[The place of scales and questionnaires in assessing the disease's severity and the long-term prophylaxis's prescribing in patients with hereditary angioedema].

Hereditary angioedema is a hereditary life-threatening disease characterized by recurrent angioedema of various strength and localization. To date, definite diseases severity criteria have not been developed. There are many different factors to consider not only the frequency of episodes, but also their duration, strength, influence on the patient's appearance, the severity of the pain syndrome. Disease related quality of life, the number of work disability days, and the patient's satisfaction with the prescribed treatment are important. In addition, there are no criteria for prescribing long-term prophylaxis, and no parameters for choosing a specific drug. The introduction of specific scales and questionnaires developed to assess such characteristics as disease activity, disease control, quality of life in patients with recurrent angioedema into clinical practice seems to be the best solution for both questions. The comprehensive understanding of the diseases severity in a particular patient can be carried out with the combined use of assessment tools.

Peculiarities of the Development of the Myocardial Infarction in ISIAH Rats.

We studied peculiarities of the development of myocardial infarction in rats with inherited stress-induced arterial hypertension (ISIAH rats). The control group consisted of Wistar rats. Occlusion of the left coronary artery (30 min) followed by reperfusion (120 min) was performed. The infarct size was determined relative to the risk zone by staining with 1% triphenyltetrazolium. BP, blood filling, and blood flow in the caudal vessels were measured. The infarct size was 31.5±3.0% of the risk zone in Wistar rats and 47.9±4.4% in ISIAH rats (p=0.026). No correlations of infarction size and BP or HR were found at the study stages. In ISIAH rats, local 30-min ischemia followed by 120-min reperfusion caused greater myocardial infarction that did not depend on BP or HR.

[Pulmonary manifestations in adult patients with a defect in humoral immunity]. / Pul'monologicheskie proyavleniya u vzroslykh patsientov s defektom gumoral'nogo zvena immuniteta.

Primary immunodeficiencies (PIDs) are a group of congenital diseases of the immune system, which numbers more than 230 nosological entities associated with lost, decreased, or wrong function of its one or several components. Due to the common misconception that these are extremely rare diseases that occur only in children and lead to their death at an early age, PIDs are frequently ruled out by physicians of related specialties from the range of differential diagnosis. The most common forms of PIDs, such as humoral immunity defects, common variable immune deficiency, X-linked agammaglobulinemia, selective IgA deficiency, etc., are milder than other forms of PID, enabling patients to attain their adult age, and may even manifest in adulthood. Bronchopulmonary involvements are the most common manifestations of the disease in patients with a defect in humoral immunity. Thus, a therapist and a pulmonologist are mostly the first doctors who begin to treat these patients and play a key role in their fate, since only timely diagnosis and initiation of adequate therapy can preserve not only the patient's life, but also its quality, avoiding irreversible complications. Chest computed tomography changes play a large role in diagnosis. These are not specific for PID; however, there are a number of characteristic signs that permit this diagnosis to be presumed.

[A place of intravenous immunoglobulins in current clinical practice: Privigen is a novel 10% immunoglobulin]. / Mesto immunoglobulinov dlya vnutrivennogo vvedeniya v sovremennoi klinicheskoi praktike: Prividzhen - novyi 10% immunoglobulin.

Intravenous immunoglobulins (IVIGs) were initially designed to treat patients with primary immunodeficiencies (PID). Due to the multidirectional effect of IVIGs on the immune system, a range of nosological entities, in which these agents are successfully administered, is steadily expanding. As of now, IVIGs are successfully used in neurology, rheumatology, hematology, and oncology and they are essential drugs for many patients. In spite of the long experience with IVIGs, their mechanism of action remains unclear, numerous investigations for their clinical introduction are being continued. Therefore, there is a growing need to increase the production of the drugs, which gives rise to the emergence of novel medications, which differ in their composition and manufacture technologies, on the pharmacological market. The 10% intravenous immunoglobulin privigen, the safety and efficacy of which has been proven in foreign practice, is a novel drug on the Russian market.

[Myocardial Infarction and Natural Defense Mechanisms: The Role of Norepinephrine Reuptake].

PURPOSE: to study effect of norepinephrine reuptake blockade in reperfusion period on size of infarct caused by local ischemia with and without ischemic pre- and postconditioning. MATERIAL AND METHODS: Wistar rats (n=46) were randomly divided into 6 groups. Group (gr) I (n=7) - 30 min occlusion of left coronary artery followed by 120 reperfusion; gr II (n=2) as in gr I +desipramine (0.8 mg/kg intravenously [i.v.]) at the start of reperfusion; gr III (n=6) - ischemic preconditioning before coronary artery occlusion; gr IV (n=7).

Myocardial serotonin during ischemia under conditions of ischemic preconditioning.

We studied the dynamics of interstitial serotonin during local myocardial ischemia under conditions of ischemic preconditioning in Wistar rats. Ischemic preconditioning increased serotonin content in the dialysate (p=0.003). During 30-min ischemia, ischemic preconditioning delayed serotonin increase just before the 20th min of ischemia. Ischemic preconditioning promoted short-term increase in the serotonin level in the myocardial interstitium but followed by prolonged ischemia, it delayed the accumulation of serotonin in the myocardial interstitium.

[Myocardial serotonin metabolism after local ischemia and ischemic precondition].

To determine the effect of ischemic preconditioning upon myocardial serotonin and 5-hydroxyindolacetic acid (5-HIAA) dynamic in myocardial ischemia and reperfusion. 28 male Wistar rats anesthetized with urethane were randomly divided into 2 groups. In the control group (n = 13) rats were subjected to 30 min coronary occlusion and subsequent 120 min reperfusion. In the ex- perimental group (n = 15) ischemic preconditioning (3 x 3 min ischemia + 3 x 3 min reperfusion) before prolonged ischemia was used. Myocardial interstitial serotonin and 5-HIAA were measured using a microdialysis technique. Myocardial serotonin and 5-HIAA significantly increased af- ter ischemic preconditioning (p = 0.00298; p = 0.00187). In prolonged ischemia interstitial serotonin level was lower in the experimental group vs. control up to 20 min of ischemia (p < 0.05). We conclude that ischemic preconditioning increases interstitial myocardial serotonin, but inhibit serotonin increase in subsequent prolonged myocardial ischemia. After 20 minutes of reperfusion the lack of correlation between serotonin and 5-HIAA levels appeared which may be the evidence of serotonin uptake activation.

Ischemic postconditioning and size of myocardial infarction during inhibition of norepinephrine reuptake.

We studied the effect of inhibition of norepinephrine reuptake during the reperfusion period on the size of infarction zone after focal myocardial ischemia and under conditions of ischemic postconditioning. In groups 1 and 2, 30-min occlusion of the left coronary artery followed by 120-min reperfusion was performed. In groups 3 and 4, ischemia was followed by ischemic postconditioning (six 10-sec occlusions alternating with 10-sec reperfusions). Ringer solution (1 ml, groups 1 and 3) and desipramine (0.8 mg/kg, groups 2 and 4) were injected intravenously at the beginning of reperfusion. The area of myocardial infarction in group 1 was 32.0±3.1% of the area of the risk zone; in groups 2, 3, and 4 the corresponding value was 46.1±3.4% (p=0.006), 22.2±2.6% (p=0.028), and 50.3±3.1% (p=0.018), respectively. It was shown that inhibition of norepinephrine reuptake in the early reperfusion period after ischemia increased myocardial injury and abolished the protective effect of ischemic postconditioning.

Inhibition of norepinephrine reuptake and size of myocardial infarction during focal ischemia and after preconditioning.

Experiments on rats showed that blockade of norepinephrine reuptake in the early reperfusion period after focal myocardial ischemia aggravates myocardial injury and abolishes the protective effect of ischemic preconditioning.

[Ischemic preconditioning and metabolism of myocardial adrenaline].

We implanted under urethane narcosis microdialysis probes into myocardium of Wistar rats. In experimental group we used ischemic preconditioning. After this left descending coronary artery was occluded for 60 minutes and then reperfused for 60 min. In control group prolonged occlusion was preceded by 30 min of rest. Significant elevation of noradrenaline concentration in myocardial interstitium was noted at 20th and 10th minutes of testing ischemia in experimental and control groups respectively. From 20th minute to the termination of occlusion noradrenaline concentration in myocardial in animals of control group was significantly higher than that in preconditioned animals. Concentration of dihydroxyphenylglycol in interstitium reflecting noradrenaline metabolism in axoplasm fell during ischemia and rose when reperfusion was started. Elevation of dihydroxyphenylglycol was statistically significant compared with both baseline level and control (p<0.005) practically at all stages of reperfusion. Thus ischemic preconditioning inhibits effectively noradrenaline accumulation in myocardial interstitium during prolonged ischemia. After ischemic preconditioning normal mechanism of noradrenaline reuptake functions longer however because of impaired storage in vesicles substantial part of noradrenaline remains in free state in axoplasm to be subjected to deamination with participation of monoamine oxidase.

[Uptake1 inibition in reperfusion: noradrenalin dynamic and myocardiola infraction size].

To determine the effect of uptake 1 inhibition in reperfusion after myocardial ischcmia upon noradrenalin dynamic and myocardial infarction size, 14 male Wistar rats anesthetized with urethane were randomly divided into 2 groups and subjected to 30 min coronary occlusion and subsequent 120 min reperfusion. In control group (n = 7) 1 ml of Ringer's solution was administered intravenously at the beginning of reperfusion. In experimental group (n = 7) instead of Ringer's solution 0.8 mg/kg of desipramine was used. Myocardial interstitial noradrenalin levels were measured using a microdialysis technique. Infarction size was determined by triphenyltetrazolium chloride staining and was related to the area at risk. Desipramine increased infraction size from 32.0 +/- 3.1 % (control group) to 46.1 +/- 3.4% (p = 0.06). Interstitial noradrenalin in experimental group did not decrease during 120 min reperfusion (p < 0.05 vs. control). The data obtained suggest that uptake 1 inhibition in reperfusion after myocardial ischemia increases myocardial infarction size through increased interstitial noradrenalin.

[Activation processes in the lymphocytes of patients with latent sensitization].

Latent sensitization is a risk factor of a clinically manifest atopic reaction. Investigation of a phenotypic composition of lymphocytes reveals function of the immune system in this condition. Indirect fluorescence assessed differential and activation lymphocyte antigens (CD4, CD3, CD8, CD16, CD20 and CD25, CD71, HLA-DR, CD95, CD23, CD54, respectively) in 15 patients with latent sensitization, 32 patients with atopic bronchial asthma and 22 healthy donors. The immune system demonstrated definite activation with involvement ofT- and B-links of the immune system. Lymphocyte activation in latent sensitization and bronchial asthma differs by high expression of CD95 apoptosis trigger receptor. Enhancement of Fas-mediated lymphocyte apoptosis may inhibit IgE synthesis and atopic pathology manifestation.

Dimethylarginines and serotonin in the blood of spontaneously hypertensive rats.

The serotoninergic system and nitric oxide system were studied in spontaneously hypertensive rats SHR and Wistar rats (control). The contents of serotonin, 5-hydroxyindoleacetic acid (serotonin metabolite), L-arginine, monomethylarginine, and asymmetric and symmetric dimethylarginines were measured in blood plasma. Serotonin content in hypertensive animals was much higher than in Wistar rats. No interstrain differences were found in the concentration of 5-hydroxyindoleacetic acid. The concentration of asymmetric dimethylarginine in SHR rats was higher than in Wistar rats. However, the concentration of monomethylarginine in SHR rats was lower than in Wistar rats. Our results and published data on the serotoninergic system indicate that SHR rats serve as a convenient model of hypertension.

[Noradrenaline dynamics in prolonged ischemia after ischemic preconditioning].

AIM OF THE STUDY: To determine the effects of two-staged ischemic preconditioning on myocardial noradrenaline in prolonged ischemia and reperfusion. METHODS: Thirty-two male Wistar rats anesthetised with urethane randomly divided into 2 groups: group 1 (ischemic preconditioning group, n = 16), and group 2 (control, n = 16). Myocardial interstitial noradrenaline levels were measured using a microdialysis technique. Ischemic preconditioning was elicited by two episodes: 5 min of ischemia and 10 min of reperfusion. The intermittent occlusions were followed by prolonged occlusion (60 min) and reperfusion (60 min). RESULTS: An increase in interstitial noradrenaline was observed in 10 min of prolonged ischemia in group 2, and in 20 min in group 1. After 20 min of myocardial ischemia there was a significant difference between groups (p < 0.05) in interstitial noradrenaline levels. In control group, it was 60% higher. In reperfusion, noradrenaline levels decreased markedly in group 1. CONCLUSION: We suggest that ischemic preconditioning by two episodes: 5-min ischemia and 10-min reperfusion prevents excessive noradrenaline interstitial accumulation, perhaps, through protection of physiological uptake I carrier.

[Determination of catechelamines, serotonin, and 5-hydroxyindoleacetic acid in a blood].

The specific features of chromatographic electrochemical detector determination of plasma catecholamines, serotonin, and 5-hydroxyindoleacetic acid (5-HIAA) are considered. Platelet-poor plasma catecholamines were concentrated on alumina. The concentrate was injected into a chromatograph. Serotonin and 5-HIAA were measured in platelet-poor plasma and thrombocytic clot. The data available in the literature and their authors' own findings of the sample preparation parameters that could minimize the artificially increased platelet-poor plasma concentrations of serotonin via thrombolysis, as well its loss on protein sedimentation.

[Changes of immune indices in pancreonecrosis and their correction]. / Izmeneniia nekotorykh immunologicheskikh pokazatelei pri pankreonekroze i ikh korrektsiia.

Indices of immune status, lipid peroxidation and intoxication syndrome were assessed in 54 patients with acute destructive pancreatitis after surgery. Immunodeficiency developed in pyoseptic complications. Polyoxidonium was used in 22 patients for correction of secondary immunodeficiency. This drug reduces number of septic complications, lethality and hospital day.

[Experience in clinical use of primalan (mequitazine) in allergology]. / Opyt klinicheskogo primeneniia primalana (mekvitazina) v allergologii.

AIM: To study efficacy of primalan (mequitasine) in the treatment of allergic rhinoconjunctivitis and chronic recurrent urticaria. MATERIAL AND METHODS: The study included 140 patients. Of them, 60 patients had allergic rhinitis, 80 patients had chronic recurrent urticaria. All the patients received primalan (mequitasin) in a dose 10 mg/day (5 mg twice daily or a single dose 10 mg). The disease symptoms and side effects of primalan were assessed for 28 days of the treatment. RESULTS: Primalan (mequitasin) proved to be highly effective against allergic rhinitis (good and very good response--76%, satisfactory--20%) and chronic recurrent urticaria (the response in 90% patients). Good primalan tolerance was reported. Side effects were moderate and did not require the drug withdrawal (sleepiness in 6.6%, dryness of the mucosa in 5%). CONCLUSION: Primalan (mequitasin) can be recommended for wide application in therapy of allergic rhinitis and chronic recurrent urticaria.

Effects of slow and rapid cooling on catecholamine concentration in arterial plasma and the skin.

Norepinephrine (NE) and epinephrine (Epi) concentrations in arterial plasma and in skin tissue were measured chromatographically before and after external cooling. Urethan-anesthetized rats were cooled either slowly (0.004-0.006 degrees C/s) or rapidly (0.03- 0.05 degrees C/s). Blood samples were drawn three times from each animal: 1) before cooling and at a rectal temperature decreased 2) by 0.5 degrees C and 3) by 3-4 degrees C. Skin samples were taken from controls and from rapidly or slowly cooled rats at a rectal temperature lowered by 0.5 degrees C. The resting mean values were 36.7 +/- 0.3 degrees C for rectal temperature, 0.62 +/- 0.079 and 1. 09 +/- 0.203 ng/ml for plasma NE and Epi, and 85.6 +/- 4.1 and 137.6 +/- 34.3 ng/g for skin NE and Epi. A decrease in rectal temperature by 0.5 degrees C at rapid cooling produced a 2.6-fold increase of NE and a 2.8-fold increase of Epi in plasma. Concomitantly, there was a significant decrease in skin NE concentration by 28% and Epi by 86%. At a rectal temperature decreased by 0.5 degrees C after slow cooling, plasma catecholamines did not change; at unaltered skin NE concentration, there was a reduction in skin Epi concentration (60%). When rectal temperature was lowered by 3-4 degrees C, the increase in plasma NE was virtually the same at both cooling rates and only plasma Epi increased more after deep rapid cooling than slow cooling. Thus the sympathoadrenal system may be differently activated depending on cooling rate. Rapid cooling, when the dynamic activity of the skin cold receptors is involved in the cold response, may provide conditions for an earlier activation of the sympathoadrenal system. This may evidence the functional significance of the dynamic activity of the skin cold receptors in the formation of the cold defense responses.

[Characteristics of responses of the sympatho-adrenal system to various types of cooling]. / Osobennosti reaktsii simpatoadrenalovoi sistemy krys pri raznykh tipakh okhlazhdeniia.

Fast cooling involving the dynamic activity of the skin cold receptors seems to establish a condition for changes in catecholamine concentration at a lesser decrease of body temperature as compared with slow cooling.