Surgical treatment of atrial fibrillation: technique of thoracoscopic radiofrequency fragmentation of the left atrium. / Khirurgicheskoe lechenie fibrilliatsii predserdii: tekhnologiia vypolneniia torakoskopicheskoi radiochastotnoi fragmentatsii levogo predserdiia.

Presented in the article is a detailed description of a modified technique of minimally invasive surgical treatment of patients with atrial fibrillation - thoracoscopic radiofrequency fragmentation of the left atrium. This modification differs from the prototype GALAXY procedure by a significant increase of the 'quantitative' rather than 'qualitative' parameter of surgical aggression in relation to the left atrium. This technique results in creation of multiple transmural continuous closed lines of lesion to the left atrium and, consequently, a reduced risk of inadequate surgical treatment for atrial fibrillation. Besides the radiofrequency action on the wall of the left atrium, the protocol of the operation included destruction of the ligament of Marshall and resection of the left atrial appendage. An indication for performing this operation is the presence of various forms of atrial fibrillation.

[Results of surgical remodeling after resection of aneurysm and plasty by Dor-II-Jatene method in patients with post-infarction aneurysms of the left ventricle].

Post-infarction remodeling was studied in 41 patients with the post-infarction aneurysm of the left ventricle and initially reduced contractive function of the left ventricle myocardium: ejection fraction from 17 to 35%. The ultrasonic pre- and postoperative investigation allowed assessment of the index of the ultimate diastolic volume, index of the ultimate systolic volume, ejection fraction, long axis of the left ventricle, apical short axis, papillary short axis, mitral short axis. In addition, impaired obliquity of the left ventricle cavity and relative thickness of the left ventricle wall and intervenricular septum at different levels were determined. Surgical remodeling using resection of aneurysm and plasty by Dor-II-Jatene method facilitated normalization of indices of the cavity geometry and reestablishment of the contractive ability of the left ventricle.

[Effect of nicotine on electrogenic contribution of the Na,K-ATPase isoforms and contractile characteristics of the rat skeletal muscle].

Nicotine in concentration 100 nM which corresponds to concentration of nicotine circulating in tobacco smokes induced hyperpolarization by approximately 4 mV of muscle fibres of the rat isolated diaphragm, as well as an increase in amplitude and acceleration of action potentials. Similar hyperpolarization was induced by nicotine and acetylcholine in the rat soleus muscle. In this muscle, the hyperpolarization developed more slowly than in diaphragm revealing initial slight depolarization. Non-competitive blocker of open channel of nicotinic acetylcholine receptor, proadifen, abolished nicotine- or acetylcholine-induced depolarization but not the hyperpolarization. In the diaphragm, the hyperpolarization was blocked by specific inhibitors of the Na,K-ATPase, ouabain (50 nM) or marinobufagenin (2 nM) suggesting an involvement of the Na,K-ATPase. Estimation of elecrogenic contributions of isoforms of the Na,K-ATPase showed that the hyperpolarization was due to an increase in electrogenic contribution of alpha 2 isoform without change in contribution of alpha 1 isoform. Nicotine did not affect parameters of muscle contractions in response to direct stimulation.

[Decrease in the electrogenic contribution of Na,K-ATPase and resting membrane potential as a possible mechanism of calcium ion accumulation in filaments of the rat musculus soleus subjected to the short-term gravity unloading].

After three days of hind limb unloading, the depolarization of muscle fibers from -71.0 +/- 0.5 mV to -66.8 +/- 0.7 mV as well as a decrease in muscle excitability and a trend to fatigue acceleration were observed. After hind limb unloading, the electrogenic contribution of the ouabain-sensitive alpha2 isoform of Na,K-ATPase, tested as depolarization due to the administration of 1 microM ouabain, decreased from 6.2 +/- 0.6 to 0.5 +/- 0.8 mV. The contribution of the ouabain-resistant alpha1 isoform, estimated as additional depolarization after the administration of 500 microM ouabain, decreased from 4.6 +/- 0.6 to 2.6 +/- 0.6 mV. After hind limb unloading, the fluorescence intensity of single muscle fibers loaded with Fluo-4-AM increased more than four times, indicating an increase in intracellular Ca2+ concentration. The effect was prevented by local delivery of nifedipine, which blocks L-type Ca2+ channels. These data suggest the existence of a selective mechanism of suppression of the alpha2-pump electrogenic contribution, which led to the depolarization of soleus muscle fibers after 3 days of hind limb unloading. The depolarization in turn may activate L-type Ca2+ channels, resulting in intracellular Ca2+ accumulation.

[Role of the alpha2-isoform of Na+, K(+)-ATPase in the positive inotropic effect of ouabain and marinobufagenin in the rat diaphragm].

It was shown that the specific inhibitors of Na+, K(+)-ATPase ouabain and marinobufagenin increased the contraction of an isolated rat diaphragm (positive inotropic effect) by up to approximately 15% in a dose-dependent manner with EC50 = 1.2 +/- 0.3 and 0.3 +/- 0.1 nM, respectively. The results indicate the involvement of the ouabain-sensitive alpha 2 isoform of Na+, K(+)-ATPase. The analysis of ouabain-resting membrane potential dose-response relationships in the presence and absence of hyperpolarizing concentration of acetylcholine (100 nM) suggests the existence of two pools of alpha 2 Na+, K(+)-ATPase with different affinities for ouabain. The pool with a higher ouabain affinity is involved in the hyperpolarizing effect of acetylcholine and, presumably, in the positive inotropic effect of ouabain, which might be a mechanism of regulation of muscle efficiency by circulating endogenous inhibitors of Na+, K(+)-ATPase.

[Effects of marinobufagenin on electrophysiological and contractile characteristics of the rat diaphragm].

Effects of Na+,K(+)-ATPase inhibitor: marinobufagenin, on contractile and electric characteristics of isolated rat diaphragm were studied for the first time. Marinobufagenin induced dose-dependent (EC50 = 0.3 +/- 0.1 nM) increase in the contraction force (positive inotropic effect). At 1-2 nM, it slowed down the fatigue induced by continuous direct stimulation (2/s) of the muscle. Marinobufagenin at the same concentrations did not affect resting membrane potential or parameters of action potentials of muscle fibers, while at 10 and 20 nM it induced hyperpolarization by approximately 2 mV. Marinobufagenin blocked dose-dependently (IC50 = 2.9 +/- 2.0 nM) hyperpolarizing effect of acetylcholine (100 nM) mediated by increase in electrogenic contribution of alpha2 isoform of the Na+,K(+)-ATPase. This result suggests a capability of marinobufagenin to inhibit this isoform of the Na+,K(+)-ATPase. Possible mechanisms of marinobufagenin effects in skeletal muscle are discussed.

[The current potentials and the role of echocardiography in the diagnosis and surgical treatment of infectious endocarditis]. / Sovremennye vozmozhnosti i rol' ékhokardiografii v diagnostike i khirurgicheskom lechenii infektsionnogo éndokardita.

The authors have analyzed results of examination of 107 patients with infective endocarditis (IE) of the natural (IENV) and artificial valves (IEAV) of the heart. It was found that the revealed ultrasonic symptoms of IE were specific in 97.7% of patients with IENV and in 100% of patients with IEAV. The sensitivity of transthoracal echocardiography was 89.6% in patients with IENV and 65% in patients with IEAV. The intracardiac morphological alterations were found to coincide with the findings of echocardiography in 78.2% of patients with IENV and in 55%--with IEAV. The authors have elaborated an algorithm of the complex diagnostic examination of patients.

[Traumatic suppurative-necrotic pancreatitis]. / Travmaticheskii gnoino-nekroticheskii pankreatit.

Among 105 patients with traumatic pancreatitis there were 32 patients with pyo-necrotic pancreatitis. The diagnosis and treatment of pyo-necrotic pancreatitis are described.