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Biomedical subjects

A D Arapov

Publications and source records attributed to A D Arapov.

At least 19 recordsLinked to original sources
PubMed1987

Ischemic heart arrest: nitrogenous metabolism in energy-depleted human myocardium.

Seventeen patients undergoing radical correction of Fallot's tetrad or defects of interventricular septum were investigated. Needle biopsies from the left ventricular apex region were obtained at the 1st min after cross-clamping of the aorta and at the end of cardiac arrest to determine adenosine triphosphate (ATP), glutamate, aspartate, alanine and ammonia. The losses of ATP during clamping period were related to decrease in glutamate. The fall in ATP by more than 20% of the initial level was accompanied by a significant decrease in aspartate, an accumulation of alanine and ammonia in cardiac tissue but did not affect glutamine content. The data obtained prove the participation of specific nitrogenous compounds of human heart, and especially glutamate, in response to energy depletion during ischemia.

Adenosine Triphosphate↗
PubMed1987

Glutamate-blood cardioplegia improves ATP preservation in human myocardium.

Two groups of patients subjected to radical correction of Fallot's tetrad and defects of interventricular septum were investigated to ascertain whether the addition of glutamic acid to blood cardioplegic perfusate could improve preservation of myocardial ATP during cardiac arrest. In the control group (17 patients) the myocardial protection was performed by repeated infusions of cold blood potassium cardioplegic solution; in the 2nd group (24 patients) cardioplegic perfusate containing glutamic acid (20 mmol/l) was used. Left ventricular biopsies were taken during the first minute after cross-clamping of the aorta and before the release of the aortic clamp to determine ATP, glutamate and lactate. The cross-clamping time averaged 32 min in both groups. In the patients of the control group the losses of ATP correlated with the decrease in glutamate during the clamping period. A maintenance of a higher myocardial glutamate content by glutamate-containing cardioplegic perfusate prevented ATP fall or increased its level in patients of the 2nd group. There was no significant difference in lactate levels between the two groups by the end of the cardiac arrest. We conclude that enrichment of blood cardioplegic solution by glutamic acid, which may act as a substrate for anaerobic energy production, provides more effective myocardial protection during ischemic heart arrest.

Adenosine Triphosphate↗
PubMed1987

[Effect of cardioplegia on nitrogen and energy metabolism of the human heart].

The interrelation between the energy and nitrogenous metabolism of the myocardium during cardioplegia has been studied in patients with congenital valvular heart disease (tetralogy of Fallot--12 patients, ventricular septal defect--5 patients). Whole body hypothermia with repeated heart reperfusion with cold cardioplegic blood perfusate was used for the protection of the myocardium. However, ATP level of the myocardium of some patients decreased by 20% and more of the baseline. This loss was accompanied by a reduction in glutamate and aspartate levels and a rise in ammonium and alanine levels in the myocardium (by 17.7 +/- 3.8; 17.6 +/- 5.9; 61.4 +/- 12.5 and 92.4 +/- 26.3% of the baseline, respectively).

Adenosine Triphosphate↗
PubMed1986

[Laser endoscopic destruction of the atrioventricular junction of the heart conduction system in an experiment].

Feasibility and degree of local AV junction destruction were studied prior to the induction of complete transversal block on the model of 18 isolated perfused dog hearts, using endoscopic laser device, employing cardiofibroscope and laser Ne: YAG. Morphological pattern in the destruction zone is presented. The technique and device can be used for transvenous AV junction destruction.

Animals↗
PubMed1979

[Recurrent right-ventricular hypertrophy in patients with congenital isolated stenosis of the pulmonary artery and outlet tract of the right ventricle in the immediate and late periods after surgery].

The degree of hypertrophy of the right ventricle is proportionate to the size of the systolic pressure gradient between the right ventricle and pulmonary artery prior to operation. The involution of hypertrophy is dependent on the type of stenosis, age of the patient and the term of surgery.

Arterial Occlusive Diseases↗