PubMed Health⌕ Search

Biomedical subjects

I N Gribkova

Publications and source records attributed to I N Gribkova.

15 recordsLinked to original sources
PubMed1992

[The clinico-electrocardiographic classification of the early ventricular repolarization syndrome].

Based on an analysis of 4980 ECGs of patients, the authors could distinguish and classify the clinico-electrocardiographic versions of the early ventricular repolarization syndrome (EVRS): permanent, occurring for the first time, suddenly disappearing, intermittent with a gigantic T wave; with a negative T wave, with a short-term T wave inversion, marked by the combination with Wolff-Parkinson-White syndrome, and additional chordae of the left ventricle. The clinico-electrocardiographic classification of the EVRS is of paramount importance for practitioners owing to an assumption that the EVRS is not only a version of the normal ECG but also can be a marker of CHD. The authors view the EVRS as an independent version of the preexcitation syndrome along with Wolff-Parkinson-White and CLK syndromes, with the manifestations of which it may combine.

Diagnosis, Differential↗
PubMed1990

[Early ventricular repolarization syndrome in patients with heart defects].

The prevalence of the early ventricular repolarization syndrome (EVRS) was examined in 129 patients with congenital and acquired heart diseases. Dynamic ECG values were assessed. The most prevalence rate was found in patients with congenital heart disease (100%), aortic (80%), mitral (51%), and aorto-mitral valvular (60%) diseases. The prevalence of EVRS, the mechanisms of its occurrence were associated with the performance of accessory pathways and the manifestation of the competitive nature of the functional interaction between the basic and accessory pathways.

Electrocardiography↗
PubMed1976

[Influence of anti-arrhythmia agents on electrolyte metabolism].

In 73 patients with hypertensive and ischemic heart diseases the total body potassium content was studied by measuring natural radioactivity with reference to K40 before and after administration of quinidine, isoptin and inderal. Furthermore, in 74 patients subject to determination was the blood plasma and erythrocytes potassium and sodium levels on application of the said agents. Following administration of quinidine and isoptin the level of total potassium in the organism was rising substantially, while taking inderal lead to a drop of the potassium concentration in the body. No clear cut parallels between the blood plasma and erythrocytes ontent and the level of total potassium in the organism could be uncovered. Mechanisms underlying the antiarrhythmic action of quinidine, isoptin and inderal are discussed.

Adult↗
PubMedDate not supplied

[Comparative evaluation of the toxicity of potassium hydrocarbonate and chloride].

The toxicity of potassium hydrocarbonate and chloride was compared in tests on 113 albino rats. It was noted that following introduction of maximal amounts of potassium chloride death occurred earlier in these animals than in the ones which received equivalent doses of potassium hydrocarbonate. Simultaneous administration of sodium hydrocarbonate reduced the toxicity of potassium hydrocarbonate and potassium chloride. Morphological investigations brought out that toxic doses of potassium hydrocarbonate led to shifts of the carbohydrate and lipids metabolism. Some mechanisms underlying the action of potassium chloride and potassium hydrocarbonate are discussed.

Animals↗
PubMedDate not supplied

[Comparative evaluation of the toxicity of potassium hydrocarbonate and potassium chloride].

The potassium hydrocarbonate and potassium chloride toxicity was compared in experiments on 113 albino rats. The death following introduction of maximal amounts of potassium chloride was noted to supervene earlier than it did in animals receiving equivalent doses of potassium hydrocarbonate. Simultaneous introduction of sodium hydrocarbonate lowered the toxicity of both potassium hydrocarbonate and chloride. Morphological investigations revealed that toxic doses of potassium hydrocarbonate bring about shifts in the carbohydrate and lipids metabolism. Some mechanisms behind the action produced potassium chloride and hydrocarbonate are discussed.

Animals↗