Structural changes in platelets in alloxan diabetes as parameters of their activation in the vascular bed and morphologic features]

The present study shows that a stable level of blood platelet number persists in diabetic rats (following 15 and 60 days after experimental alloxan injection) Unusual platelet megaforms are seen accumulating (up to 36%), having no size analogs in control animals. A quantitative electron-microscopic analysis demonstrated that the enlargements of diabetic platelets was accompanied by their rounding in shape and by a more frequent (by 2.0-2.6 times) generation of surface pseudopodia. The share of platelets increased in two independent fractions, with considerable deflexion over the normal range limit variations in the number, size and general volume of their alpha-granules (cutting down) or dense (increase) bodies. At the same time a common decrease in these indexes for different types of grains in platelets of various dimensions occurred. The integral picture of the platelet granular apparatus (image of granular apparatus), that demonstrates quantitative proportions between the number and size indexes of different grain types, is found distorted in diabetic rats.     

Method of quantitative assessment of morphological changes in the central nervous system]

The author present a variant of quantitative assessment of the degree of morphological changes in the central nervous system neurons. It is suggested that the following groups of the changed neurons should be distinguished: swollen neuron with the initial manifestations of breaking large tigroid lumps into smaller ones; swollen neuron with marked phenomena of breaking large tigroid lumps into smaller ones and initial phenomena of hypochromatosis; swollen neuron with total tigrolysis with hyper- and hypochromatosis; dehydrated hyperchromic neuron; vacuolized neuron; contracted atrophic neuron; perished neuron. Each of the mentioned groups is given a mark, characterizing the degree of morphological changes. A formula for the assessment of the degree of morphological changes for individual formations and zones of the central nervous system is suggested.     

Tempol improves vascular function in the mesenteric vascular bed of senescent rats

Ageing is associated with structural and functional alterations of the vasculature. The nature of age-related vascular disorders is not completely understood. Oxidative stress is hypothesized to play a crucial role in the pathophysiology of vascular complications. We investigated the effects of chronic treatment with the superoxide dismutase mimetic tempol (4-hydroxy-2,2,6,6-tetramethyl piperidinoxyl) on vascular function in the mesenteric vasculature of aged rats. Young (3 weeks) and old (40 weeks) Sprague-Dawley rats were treated with tempol (1 mM in drinking water) or vehicle for 3 weeks. Arterial blood pressure was slightly, but significantly, higher in old than in young rats. Tempol had no effect on arterial blood pressure. The vasoconstrictor responses to norepinephrine (NE) and serotonin (5-HT) were exaggerated in the mesenteric vascular bed (MVB) removed from old rats. Vasodilator responses to acetylcholine (ACh), papaverine (PPV), and isoprenaline (ISO) were reduced in the MVB of old rats in comparison with young rats. Chronic treatment of old rats with tempol normalized their responses to NE and 5-HT. The dilator responses to ACh, PPV, and ISO were similar between old rats receiving tempol and young rats. The present findings suggest that oxidative stress contributes to vascular dysfunction in the mesentery of old rats. The vasculoprotective effects of tempol remain to be elucidated.     

Histophysiology of the microvascular bed in experimental trauma

1. Morphohistological changes in a focus of spinal cord trauma have a phasic character, with a period of primary lesions (5-30 min after traumatization) and a period of secondary lesions (1-23 h after traumatization). 2. Variation of transport enzyme activities in the walls of the microvessels of the traumatized spinal cord is characterized by an undulating course and by asynchrony of the peaks of Mg-dependent ATPase and alkaline phosphatase activity. 3. With reference to the rapid drop in the given enzyme activities and to progressive necrotic changes in the traumatized spinal cord, it is desirable that the cord circulation should be corrected within the first few hours after traumatization.     

Pharmacokinetic studies of methionine in rats using deuterium-labeled methionine quantitative assessment of remethylation

The pharmacokinetics of methionine has been studied in rats by means of stable isotope methodology. After the i.v. bolus injection of [2H7]methionine (5 mg/kg body wt.), the plasma concentrations of [2H7]methionine, demethylated [2H4]homocysteine and remethylated [2H4]methionine were determined simultaneously with endogenous methionine and homocysteine by gas chromatography-mass spectrometry. The half-life for [2H7]methionine were 35.0 +/- 6.9 min. The appearance of the metabolites, [2H4]homocysteine and [2H4]methionine, in the plasma was very rapid. The fraction of [2H7]methionine that remethylated to [2H4]methionine through [2H4]homocysteine were 0.185 +/- 0.028. The administered [2H7]methionine did not influence the plasma levels of endogenous methionine and homocysteine. The present stable isotope methodology has made it possible to evaluate the pharmacokinetics of methionine, including the estimation of remethylation.     

Concentration of erythrocyte-based magnetic carriers in the vascular bed

The in vivo and in vitro experiments have shown that magnetic erythrocytes (loaded with ferromagnetic material) can be retained in certain sites of the vascular bed. Magnetic erithrocytes could be concentrated in the abdominal part of the dog aorta using a small permanent magnet fixed on the outer wall of the aorta.     

Status of the circulatory bed of the vascular membrane of the eyeball and retrobulbar structures during experimental venous stasis

In 43 test animals the state of the blood bed in the retrobulbar formations and the eyeball vasular tunic has been studied under venous congestion produced by ligation of the anterior vena cava (in dogs) and both external jugular veins (in rabbits). A complex of histological, histotopographic, morphometric and variation-statistical techniques has been used. The results obtained demonstrate that disturbances in the venous outflow in the anterior vena cava system produce certain responses in all parts of the retrotubular adipose tissue, of the eyeball muscles, of the optic nerve tunics, of the vascular tunic. Certain stageness is noted in the course of venous congestion. Places of the greatest morphological changes in the eyeball vascular tunic are determined. They are zones of vorticose veins formation and the area corresponding to the posterior pole of the eyeball. The analysis of the specific areas of the intermuscular arteries and veins cross sections demonstrates that in the reaction of these vessels to the different venous outflow in the anterior vena cava system these is certain unevenness in different ofthalmic muscles.     

The generation of prostacyclin by arteries and by the coronary vascular bed is reduced in experimental atherosclerosis in rabbits.

Experimental atherosclerosis in rabbits was associated with a suppression of prostacyclin generation from exogenous arachidonic acid by the coronary vascular bed. The spontaneous formation of prostacyclin by incubated rings of mesenteric artery was also diminished. These results suggest that in atherosclerosis an impaired activity of the endothelial prostacyclin synthexizing system contributes to the intra-arterial formation of thrombi.     

A comprehensive approach to visual and functional assessment of experimental vascular lesions in vivo

The role of metabolic factors derived from cardiac muscle in the development of reactive hyperemia after brief occlusions of the coronary circulation seems to be well established. However, the contribution of occlusion-induced changes in hemodynamic forces to eliciting reactive hyperemia is less known. We hypothesized that in isolated coronary arterioles changes in intraluminal pressure and flow, during and after release of occlusion (O/R), themselves via activating intrinsic mechanosensitive mechanisms, elicit release of vasoactive factors resulting in reactive dilations. Thus in isolated coronary arterioles (diameter: 88 +/- 8 microm) changes in diameter to changes in pressure or pressure plus flow (P+F) during and after a brief period (30, 60, and 120 s) of O/R of cannulating tube were measured by videomicroscopy. In response to both types of O/R, diameter first decreased, then, subsequently increased during occlusions. When only pressure was changed (from 80-10-80 mmHg), after release of occlusion, peak dilations increased as a function of the duration of occlusions. After flow was established (30 microl/min), O/R elicited changes in both pressure and flow (from 80-10-80 mmHg and from 0 to 30 microl/min). In these conditions, after the release of occlusions, not only the peak but also the duration of reactive dilation increased significantly as a function of the length of occlusions. The dilations during, and peak dilations after occlusions both in pressure and P+F protocols were significantly reduced by the inhibition of NO synthase with Nomega-nitro-L-arginine-methyl-ester (L-NAME) or by endothelium removal, whereas duration of postocclusion dilations were reduced by L-NAME or by endothelium removal only in P+F protocols. Furthermore, in both protocols, catalase significantly reduced the peak but not the duration of reactive dilations. Thus, mechanosensitive mechanisms that are sensitive to deformation, pressure, stretch, and wall shear stress elicit release of NO and H2O2, resulting in reactive dilation of isolated coronary arterioles.