[Effect of Visken therapy on the lymphocyte beta2-adrenoceptor-dependent adenylate cyclase system in essential hypertension].
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Biomedical subjects
Publications and source records attributed to V P Masenko.
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Ventricular arrhythmias were analysed in 38 patients with Stages I-IIB heart failure from 24-hour Holter monitoring data obtained before and after digoxin therapy by comparing with the concentrations of catecholamines. There was a direct relationship between the plasma levels of epinephrine and norepinephrine and the severity of ventricular arrhythmias, as well as between the changes in cumulative catecholamine levels and ventricular arrhythmias during digoxin therapy. Virtually in all cases, the antiarrhythmic effect of the drug was accompanied by lower plasma catecholamine concentrations whereas the levels of norepinephrine and epinephrine remained nearly unchanged or increased with the tentatively arrhythmogenic action. The findings may suggest that hypercatecholaminemias are essential in the genesis of ventricular arrhythmias in heart failure. Cardiac glycosides can heterogeneously affect ventricular arrhythmias by modifying the activity of the sympathoadrenal system.
The results from recent studies suggest that the endogenous opioid beta-endorphin (beta-E) is related to pain modulation. Therefore, plasma beta-E levels were studied in 23 patients with essential hypertension (EH) and in 7 patients with coronary artery disease (CAD) during asymptomatic ischemic events and in 5 patients with CAD during symptomatic ischemic events. Blood samples for beta-E were taken at the moment of silent ST depression, pointed with alarm by the real time ECG monitor "Q Med Monitor" (USA). Control blood samples were taken under the same conditions without ischemic events. Control plasma beta-E levels were significantly higher (p less than 0.01) in patients with EH as compared to that in both groups of patients with CAD (22.9 +/- 4.0 vs 7.0 +/- 1.9 and 4.5 +/- 1.6 pmol/l). At the time of silent ischemia, beta-E showed a significant increase in patients with EH (+10.1 +/- 2.1 pmol/l, p less than 0.01) and in patients with CAD (+10.7 +/- 1.3 pmol/l, p less than 0.05) as compared to the control levels. However, plasma beta-E showed no increase (+1.0 +/- 0.6 pmol/l, p greater than 0.1) during symptomatic ischemia as compared to the control levels. Thus, differences in the circulating levels of beta-E may be associated with the presence or absence of pain during myocardial ischemia.
Platelet aggregation and prostaglandin levels were examined in 50 patients with coronary heart disease concurrent with Functional Classes II-III angina who received nitroglycerin-retard (n = 20; Group 1), corovas (n = 20; Group 2), and placebo (n = 10; Group 3). Long-acting nitrates were found to exert a positive action on thrombocytic hemostasis as decreased platelet aggregation and reverse aggregation in 25% of the corovas-treated patients. Placebo failed to have the same action. Nitroglycerin-retard caused an increase in prostacyclin concentrations. Nitroglycerin-retard and corovas produced a clear-cut antianginal effect. They promoted the reduction in the number of anginal episodes and of nitroglycerin tablets used. No antianginal effect was absent when placebo was used.
The purpose of the study was to explore the dynamics of the concentration of atrial natriuretic hormone (ANH) in response to changes in arterial pressure including those induced by hypertonic crisis, 7-day hypotensive monotherapy with the drugs having different action mode, and the acute test with the basic hypotensive drugs. 75 patients suffering from arterial hypertension were entered into the study. Measurements of the concentration of ANH in blood plasma were performed by radioimmunoassay with the aid of the kits manufactured by the Amersham Company (Great Britain). The activity of renin and aldosterone was determined by radioimmunoassay according to the standard technique. A strong positive correlation was revealed between the concentration of ANH and the level of both systolic and diastolic AP. A significant rise of the concentration of ANH elicited by hypertonic crisis reflects the growth of the tension of the depressor mechanisms by which AP is regulated. The lack of significant changes in the level of ANH during the acute pharmacological tests and effective continuous treatment with the hypotensive drugs attests to the existence of the complex mechanisms that regulate ANH secretion, determined not only by the level of AP.
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The examination comprised 58 patients with essential hypertension and 17 with nephrogenic arterial hypertension. An analysis of the baseline levels of natural natriuretic factor in patients with essential and nephrogenic hypertension revealed no intergroup differences (55.3 +/- 3.0 and 45.7 +/- 5.2 ng/ml, respectively). The concentration of natural natriuretic factor was significantly higher in even patients with mild arterial hypertension than in healthy persons (28.4 +/- 4.7 and 17.4 +/- 2.9 ng/ml). There was a direct correlation between the level of natural natriuretic factor and blood pressure and left ventricular myocardial hypertrophy. There were higher positive correlations between the levels of natural natriuretic factor and those of hormones of the renin-angiotensin-aldosterone system and catecholamines in patients having a diastolic pressure of greater than 115 mm Hg. A significant increase in natural natriuretic factor levels (92.1 +/- 11.8 ng/ml) was found in the presence of hypertensive crisis.
Serum neopterin was measured over time (from 3 to 24 months) by RIA in 15 patients with dilated cardiomyopathy. Comparison with the clinical data revealed that the initially normal concentration of neopterin (less than 9 nM/l) was associated with a stable disease course on a long-term observation (group I). The second group with an initially high neopterin concentration showed an objective improvement of the health status together with normalization of the neopterin level. The third group of patients were characterized by an increase of the neopterin level measured over time, coupled with a disease progress. It should be noted that 5 out of 8 patients died. In addition to neopterin measurements, the patients with dilated cardiomyopathy were examined for serum beta-2-microglobulin (beta-2M). Analysis of the data obtained has demonstrated a similar relationship between the level of neopterin and beta-2M and the clinical course of dilated cardiomyopathy. Still, neopterin is a more sensitive marker. Therefore, the data obtained attest to a possibility of the use of serum neopterin as a prognostic marker in patients suffering from dilated cardiomyopathy.
The article deals with experience in the first transplantation of a heart-lung complex in the USSR. The recipient was a 34-year-old male with dilation cardiomyopathy. It was decided to perform the transplantation because the terminal stage of cardiac failure and secondary pulmonary hypertension developed (cardiac index 1.3 l/m, pressure in pulmonary artery 80/50 mm Hg, resistance of pulmonary vessels 10.4 units after Wood). The heart and lung were transplanted from a 19-year-old male who died from a craniocerebral injury. Cyclosporine, metipred , imuran, dopamine in small doses, cardiotonics, and antibiotics were given in the postoperative period; the patient was kept on artificial respiration for 48 hours. For up to 10 days the patient's condition was relatively stable and his consciousness was clear. Bilateral pneumonia developed, however, from which he died on the 12th postoperative day. The article discusses organizational problems and some questions of immunosuppressive therapy, immunological monitoring, and the management of patients after transplantation of a heart-lung complex.
Adrenal glucocorticoid function was studied in 56 newborns with natal injuries of the cervical section of the spine and the contribution of the hypoxic factor to such injuries defined. The babies were examined by the cliniconeurologic and electron-neuromyographic methods in order to specify the level of the injury. Blood serum and umbilical blood hydrocortisone levels were radioimmunoassayed immediately at birth and on days 5-7 of life. Spinal injury at the C1-C4 level was associated with low hydrocortisone levels, that may be regarded as an additional criterion for the differentiation of the level of injury in traumas of the cervical portion of the spine in the newborns.
A radioimmunoassay study of procollagen type III end protein (PEP) was conducted in the serum of 11 patients with confirmed dilated cardiomyopathy (DCMP) and 9 patients with coronary heart disease. For DCMP patients PEP levels averaged 8.8 +/- 7.9 micrograms/l, for coronary patients 4.4 +/- 1.6 micrograms/l, in donors 1.7 +/- 1.4 micrograms/l. Thus, the difference between DCMP and coronary patients, donors appeared significant (p less than 0.05). PEP concentrations over 4.5 micrograms/l occurred in 54% of DCMP patients. Growing of PEP turned out most substantial in severe disease (circulatory failure stage IIB-III, pulmonary thromboembolism). Determination of PEP is thought valid for laboratory diagnosis of myocardial inflammation and fibrosis. The discussion covers possible causes and mechanisms underlying high production of PEP from the view point of impaired collagen production.
A relationship was examined between blood vasopressin levels and the fibrinolytic system in 35 patients with angina pectoris (16 with vasospastic angina (VA) and 19 with exercise-induced angina) who had undergone vein occlusion testing. There was a positive correlation between the post-testing vasopressin levels and the activity of tissue plasminogen activator inhibitor (TPAI) (r = 0.54) which was more high in patients with VA (r = 0.61). Only did the patients with VA show a direct relationship between the vasopressin concentrations and the activity of tissue plasminogen activator (TPA) (r = 0.63), the concentration of fibrinogen-fibrin degradation products (FFDP) (r = 0.88). Thirteen patients having higher vasopressin levels (over 3.4 ng/ml) displayed a greater TPAI activity than did the patients with vasopressin levels of at least 3.4 ng/ml (26.2 +/- 4.9 and 15.0 +/- 1.42 IU/ml, respectively; p less than 0.05). There was a direct relationship between the vasopressin levels and the activity of TPA (r = 0.65), the concentration of FFDP (r = 0.78) in patients having a vasopressin level of above 3.4 ng/ml. The findings are in agreement with the concept that endogenous vasopressin is involved in the regulation of the blood fibrinolytic system.
Seventy four patients aged 35-74 years who had mitral valvular disease were examined for renin, angiotensin II, aldosterone, and vasopressin, of whom 49 patients were diagnosed as having a mitral valve defect with prevalent stenosis, 25 presented with a mitral valve defect with prevalent heart failure. Circulatory disorders, Stages I-II, were found in 41 patients, Stage IIB in 23, and Stage III in 10 patients. There were no significant differences in the parameters of the renin-angiotensin-aldosterone system (RAAS) and vasopressin in untreated adult and elderly patients with mitral valvular disease at rest. As circulatory disorders progressed, the RAAS parameters significantly increased in all the groups. However, the patients with prevalent stenosis showed higher blood renin levels than did those with prevalent heart failure, irrespective of its severity. In refractory heart failure, the significant differences remained to a greater extent only for renin. The treatment with peripheral vasodilators (isosorbide dinitrate and corinfar) resulted in compensatory activation of the neurohumoral vasoconstrictive system, thereafter the RAAS parameters significantly increased after the drugs.
A study was made of the concentration of endothelin (ET) in the plasma of patients suffering from arterial hypertension (AH), heart failure (HF) and in that of healthy volunteers. The concentration of ET in the normal subjects was within 4.0-8.6 pg/ml, in the patients with AH, it varied from 5.7 to 64.5 pg/ml, and in the patients suffering from HF, from 8.8 to 94.0 pg/ml. A subgroup of patients with essential hypertension, stage II B, showed a tendency towards a rise of the ET concentration in response to orthostatic load that was associated with an increase of the concentration of angiotensin-2.
Seventy-six patients with chronic heart failure, stages I-III, that developed after different heart diseases were examined. Catheterization of the right heart was carried out in 51 patients. The concentration of immunoreactive atrial natriuretic factor (ANF) in peripheral blood plasma and in the blood from the right atrium was increased in patients and rose as heart failure progressed. No correlation was discovered between the character of heart disease and the concentration of immunoreactive ANF in the plasma. The latter one was directly dependent on the wedging pressure in the pulmonary artery and on the pressure in the right atrium. The level of immunoreactive ANF in the atrium was higher than in the periphery. However, that was not of statistical power.
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Renin-angiotensin-aldosterone++ system was investigated in 60 patients suffering from rheumatoid arthritis. Forty-four of them (group 1) had arterial hypertension (144 +/- 4/94 +/- 2 mm Hg), sixteen were free of hypertension (120 +/- 3/80 +/- 1 mm Hg). Twenty-nine control subjects comparable by AH standing and demographic parameters had essential hypertension stage IB-IIA by A. L. Myasnikov classification (141 +/- 3/89 +/- 1 mm Hg). A tendency to renin suppression was dominating in 72% of group 1 patients (plasma renin activity less than 1.0 ng/ml/h). In this group there appeared high concentrations of A II (14.2 +/- 3.1 pg/ml) and plasma aldosterone++ (238 +/- 94 ng/ml). Rheumatoid vasculitis manifested in 86% of patients. Control subjects exhibited plasma renin activity greater than 3.0 ng/ml/hin 48%, average A II concentration was similar to that of group 1 (12.4 +/- 2.7 ng/ml/h, p greater than 0.05), plasma aldosterone++ level was significantly lower (176 +/- 29 ng/ml, p less than 0.05). Correlations were established between A II concentration and ESR (r = 0.39, p less than 0.05), A II and rheumatoid factor titers (r = 0.40, p less than 0.05). These indicate that immunopathological reactions are responsible for shifts in renin-angiotensin-aldosteron system in hypertensive rheumatoid arthritis subjects.
Fifteen patients with essential hypertension underwent treatment with captopril (7 patients) and ramipril (8 patients). The drugs belong to angiotensin-converting enzyme (ACE) inhibitors. Pretreatment immunological examination and that after a 10-15-week course of the above therapy involved measurements of IgG, IgA, IgE and beta 2-microglobulin. The analysis of the trend in the immunological indices demonstrated that captopril, distinct from ramipril by the presence of a sulfhydryl group, caused a decrease in immunological parameters suggesting a potential role of culfhydryl groups in mediating ACE inhibitor action on the immune system. The immunological properties of captopril may appear useful in various systemic diseases.