[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.

[Apoptosis and hibernation of cardiomyocytes of periscar zone as factor of chronic cardiac aneurysm progression]. / Apoptoz i gibernatsiia kardiomiotsitov perirubtsovoi zony kak faktor progressirovaniia khronicheskoi anevrizmy serdtsa.

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.

[Comparative morpho-functional assessment of the impact produced by prolonged infusions of prostaglandins E and F on the course of genetically preconditioned arterial hypertension]. / Sravnitel'naia morfofunktsional'naia otsenka vliianiia prolongirovannykh infuzii prostaglandinov E i F na techenie geneticheski obuslovlennoi arterial'noi gipertonii.

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.

[Hibernation and stunning as manifestations of ischemic dysfunction of the myocardium]. / Gibernatsiia i stanning kak proiavlenie ishemicheskoi disfunktsii miokarda.

Current information on hybernation and stunning which are the basis of myocardial dysfunction resulting from chronic ischemic heart disease and revascularization is provided. Myocardial stunning is an acute disturbance of a contractile function of ischemic myocardium at the moment of coronary circulation restoration done by various methods (coronary shunting, angioplasty, thrombolysis). Myocardial hybernation is a chronically developing foci of subnormal contractility in the region of stenotic artery. The difference between them is that stunning is a complex of structural and metabolic damages under the condition "ischemia-reperfusion" while hybernation is an adaptation of the myocardium to chronic ischemia by metabolism switching to anaerobic glycolysis. The study of pathophysiology and morphology of hybernating and stunned myocardium is necessary for developing methods of myocardium protection from ischemic damage.

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.

[Hyperplastic changes and aldosterone content in the adrenal cortex in essential hypertension and primary aldosteronism]. / [Giperplasticheskie izmeneniia i soderzhanie al'dosterona v kore nadpochechnikov pri éssentsial'noi gipertonii i pervichnom al'dosteronizme.

Autopsy and operative material (adrenalectomy for hyperaldosteronism) was studied to elucidate morphology, incidence of nodules, aldosterone content in the adrenal of patients with essential hypertension (EH). It was established than nodular masses in the adrenals in the form of micro and macronodules are present in 80% of EH patients. Aldosterone content in the adrenals in both nodules and in the adjacent cortex is significantly higher than in the adrenals of patients without EH. This fact as well as increased cell nuclei size in the fascicular and glomerular zones indicate high secretory activity of the adrenals in EH. Clinicomorphological comparisons in patients after adrenalectomy because of hyperaldosteronism syndrome allow to conclude that grave forms of EH may be followed by aldosteronism syndromes with nodular hyperplasia of the adrenal cortex being the basis of the syndrome. Indications to adrenalectomy require clear criteria of differential diagnosis with primary aldosteronism.

[Mediacalcinosis of the aorta (pathomorphology and pathogenesis of arterial calcification and its relationship to atherosclerosis)]. / Mediakal'tsinoz aorty (k voprosu patomorfologii i patogeneza kal'tsifikatsii arterii i vzaimootnosheniia s aterosklerozom).

It is established on the material of 116 legal-medical autopsies of 11-50-year-old subjects deceased of occasional causes that calcinosis of the aorta media appears in subjects under 20 years and progresses with age. As distinct from the aorta, the first calcium deposits in the coronary arteries appear in the intima, in the foci of muscular-elastic hyperplasia. Calcium deposits in the coronary and other arteries appear a decade later than in the aorta. The beginning of the mediacalcinosis coincides in time with focal intima lipoidosis but the correlation between the intima thickening and the intensity of mediacalcinosis is not observed. Calcinosis of the atherosclerotic plaques appears in preexisting mediacalcinosis. Calcium deposits are closely linked with the elastica, and the media calcinosis occurs in the elastica destruction and is not followed by proliferation of the smooth cells. Cell membrane fragments and vesicular structures are found ultrastructurally in the calcinosis foci, this suggesting that the mediacalcinosis is connected with the elastica destruction and the smooth cell death.

[The effect of captopril on the arterial pressure, structural resistance and vascular reactivity of the kidney in rats with nephrogenic hypertension]. / Vliianie kaptoprila na arterial'noe davlenie, strukturnoe soprotivlenie i reaktivnost' sosudov pochi u krys s nefrogennoi gipertenziei.

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.

[Functional state of the adrenals in various forms of arterial hypertension]. / Otsenka funktsional'nogo sostoianiia nadpochechnikov pri nekotorykh formakh arterial'noi gipertenzii.

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.

[Significance of single-dose captopril test in the differential diagnosis of primary aldosteronism]. / Znachenie testa s odnorazovym priemom kaptoprila v differentsial'noi diagnostike pervichnogo al'dosteronizma.

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.

[Plasma mineralocorticoids--aldosterone and desoxycorticosterone-- in patients with"low-renin"arterial hypertension]. / Mineralokortikoidy plazmy--al'dosteron i dezoksikortikosteron-- u bol'nykh s "nuzkoreninovoi" arterial'noi gipertoniei.

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.

[Hypertensive disease and renal hypertension (structural and functional studies of the kidneys using dynamic computerized tomography)]. / Gipertonicheskaia bolezn' i pochechnye gipertonii (strukturnoe i funktsional'noe issledovanie pochek s ispol'zovaniem dinamicheskoi kompiuternoi tomografii).

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.

[Morphofunctional characteristics of endocrine nephropathy in primary aldosteronism]. / Morfofunktsional'naia kharakteristika éndokrinnoi nefropatii pri pervichnom al'dosteronizme.

Tubular functions and the state of renal parenchyma were evaluated in 45 patients with primary aldosteronism (PA) in order to assess morphological and functional characteristics of PA-associated endocrine nephropathy. Data on acid excretion and concentration activities were compared to morphologic findings in renal biopsy specimens, obtained at adrenalectomy. It is demonstrated that endocrine nephropathy may be manifested clinically in two ways: 1) increased secretion combined with a reversibly depressed maximum osmotic urinary concentration; and 2) persistent depression of both functions. The first variant can be seen in cases of high aldosteronemia, marked hypokalemia and recent disease. The morphological substrate of these disorders is hypokalemic tubulopathy, reflected in tubular epithelium vacuole dystrophy of varying degrees. The other variant is seen in cases of moderate aldosteronemia and hypokalemia and long duration of the disease, involving severe hypertension. The morphologic substrate of these tubular disorders is nephropathy with a marked tubulo-interstitial component (chronic tubulo-interstitial nephritis).

[Clinico-morphologic characteristics of 2 tumor forms of primary hyperaldosteronism]. / Kliniko-morfologicheskaia kharakteristika dvukh opukholevykh form pervichnogo gipera'ldosteronizma.

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.

[A comparison of selective microproteinuria with histomorphology of the kidneys in patients with arterial hypertension]. / Sopostavlenie selektivnoi mikroproteinurii s gistomorfologiei pochek bol'nykh s arterial'noi gipertoniei.

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.

[The diagnosis of hypertension (research on kidney biopsies and microalbuminuria]. / Diagnostika gipertonicheskoi bolezni (issledovanie bioptatov pochek i mikroalbuminurii).

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.

[Renin-angiotensin system in sudden cardiac death: biochemical and morphological aspects]. / Renin-angiotenzinnaia sistema pri vnezapnoi sedechnoi smerti: biokhimicheskie i morfologicheskie aspekty.

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.