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Biomedical subjects

R I Sokolova

Publications and source records attributed to R I Sokolova.

At least 19 recordsLinked to original sources
PubMed2005

[Hibernation and stunning as manifestations of ischemic dysfunction of the myocardium].

Hibernation and stunning are phenomena which constitute a basis of dysfunction of the myocardium appearing as a consequence of chronic ischemic heart disease and of myocardial revascularization. Myocardial stunning is an acute derangement of contractility of ischemic myocardium at the moment of restoration of coronary blood flow by various interventions (bypass grafting, angioplasty, thrombolysis). Myocardial hibernation implies presence of chronically developing foci of reduced contractility located in the area of myocardium supplied by obstructed artery. There is a following difference between these phenomena: stunning is a complex of structural and metabolic disorders during the state of "ischemia-reperfusion" while hibernation is a process of adaptation of the myocardium to chronic ischemia consisting in switch of metabolism to alternative type of energy production (anaerobic glycolysis). Exploration of pathophysiology and morphology of hibernating and stunned myocardium is necessary for elaboration of methods of protection against ischemic injury.

Diagnosis, Differential↗
PubMed2004

[Apoptosis and hibernation of cardiomyocytes of periscar zone as factor of chronic cardiac aneurysm progression].

Tissue specimen from chronic aneurysms and adjacent myocardium obtained at aneurysmectomy and coronary bypass surgery from 46 patients were subjected to morphological study. Immunohistochemical methods and electronic microscopy were applied for detection of apoptosis and hibernation of cardiomyocytes in 11 cases and histochemical determination of activity of energetic enzymes succinate and lactate dehydrogenase was used in 5 cases. Cardiomyocytes from peri and intra scar layers of myocardium were found to be in a state of hibernation while some of them were in a state of apoptosis. Extent of apoptosis was different in aneurysms on different stages of organization. Number of altered cardiomyocytes was the greatest in immature aneurysms. Basing on these findings apoptosis of hibernating cardiomyocytes was suggested to be one of factors of expansion of sclerotic zone and aneurysm formation.

Apoptosis↗
PubMed2003

[Comparative morpho-functional assessment of the impact produced by prolonged infusions of prostaglandins E and F on the course of genetically preconditioned arterial hypertension].

The administration of prolonged intravenous infusions of prostaglandins is defined; the method provided for specifying a long-term impact produced by prostaglandins on a nature of the course of genetically preconditioned arterial hypertension (AHT) in rats. Infusions of PGE-2 bring about a prolonged and stable reduction of mean arterial presser (AP) by 10% versus its original value; they intensify 2-fold the depressor baroreflectory regulation and stimulate the urinary excretion of endogenous renal PGF-2 alpha; besides, they contribute to a better blood supply to organs, i.e. an increased perfusion of the cortical and medullary layers of the kidneys and of the brain substances; and dilatation of the intramural branches of the coronary arteries, due to which the AP becomes milder. Infusions of PGF-2 alpha contribute to a prolonged and stable elevation of mean AP by 12% versus the original value; they inhibit the depressor baroreflectory regulation and intensify the pressor baroreflectory regulation; they, additionally, induce the urinary excretion of endogenous renal PGF-2 alpha and correct the lesions in the blood supply to organs, i.e. pathological microcirculation, anemia and spasm of the renal parenchyma, ischemic foci in the myocardium, spastic contraction of small cerebral arteries, edema and destructive changes (of the local necrosis variation) in the cerebral substance microvessels concomitant with a commencing diapedetic hemorrhages. Finally, all above listed lesions are signs of the malignant AP course.

Animals↗
PubMed1999

Evidence for an antihypertensive factor from the adrenal medulla of SHR modulating neurogenic vasoconstriction.

The aim of this study is to investigate some vasoactive properties of the blood of spontaneously hypertensive rats (SHR). Isolated segments of rat tail arteries obtained from normotensive rats (Wistar-Kyoto (WKY) and Wistar) were perfused with blood from conscious donor rats (WKY, Wistar or SHR). Alterations of the neurogenic constrictor responses (NCR) of the isolated segments evoked by electrical stimulation were studied. The amplitude of NCR of the isolated arteries was studied during perfusion with blood according to the perfusion scheme WKY1(1)-SHR1(2)-WKY1(3) and WKY1(1)-WKY2(2)-WKY1(3). The release of 3H-noradrenaline ([3H]-NA) from vascular sympathetic fibres was measured. The influence of adrenal demedullation on NCR was estimated. We have shown that NCR of isolated arteries decreased by 28.3 +/- 7.9% (P < 0.05 vs. WKY1(1)) during perfusion with blood from SHR (scheme WKY1(1)-SHR1(2)-WKY1(3)). In these experiments, release of [3H]-NA from sympathetic fibres of the artery segments decreased by 39.9 +/- 9.6% during the perfusion with blood from SHR vs. WKY1(1) (P < 0.05). Adrenal demedullation prevented the decrease of NCR during perfusion of the arteries with blood from SHR. In conclusion, the blood of SHR has some antihypertensive factor(s), which causes decrease of NCR in the tail artery from normotensive rats. This decline is accompanied by the decrease of release in [3H]-NA from the transmural sympathetic fibres and is abolished after adrenal demedullation of blood donor rats.

Adrenal Medulla↗
PubMed1993

[The effect of captopril on the arterial pressure, structural resistance and vascular reactivity of the kidney in rats with nephrogenic hypertension].

The angiotensin-converting enzyme inhibiting agent captopryl suppressed a moderate hypertension in rats with pyelonephritis and with ureteral obstruction, but not in rats with ureteral obstruction combined with the renal artery constriction. The suppression of the hypertension was accompanied by a reversion of structural alterations in the blood vessels.

Animals↗
PubMed1992

[Functional state of the adrenals in various forms of arterial hypertension].

The study of structural changes and changes of the aldosterone content (AC) in the surgically removed adrenals of patients with different clinical variants of combination of the arterial hypertension (AH), low--renin hyperaldosteronism and space--occupying lesions in the adrenals found by CT was carried out. In 15 of 20 patients after adrenalectomy the diagnosis of the primary aldosteronism (PA) was established, in 4 cases diagnosis of the hypertension, 2B degree, and in one case the diagnosis of Cushing disease. The functional state was evaluated according to AC in the adenomas and macronodes and in the adjacent cortex as well as by nuclei size of cells producing aldosterone. The aldosterone hyperproduction was shown to be associated with local adenoma in some cases and with hyperactive cortex in the others this being reflected in the course of AH and in the adrenalectomy hypotensive effect.

Adenoma↗
PubMed1990

[Plasma mineralocorticoids--aldosterone and desoxycorticosterone-- in patients with"low-renin"arterial hypertension].

The plasma aldosterone (A) and desoxycorticosterone (DOCS) levels were measured in 10 patients with primary aldosteronism and in 2 subgroups with low-renin hypertensive disease (LRHD): (1) those with normal adrenal glands++ (n - 11) and (2) those with structural changes in the cortex (n - 11). The patients from Subgroup 1 showed the lowest basal A and DOCS levels (107.29 +/- 12.90 and 0.080 +/- 0.013 ng/ml, respectively) and low concentrations of the two hormones after stimulation of 4-hour walk (211.57 +/- 30.47 and 0.095 +/- 0.024 ng/mg, respectively). In the patients from Subgroup 2, the basal and 4-hour post-walk++ A and DOCS contents were increased in the cortex (basal 201.50 +/- 41.59 and 0.177 +/- 0.36 ng/mg and poststimulation 331.33 +/- 30.47 and 0.302 +/- 0.061 ng/ml, respectively). Some patients with primary aldosteronism displayed the same DOCS response to stimulation as did those with LRHD in the presence of structural cortical changes. Histological examination of operative biopsy specimens indicated that higher DOCS levels were associated with diffuse nodal hyperplasia of the zona fasciculata in the cortex. The results suggest that there may be a LRHD variant running with excessive DOCS secretion and related to pathogenetically related to hyperplasia of predominantly the zone fasciculata in the adrenal cortex.

Adrenal Cortex↗
PubMed1990

[Significance of single-dose captopril test in the differential diagnosis of primary aldosteronism].

The captopril test was used to make a differential diagnosis of various types of primary aldosteronism. After captopril, there was no change in the activity of the renin-angiotensin-aldosterone system only in the group of patients with aldosterone-producing adenomas in a histological variant of "adenoma and atrophy". The findings suggest that aldosterone secretion regulation is autonomic in the adenoma unassociated with the function of the renin-angiotensin-aldosterone system only in the case of isolated adenoma with a histological variant of adenoma and atrophy. In patients with aldosterone-producing adenomas in the presence of the variant "adenoma and hyperplasia", aldosterone secretion retains sensitivity to the renin-angiotensin-aldosterone system as in patients with idiopathic hyperplasia and hypertensive disease, which indicates that it is possible to differentiate isolated "adenoma and atrophy" from hypertensive disease and idiopathic hyperplasia, despite its combination with tumor by using the captopril test.

Adenoma↗
PubMed1989

[A comparison of selective microproteinuria with histomorphology of the kidneys in patients with arterial hypertension].

Urinary excretion of individual proteins has been examined in 30 patients suffering from arterial hypertension, subjected to renal biopsy. The findings indicate an increased excretion of the proteins associated with the localization of the morphologic shifts in the kidneys. Thus, glomerular abnormalities are characterized by a 10-30-fold increase of albumin and IgG excretion with the urine and normal values of beta-2-microglobulin (beta-2-MG); canalicular abnormalities are associated with normal urine albumin or microalbuminuria and 10-40-fold increased excretion of beta-2-MG, paralleled by increased urine N-acetyl-B-glucosaminidase activity, this latter shift indicating grave tubulointerstitial changes. Hypertensive changes of the vessels involve microalbuminuria. Quantitative and qualitative characteristics of proteinuria may become an additional test in the differential diagnosis of symptomatic arterial hypertension.

Adult↗
PubMed1989

[Hypertensive disease and renal hypertension (structural and functional studies of the kidneys using dynamic computerized tomography)].

Renal functional and structural studies were performed in 46 patients with arterial hypertension: out of them 12 had hypertensive disease, 13, chronic pyelonephritis, 21, a hypertensive type of chronic glomerulonephritis. In each case, the clinical diagnosis was evidenced by one of the invasive techniques. Dynamic computed tomography was conducted by the original methods; the findings were analyzed by taking into account time-density curves which made it possible to gain an insight into the status of blood flow and filtration in each individual kidney. Computed tomography and dynamic computed tomography revealed that hypertensive disease was characterized-by normal volume and thickness of the renal cortical layer and symmetric time-density curves, whereas a hypertensive type of chronic glomerulonephritis featured lower renal cortical layer thickness, reduced renal volume, symmetrically decrease amplitudes of the first and second peaks of the time-density curve, chronic pyelonephritis showed asymmetric time-density diagrams due to the lower density areas in the afflicted kidney.

Adult↗
PubMed1989

[The diagnosis of hypertension (research on kidney biopsies and microalbuminuria].

Patients with essential hypertension, hypertonic glomerulonephritis and Conn's syndrome were examined for excretion of albumin, immunoglobulin G and beta 2-microglobulin. The results obtained were correlated with pathological changes in liver parenchyma according to biopsies withdrawn from the patients. Essential hypertension running a benign course was not characterized by pronounced changes in excretion of the above proteins. Injury to the glomerular apparatus of the kidneys in glomerulonephritis was attended by considerable rise of albumin and immunoglobulin excretion whereas injury to the tubular structures by the increase of beta 2-microglobulin excretion. It is suggested that analysis of microalbuminuria can be used in the differential diagnosis of arterial hypertension running its course in association with the minor urinary syndrome.

Albuminuria↗
PubMed1989

[Clinico-morphologic characteristics of 2 tumor forms of primary hyperaldosteronism].

Unilateral adrenalectomy was performed in 32 patients with primary hyperaldosteronism due to tumour of the adrenal gland and with arterial hypertension (AH) of various degree of severity. Stable normalization of AH occurred in 14 patients and in 18 its course improved. The results of a retrospective analysis of a hypotensive effect, the morphological picture of the removed adrenal and the findings of clinico-biochemical and instrumental study made it possible to establish preoperatively the diagnostic criteria for the identification of two tumorous forms of primary hyperaldosteronism: aldosterone-producing adenoma proper and the tumorous form of adrenocortical hyperplasia. They have different pathogenesis and postadrenalectomy hypotensive effect.

Adenoma↗
PubMed1989

[Renin-angiotensin system in sudden cardiac death: biochemical and morphological aspects].

The renin activity of the blood plasma (RAP), renal cortex (RARC), juxtaglomerular apparatus (JGA) and renal microcirculation were studied in 330 male patients after sudden death. The activity of the renin-angiotensin system (RAS) is shown to be increased in sudden cardiac death (SCD) particularly in patients dying in the presence of alcoholic intoxication. The values of RAP and RARC and their correlation depend on the ethanol concentration in the blood. In cases of SCD with chronic alcoholic intoxication the signs of JGA hyperfunction are found (diffuse hypertrophy of the JGA structural elements). The investigation of the kidney microcirculation revealed two main phenomena of the circulation disturbance--juxtamedullary shunting and congestion. The interconnection between the degree of RAS activity and the type of the microcirculatory damage is established. The congestion was more frequently observed at the low and medium RAP values while the juxtamedullary shunting--at the high levels of the renin activity.

Alcoholic Intoxication↗
PubMed1988

[Myocardial hypertrophy, arterial hypertension and sudden cardiac death].

721 cases of sudden coronary death (SCD) of men aged 30-59 were studied. It was found out that SCD happened in majority of cases in subjects with increased weight of heart: 44.2% of patients had heart weight of 500 g or more. A special histomorphometric study of kidneys (345 cases of SCD) revealed arterial hypertension (AH) in 41.2% of cases, which far exceeded AH incidence in the population of men of equal age. Nevertheless, not in all cases of SCD was myocardial hypertrophy caused by AH. In patients with no AH myocardial hypertrophy was usually caused by postinfarction cardiosclerosis. In certain cases of SCD without cardiosclerosis accompanied by manifest myocardial hypertrophy there were signs of dilatative or hypertrophic cardiomyopathy. The obtained results suggest that AH and increased weight of heart should be considered factors predisposing to SCD.

Adult↗
PubMed1988

[Tubulointerstitial nephritis in Conn's syndrome].

The evaluation of 79 renal biopsies from patients with primary aldosteronism established pathology in one-fourth of the examinees. There were specific dystrophic and atrophic lesions of the tubular apparatus, focal interstitial sclerosis and disseminated round-cell infiltrates. Immunomorphological evaluation showed these to have macrophages and T lymphocytes as cellular components. The process manifested clinically by steady hypofunction of osmotic diuresis in the absence of bacterial inflammation and calycine-pelvic destruction. No relation of this condition with inflammation in onset and signs of immune origin of such give good grounds to refer the pathology to tubulointerstitial nephritides of immune genesis.

Antibodies, Monoclonal↗