood pressure. This relationship was reverse in the event of intact NO-synthase and linear in the event of NO synthesis depression. These data point to the significance of NO secretion for as baseline BD values, so mechanisms of orthostasis-induced hypotension.

Experimental data on the effect of NO synthase inhibition on hemodynamic changes (blood pressure, cardiac output, and peripheral resistance) induced by an increased (polyglucin infusion) or decreased (orthostasis) cardiac output are presented. Under conditions of NO synthase inhibition, the pressor effects of polyglucin and orthostatic hypotension increased by 70 and 72%, respectively. The response of peripheral resistance had a similar trend. Significance of NO secretion by vascular endothelium for the development of systemic hemodynamic responses is proposed.

An analysis of risk factors of incompetence of the bronchus stump or tracheobronchial anastomosis has shown that the statistically reliable factors (p < 0.05) were: male gender of the patient, neglected lung cancer, high degree of purulent intoxication, preoperative gamma-therapy, certain kinds of performing sutures, the degree of acute respiratory insufficiency. The traditional methods of plasty of the primary bronchus stump or tracheobronchial anastomosis in patients with the high objective risk of the development of incompetence of their sutures are known to be not effective. An experience with 70 prophylactic and curative omentoplasties has shown than the application of the greater omentum for plasty can substantially reduce frequency of the formation of acute bronchopleural fistulas, but the technique of fixation of the omentum to the trachea and opposite primary bronchus is of great significance for realization of the omentum plasty potential.

Blockade of NO synthesis in anesthetized rats significantly potentiated pressor responses to Polyglucin (by 70%) and considerably increased total peripheral resistance. It was concluded that vasodilatation induced by increased systemic blood flow (cardiac output) modulates pressor responses under conditions of increased blood volume.

In anaesthetised rats, effects of blockade of the NO-synthetase upon hemodynamic shifts were studied (arterial pressure, cardiac output, general peripheral vascular resistance), the shifts being evoked either by increase (infusion of polyglucon) or by decrease (orthostasis) in the cardiac output. Under the blockade of the NO-synthetase, the pressor effects of polyglucon increased by 27% and the orthostatic hypotension by 72%. Responses of general peripheral vascular resistance changed in the same direction. The findings suggest importance of the NO secretion by the vessels' endothelium for formation of the systemic hemodynamics responses.

Systemic vasodilation produced by sodium nitroprusside in various concentrations and accompanied by a decrease in baseline blood pressure was followed by progressive reduction in pressor responses to alpha-adrenoceptor agonist phenylephrine (mesatone) in rats. In a blood pressure range of below the physiological level (80-100 mm Hg), a positive linear correlation was revealed between the decrease in baseline blood pressure and pressor effect of phenylephrine.

In anaesthetised rats, bending of the body for 30 degrees and 45 degrees entailed a reverse linear dependence between the systolic and diastolic pressures under conditions of initial blood pressure over 95 mm Hg, whereas in initial blood pressure lower than 95 mm Hg the dependence is direct. In bending of the body for 60 degrees the dependence was direct and only present in initial blood pressure lower than 95 mm Hg. Pressor effects of mesaton in orthostasis directly depended on the level of the initial blood pressure. Any dependence of the cardiac output shifts on the initial blood pressure was absent. The direction and the degree of the arterial system reactivity's changes in response to orthostasis and adrenergic effect of mesaton was found to depend on the bending angle and the initial blood pressure level.

Experiments with unconscious rats showed that blocking of NO secretion intensifies orthostatic hypotension (mean arterial pressure drops by 72%) and reduces proportionally the calculated total peripheral resistance. A supposition has been made concerning involvement of the endothelial relaxing factor in orthostatic hypotension development, since in orthostasis cardiac output (systemic blood circulation) losses its influence on the endothelial NO secretion.

In anaesthetised rats, dependence of haemodynamics upon increase in the blood volume due to infusion of polyglucin in amounts 1.2 and 2.4 ml (8% and 16% of the blood volume in rats, respectively) < was studied. In the former case the initial blood pressure increased by 30%, in the latter case--by 42%; cardiac output--by 16% and 40%. The metasone pressor effects, at the were reliably decreased by 27% and 65%, and those of general peripheral resistance--by 40% and 80, respectively. The cardiac output changes did not differ significantly. The data obtained suggest an effect of the blood volume increase upon a drop of the arterial system's adrenoreactivity as a result of increase in initial blood pressure.

A stepwise decrease in the blood pressure by means of sodium nitroprusside infusion led to progressing diminishing of mesatone pressor effects in anaesthetised rats. Cardiac output changes due to mesatone administration did not depend on the initial blood pressure. The latter being lower than physiological limits, a direct linear correlation occurred between pressor responses and shifts of general peripheral resistance, on one hand, and the degree of the blood pressure initial drop, on the other hand. The constrictor responses under study are discussed in respect to their dependence on initial tone of arterial vessels.

Experience of treatment of 355 patients with large, gigantic, complex postoperative abdominal hernia, operated in the planned order in 1983-2000 yrs, is presented. Ventroplasty, using tissues of patients of their own, was done in all the patients. The one-stage, staged, T-like plasty was done, the hernial sac plasty, methods of trebled, quadrypled and increased sixfold were performed as well. The abovementioned ventroplasty methods application have permitted to eliminate the defects in musculoaponeurotic layer of abdominal wall of any size, localization and compexity. Immediate and late result was favourable. Mortality had constituted 0.6% (two patients died). Absence of hernial recurrency for follow-up to 17 years in 95.8% patients trusts efficacy of these methods of treatment and makes possible to recommend them for application in clinical practice.

Reported are data of experiments with unconscious tilted rats (30 degrees, 45 degrees and 60 degrees) in which a dependence of orthostatic hypotensive reactions of systolic (APs) and diastolic (APd) pressure on spontaneous level of baseline mean arterial pressure (APb.mean) was established. Rats tilted at 30 degrees and 45 degrees, APs and APd were in inverse linear dependence with APb.mean above 95 mm Hg and in direct dependence with APb.mean below 95 mm Hg. Pressor effects of phenylephrine correlated directly and to the same extent with APb.mean only below 95 mm Hg in the 30 degrees and 45 degrees tilt and both above and below 95 mm Hg in the 60 degrees tilt. Mean values of the pressor effect before and after experiment were different in animals tilted at 60 degrees. No dependence of cardiac output on APb.mean was determined. Therefore, the trend and depth of changes in the arterial system reactivity to tilt are dependent on the degree of inclination and the APb.mean range. Reactivity to the adrenergic agent alters only when inclination is greater than 45 degrees.

In anesthetized rats, a reverse linear correlation of arterial pressure (AP) shifts was found within the range of initial AP over 95 mm Hg under the head-up tilts at 30 and 45 degrees. Within the range beneath 95 mm Hg this correlation was transformed into the direct one. Under 60 degrees tilt such correlation only occurred within the range beneath 95 mm Hg. The direction and degree of the arterial system responsiveness seems to depend on the tilt value as well as on the range of the initial AP.

The correlation analysis revealed no correlation within the range 110 to 80 mm Hg further transforming into a direct (within the range lower than 80 mm Hg) dependence of the pressure responses to mesatone on the reduction of initial mean arterial pressure under orthostatic hypotension in anaesthetised rats. Under paraverine hypotension a reverse correlation within the range 110-80 mm Hg transforming into a direct dependence (within the range lower than 80 mm Hg) of the responses to mesatone were observed. The dependence of cardiac shifts to mesatone on the initial arterial pressure was not occurred. The mechanisms of dependence of the systemic vascular responses on initial tone of arterial vessels, are discussed.

The effect of the elevated arterial tone on pressure responses to stimulation of arterial alpha-adrenoreceptors by phenylephrine hydrochloride was studied in anesthetized Wistar rats. Different levels of the arterial tone and, hence of the mean arterial pressure, were established by means of angiotensin II infusion in the range from 101 to 160 mmHg. An elevation of the arterial tone led to a significant reduction of the arterial pressure and peripheral resistance rise produced by phenylephrine. The degree of relative reduction of the increase in the diastolic pressure exceeded 1.3 times that in the systolic pressure. The shifts of cardiac outputs remained unchanged. After cessation of angiotensin II infusion the restoration of the arterial pressure took place almost till the initial level. At this time the pressure effects of phenylephrine were tended to recovery. It is suggested that the elevated arterial tone attenuates the systemic pressure response to stimulation of arterial alpha-adrenoreceptors by a vascular mechanism based on a transmural pressure changes evoked by the constriction of the arterial vessels.

The correlation analysis revealed a direct (within the range 80 to 120 mm Hg) further transforming into a reverse (within the range 121 to 160 mm Hg) dependence of the blood pressure depressor shifts on the initial mean arterial pressure in anaesthetised rats. Within the physiological range of arterial pressure (70 to 130 mm Hg) there is no difference in responses to nitro-glycerine from their initial values. The mechanisms of dependence of the systemic vascular responses on initial tone of arterial vessels, are discussed.

A significant decrease of arterial pressure in response to isoproterenol occurred in anaesthetised rats with the initial pressure 101-130 mm Hg. Elevation of the initial pressure up to 131-180 mm Hg led to a significant attenuation of the depressor effect. The correlation analysis revealed transformation of direct correlation into inverse one between the depressor responses to isoproterenol and the degree of elevation of the initial arterial tone, as well as lack of such a dependence in the cardiac output shifts.

A significant decrease in arterial pressure and total peripheral resistance occurred following elevation of the initial blood pressure to 160 mm Hg with mesathone in anesthetised rats. The increase in the cardiac output remaining unchanged. Vascular and cardiac mechanisms of the revealed relationships are discussed.

A considerable decrease in pressor responses to polyglykine at an elevated arterial tone and constant increase of cardiac output occurred in anesthetised rats. Vascular and cardiac mechanisms of the interrelationship are discussed.

Contribution of the original angiotensin-2 controlled arterial tone to the shifts in systolic and diastolic arterial pressure (AP) was assessed in unconscious rats during tail-suspension. With this technique, values of original mean AP were elevated from 80-110 to 111-140 mm Hg. In the head-down position, rise in the tone was concurrent to a twofold increase in the number of "uncompensated" responses and a similar decrease in the number of test-resistant responses. The original arterial tone high, maximum decline of diastolic pressure was significantly less pronounced. Recovery of both systolic and diastolic arterial pressures was more dynamic against the background of high original tone. Magnitude of the diastolic AP variation dominated over that of systolic AP. These results are being analyzed in comparison with the data about orthostatic compensatory reactions.