[Five-year dynamics adrenergic reactivity of erythrocytes after radio-frequency sympathic denervation of renal arteries in patients with resistant arterial hypertension].

AIM: To study the initial state of adrenergic reactivity and the five-year dynamics of the beta-adrenergic reactivity index of erythrocyte membranes and the manifestation of the antihypertensive effect of the procedure for radiofrequency destruction of sympathetic structures of the renal artery in patients with resistant arterial hypertension. SUBJECTS AND METHODS: The analysis included 42 patients with resistant arterial hypertension (RH). The renal denervation (RD) procedure of the kidneys was performed by endovascular bilateral transcatheter radiofrequency ablation of the renal arteries. The study of 24-hour blood pressure monitoring (BPM) and the determination of ß-adrenoreactivity of erythrocytes (ß-ARM) by changes in the osmoresistance of erythrocyte membranes were performed initially, 1 week, 6 months, 1, 2, 3 and 5 years after RD. Patients retrospectively, at a follow-up period of 6 months after RD, were divided into responders (decrease in blood pressure by 10 or more mm Hg) and non-responders (decrease in blood pressure less than 10 mm Hg). RESULTS: 6 months after the RD, the number of responders was 28 people (66.7%), after 5 years - 31 people (73.8%). At the time of inclusion in the study, the median ß-ARM in the group of non-responders was not significantly higher than in the group of responders. After 6 months after the RD procedure, the ß-ARM indicator in the non-responder group was significantly lower than in the responder group (p = 0.043). With further follow-up in the group of responders, an increase in the median ß-ARM was noted, which reached significant differences relative to the baseline values in the group at follow-up periods of 1 year (p = 0.036) and 5 years (p = 0.004) after RD. The change in the ß-ARM indicator in the non-responder group was wavy in nature, the changes did not reach the significance criteria. CONCLUSION: Renal denervation in 73.8% of cases is accompanied by a stable antihypertensive response for 5 years of observation and an increase in ß-ARM, which may indicate the implementation of compensatory mechanisms in conditions of increasing activity of the sympathoadrenal system in response to a decrease in blood pressure.

[Dynamics of adreneractivity after transfer of myocardial infarction: annual observation].

AIM: To study the change in the -adrenergic reactivity of red blood cell membranes in patients during the first year after acute myocardial infarction. MATERIALS AND METHODS: The study included 25 patients with acute myocardial infarction (AMI) who signed informed consent to participate in the study. The erythrocyte membrane -adrenoreactivity index (-ARM) was determined in venous blood samples upon admission to the intensive care unit, one day after admission, 6 and 12 months after the index MI was transferred using the BETA-ARM-AGAT reagent kit (Agat-Med, Russia). RESULTS: According to the results of dynamics assessment of -APM during the first day, patients included in the study were divided into 2 groups. Group 1 (n=14) included patients who had an increase in -APM in the first day, and group 2 (n=21) included patients in whom -ARM either did not change or decreased. At the time of admission to the hospital in the formed groups, there were no differences in the -APM index and clinical and anamnestic characteristics. A day after hospitalization, the value of -APM in group 1 significantly exceeded the same indicator in group 2 (p=0.02). At the periods of 6 and 12 months, the -APM indices in the groups did not differ. In the 2nd group of patients, the progression of chronic heart failure to one or more functional classes (NYHA) was significantly more often compared with the 1st group. CONCLUSION: The study showed that on the first day in patients with AMI, both an increase and a decrease in the activity of the sympathoadrenal system are possible with a further leveling of these differences over the next year. For a group of patients with decreased activity of sympathoadrenal system on the first day, a more unfavorable course of heart failure in the post-infarction period is characteristic.

[Age-dependent changes in adrenoreactivity in experimental postinfarction cardiosclerosis.]

Presently, there is growing interest in studying the activity of the sympathoadrenal system in the aging process of the body and the development of diseases of the cardiovascular system associated with age. The intention of the research is evaluation of ß-adrenoreactivity of erythrocyte membranes (ß-ARM) of intact rats and rats with postinfarction cardiosclerosis at the age of 4, 12 and 24 months: the first group contained twenty 4 months old animals; the second group - twenty 12 months old animals; the third group - twenty 24 months old animals. In the each group were distinguish 10 intact rats and 10 experimental rats, that have postinfarction cardiosclerosis (PICS) modeled by coronary occlusion. The experiments was completed on 60 male-rats. It was shown, that in intact animals the indicator of ß-ARM significantly decreases by 12 months in relation to the group of 4 monthly animals. In the groups of intact animals of 12 and 24 months, there were no significant differences in ß-ARM. The severity of cardiac hypertrophy in animals with PICS was inversely related to age - 4>12>24 months old. Formed PICS in animals aged 4 and 12 months was accompanied by a expressed increase of ß-ARM, in animals 24 months with PICS ß-ARM did not significantly change. Changes in the ß-ARM index characterizing the state of the CAS receptor link under PICS conditions are age-related, in adults 12 months of age with PICS, an increase in ß-ARM relative to the parameter at 4 months. animals indicates compensatory desensitization of ß-adrenergic receptors upon activation of CAS in response to the development of contractile myocardial insufficiency. In the age group of 24 months with the formed cardiosclerosis, compensatory activation of CAS is manifested to a lesser extent.

Stimulation of mu and delta-Opiate Receptors and Tolerance of Isolated Heart to Oxidative Stress: the Role of NO-Synthase.

Preliminary intravenous injection of delta-opiate receptor (OR) agonists DSLET (0.1 mg/kg) or DTLET (0.1 mg/kg) increased tolerance of isolated perfused myocardium to damage by oxidative stress simulated in vivo with FeSO4 + ascorbic acid. This manifested itself by a decreased level of creatine phosphokinase (CPK) in the perfusate flowing out of the heart during the oxidative exposure. The preliminary systemic injection of mu-agonists DAMGO (0.1 mg/kg) or DALDA (0.1 mg/kg) failed to affect the release of CPK from the myocardium. The cardioprotective effect of the delta-agonist DSLET was completely abolished by preliminary intravenous injection of the delta-OR antagonist ICI 174,864 (2.5 mg/kg). The intravenous injection of the NO-synthase inhibitor L-NAME (50 mg/kg) also completely abolished the cardioprotective effect of delta-OR stimulation. The preliminary injection of DSLET but not of DAMGO prevented an increase in the level of diene conjugates and a decrease in the activity of superoxide dismutase (SOD) in the isolated myocardium tissue. Thus, the in vivo stimulation of delta-OR increased the tolerance of the heart to oxidative stress through activation of NO-synthase and SOD.

Activation of mu-opiate receptors as a factor of regulation of heart resistance to ischemia-reperfusion and oxidative stress.

Intravenous injection of the selective mu-opiate receptor agonist DAMGO (0.1 mg/kg, 15 min before isolation of the heart) improved resistance of isolated perfused rat heart to ischemia (45 min) and reperfusion (60 min) damages. In vivo administration of DAMGO prevented reperfusion-induced damages to cardiomyocytes and decreased the content of conjugated dienes in the myocardium during ischemia-reperfusion in vitro. Furthermore, stimulation of mu-opiate receptors promoted recovery of myocardial contractility during reoxygenation, but had no effect on heart resistance to free radical-induced damages during perfusion of isolated heart with a solution containing Fe2+ and ascorbic acid.