Ultrastructural changes in the microcirculatory bed and filtration-reabsorption barrier of the kidney during temporary ischemia after unilateral nephrectomy

Ultrastructure of cellular elements of the microcirculatory bed and filtration-reabsorption barrier has been studied in 150 mature white rats, in which vascular fasciculus of the left kidney has been compressed for 30 min, 1-2 h with a subsequent restoration of the blood stream in the organ undergone ischemia on the 3rd, 7th, 14th, 30th, 60th, 180th, 360th days under conditions of the preliminarily right kidney nephrectomy. On the 3rd day after ischemia of the remained kidney for 30 min, structural components of the walls of the glomerular arterioles and those of the filtration-reabsorption barrier undergo certain ultrastructural changes, that with time elapsed (7, 14 days) gradually pass away, and amount of cells with hypertrophic processes increases. Ischemia for 1 h in the remained kidney with subsequent restoration of the blood stream on the 3rd, 7th days produces in the structures mentioned more pronounced destructive changes. During subsequent compensatory hypertrophy (the 30th, 60th days) of the remained kidney after its ischemia, in the microcirculatory bed elements and in the convoluted canal epitheliocytes intracellular regenerative and hyperplastic processes develop. However, ischemia for 2 h in the remained kidney produces severe destructive-necrotic phenomena in ultrastructure of the microcirculatory bed and of the filtration-reabsorption barrier.     

Morphological and ultrastructural changes in the rat kidney after experimental sepsis

Experimental sepsis was investigated in 42 male white Wistar rats. The animals were divided into 7 equal groups. Suspended E. coli cells (2 x 10(7) per 100 g body weight) were injected into the tail vein in groups I-VI, group VII served as a control group. The rats were sacrificed with cervical dislocation at different times after injection: in 45 min (group I), 2 h (group II), 6 h (group III), 24 h (group IV), 48 h (group V), and 120 h (group VI). Samples of kidneys were taken and embedded in paraffin and EPON-812 for histological and electron microscopical evaluation, respectively. Results: histological examination demonstrated that changes in kindeys started in 2 h after infection to achieve the maximum level in 24 h, showing thereafter a tendency to decrease. A significant tissue damage was first seen in the loop and distal tubules of nephrons, and then expanded to the proximal tubules. Electron microscope examination demonstrated that changes in podocytes and cytopodia could be distinctly differentiated in 2 h after infection and obviously increased in the course of the experiment. The podocytes were enlarged, the processes were expanded and adhered to each other. For that reason the number of filtration pores in the glomerular basal membrane decreased. The count of mesangial cells in the glomerulus was increased.     

Ultrastructural changes in the microcirculatory bed of the lungs in endotoxin shock

The electron microscopic study of the lungs during the initial and intermediate stages of endotoxin shock has revealed the manifestations of thrombo-hemorrhagic syndrome. Three days later interstitial fibrosis developed. Ultrastructural alterations of microcirculation become the basis for the formation of acute pulmonary failure.     

Systemic and organic changes in the microcirculatory bed in experimental dehydration of the body

Among systemic mechanisms of microvascular reactivity of the musculus spinotrapezius, pancreas and small intestine mesentery at dehydration, a special role play the changes directed to maintenance of harmony between the capacity of the blood bed and volume of the circulatory blood, morpho-functional factors on regulation of hemodynamics, as well as mechanism of liquor resource++ elimination from the blood bed. The organic peculiarities of the microvascular reactivity at dehydration are determined by topic and quantitative character of their changes.     

Effect of elevated systemic arterial pressure on neurogenic vasoconstriction in the microcirculatory bed of rat skeletal muscles

Vasomotor reactions produced by electrical stimulation of the sympathetic tract were studied in anesthetized rats by intravital microscopy of the skeletal muscle (extensor hallucis proprius). Experiments were made in normal and elevated blood pressure. The stimulation itself did not change BP but led to an appreciable decrease in the initial diameter of the arterioles (28.6 +/- 1.4 m). The constriction amounted to 21%. The lumen decreased by 38.9%. Injection of felypressin (Sandoz) in a dose of 6 to 8 IU/100 g produced the pressor reaction. The 27.4% rise of BP during primary phase of the pressor response inhibited the development of the neurogenic vasoconstriction which was 11.5% for arteriolar diameter and 20.4% for lumen. The data suggest that inhibition of the neurogenic vasoconstriction is caused by an increase in arteriolar pressure. Consequently the elevation of intralumen pressure is considered as a protective mechanism of the drop of the tissue blood flow because of the sympathetic vasoconstriction.     

Morphofunctional changes in the microcirculatory bed of the synovial membrane in antigen-induced arthritis

Ultrastructural changes of synovial capillary and venule wall have been investigated in rabbits with antigen-induced arthritis, with the permeability of microcirculatory bed determined using 99mTc pertechnetate. The correlation between the incidence of ultrastructural microvascular damages in exudative phase of arthritis and the increased permeability has been established. Ultrastructural changes occurring in proliferative phase of arthritis are considered as adaptive to conditions of increased permeability.     

Morpho-functional changes in the muscles of the limbs and their microcirculatory bed in acute ischemia

On 26 mature dogs in a chronic experiment the character of compensatory-adaptive changes in muscles and their blood capillaries have been studied in dynamics of an acute ischemia of the extremity and at some stages of recirculation. After strangulation for two hours, thanks to joining in the compensatory-adaptive mechanisms, certain morphofunctional changes in the extremity tissues are revealed. As the duration of hypoxia increases (6-9 h), the destructive changes in the tissues become more severe. They are inherent in an acute hypoxia and accompanied with disaggregation and hydratation of cell membranes of endotheliocytes, with formation of vesicles and spherules, with increasing microclasmatosis, formation of myelin-like bodies, with destructive changes of organelles, with destruction of sarcoplasmic reticulum, with focal discoid necrosis, myocytolysis and sequestration of autolysis altered groups of muscle fibers. The data obtained serves as a base for elaboration of a pathogenically adequate surgical treatment of severe forms of an acute ischemia of extremities.     

Morphologic changes in the microcirculatory bed at stages of prolonged experimental fasting in animals

In 40 white male rats with body mass 180-200 g, by means of silver nitrate impregnation, morphological changes have been studied in the blood microcirculatory bed of the small intestine mesentery, spinal trapezoid muscle and eye ball conjunctiva at various stages of a prolonged fasting. With an increasing time of the experiment, a gradual undirected character of the changes in the microvessels is noted. After 3 days of fasting the changes in diameters of the microvessels, comparing to the control ones, have not any significant values in all the organs studied. After 6 days of fasting significant changes in diameters in all the links of the microcirculatory bed of the eye ball conjunctiva and in that of the spinal trapezoid muscle are observed. The microvascular changes are mostly pronounced on the 9th day of fasting. The maximal decrease of the microvessel diameters is noted in the eye ball conjunctiva, and the minimal--in the small intestine mesentery. The changes in the spinal trapezoid muscle are of intermediate character. The highest points of the structural lability gradient fall on the capillary and postcapillary-venular links of the blood microcirculatory bed.     

Morphofunctional changes in the lymph nodes and microcirculatory bed of small-intestinal mesentery of dogs in septic peritonitis after endolymphatic administration of ampicillin

With the aim to study effectiveness+ of endolymphatic (EL) administration of ampicillin (AC), using the model of an acute diffuse septic peritonitis in dogs, the morphological and morphometrical investigation has been performed concerning the state of the lymph nodes (LN), which are regional as regards the pathological focus (pelvic) and remote (tracheobronchial, mesenteric) and hemomicrocirculatory bed (HMCB) of the small intestine mesentery. All LN groups studied are involved in the pathological process, that produces certain increasing disturbances in the structure and cell composition in LN. In 6 h the changes are especially manifested in the pelvic LN, and in 18 h--in the animals without application of AC, or at its intramuscular injection LN lose their typical structure. Their dimensions and number of lymphoid nodules++ and medullary cords decrease, a sharp impoverishment of lymphocytes in LN is observed. By this time critical disturbances in the HMCB structure develop; they are characterized as presence of great amount of avascular areas in the mesentery, extended capillary loops, plasmatic saturation of interstitium. When AC is injected endolymphatically, simultaneously with peritonitis modelling T- and B-dependent zones in LN are preserved, a high volumetric part of lymphocytes is kept in all groups of LN, structure and function of HMCB are normalized. The pronounced delay in development and decreasing manifestation of infective-toxic disorder in LN and HMCB depend on effective concentrations of the antibiotic, produces in the lymphatic system.     

The microcirculatory bed of the human heart

Using a complex approach in studying microcirculatory bed of the human heart, possibilities of scanning electron microscopy of corrosive preparations, those of silver nitrate impregnation after V. V. Kuprianov are demonstrated. The silver nitrate impregnation makes it possible to study the wall structure of the microcirculatory pathways, to analyse arrangement of nuclei in the endothelial and muscle cells of the microcirculatory links, to reveal together with the vessels the surrounding tissues. Scanograms of the corrosive preparations of the arterioles demonstrate "circulatory strips", that are absent in the venular part. The relief of the luminal casts of the microcirculatory bed vessels in the human heart is presented as impresses of nuclei of the endothelial and smooth muscle cells. Peculiarities in form and distribution of these nuclei in various links of the microbed are demonstrated.     

Development of the uterine microcirculatory bed in postnatal ontogeny

Age peculiarities of common structure of the microcirculatory pathways, specific volumes and amount of microvessels, zonal parameters of pericapillary microcirculation of metabolites, glycosamine glycans and glycoproteins contents, phosphatase and ATPase activity, collagen and elastic fibers of the microcirculatory bed vessels have been studied in 190 unchanged uteri, beginning from 36-week-old fetuses up to 35 years of age. The microcirculatory bed of myometrium during the period of postnatal ontogenesis investigated possesses a polymer-homonomous structural organization; its base make myoangiomas, including the terminal arteriole with precapillaries and collecting venule, that run from it. Similar structure of the myometrium microcirculatory pathways is already observed in fetuses of late antenatal period. In endometrium formed glanduloangionomas are revealed in the prepubertal age. Increase in glycosamine glycans contents is stated in the microvessel walls and in the uterine stroma during the process of its development. Compensatory-adaptive changes in the uterine microcirculatory bed are described during the newborn period up to the puberty. Functionally mature structures of the microcirculatory pathways in the submucosal and vascular layers of myometrium, endometrium and in the cervix uteri are found to be formed earlier than in other areas of the organ.     

Coronary microcirculatory vasoconstriction is heterogeneously distributed in acutely ischemic myocardium

The classical model of coronary physiology implies the presence of maximal microcirculatory vasodilation during myocardial ischemia. However, Doppler monitoring of coronary blood flow (CBF) documented severe microcirculatory vasoconstriction during pacing-induced ischemia in patients with coronary artery disease. This study investigates the mechanisms that underlie this paradoxical behavior in nine patients with stable angina and single-vessel coronary disease who were candidates for stenting. While transstenotic pressures were continuously monitored, input CBF (in ml/min) to the poststenotic myocardium was measured by Doppler catheter and angiographic cross-sectional area. Simultaneously, specific myocardial blood flow (MBF, in ml.min(-1).g(-1)) was measured by 133Xe washout. Perfused tissue mass was calculated as CBF/MBF. Measurements were obtained at baseline, during pacing-induced ischemia, and after stenting. CBF and distal coronary pressure values were also measured during pacing with intracoronary adenosine administration. During pacing, CBF decreased to 64 +/- 24% of baseline and increased to 265 +/- 100% of ischemic flow after adenosine administration. In contrast, pacing increased MBF to 184 +/- 66% of baseline, measured as a function of the increased rate-pressure product (r = 0.69; P < 0.05). Thus, during pacing, perfused myocardial mass drastically decreased from 30 +/- 23 to 12 +/- 11 g (P < 0.01). Distal coronary pressure remained stable during pacing but decreased after adenosine administration. Stenting increased perfused myocardial mass to 39 +/- 23 g (P < 0.05 vs. baseline) as a function of the increase in distal coronary pressure (r = 0.71; P < 0.02). In conclusion, the vasoconstrictor response to pacing-induced ischemia is heterogeneously distributed and excludes a tissue fraction from perfusion. Within perfused tissue, the metabolic demand still controls the vasomotor tone.     

Structure and function of the microcirculatory bed in the preserved heart]

The morphological analysis of the state of the heart during hypertermal perfusion with different conservants reveals clear dependence of the microcirculation and the activity of the heart upon the type of the conservant. Perfusion with a salt solution and hemodilution is accompanied by pronounced disorders in microcirculation and unsatisfactory parameters of the cardiac activity. Conservation with cryoprecipitated plasma is characterized by comparatively less microcirculatory disorders, but fails to give a reliable safety of the heart. When using medium 199, changes in microcirculation were found to be minimal and parameters of cardiac activity were satisfactory. In the complex of non-specific changes in microcirculatory vessels the maximum structural lability was revealed in blood capillaries and vessels of the postcapillary-venular link.     

Organ and tissue-specific properties of the microcirculatory bed of the heart

The auricular and ventricular microcirculatory bed has been studied in persons of mature age, not suffering from any cardio-vascular diseases during their life. As a whole, 48 objects have been studied. The microcirculatory bed has been revealed in sections of the cardiac wall 70-100 mcm thick using silver nitrate impregnation after V. V. Kuprianov. Organ- and tissue-specific properties of the vascular microcirculatory bed are revealed in interrelations of the vessels and the structural elements of the cardiac wall (myocardium, and connective tissue structures), in position of nuclei of the endothelial cells of the capillary wall and in places of the capillary branchings. Principle differences in structure of the auricular and ventricular microcirculatory bed are demonstrated. The notion the organ- and tissue-specific properties of the microcirculatory bed vessels is discussed.