Biomedical subjects
Publications and source records attributed to A K Kirsanova.
We revealed a relationship between water balance and LPO in the myocardium, liver, and blood plasma during massive blood loss and irradiation with He-Ne laser. Low-intensity laser irradiation of the plasma inhibits LPO and normalizes water balance in rat tissues during massive blood loss.
Blood loss leads to the reduction in vitality of red blood cells (RBCs). However, the changes in morphology at different stages of hemorrhagic shock have not been studied. Thus, the aim of this study was to identify and quantitate the sequence of morphological changes in RBCs during hemorrhage. This study was performed on 15 adult inbred dogs. Blood samples were taken before hemorrhage, when the mean arterial pressure reached 40 mm Hg (initial stage of shock), and at a mean arterial pressure level of 20 mm Hg (decompensated stage of shock). The volume of blood removed averaged 33.6+/-8.9 and 55.1+/-6.9 mL/kg, respectively. Evaluation of RBC morphology was performed by computerized light microscopic morphometry and scanning electron microscopy. At the early stage of hemorrhage the number of "young-appearing" RBCs with large visible surface areas (41-50 microm2) increased from 17.7%+/-3.1% to 26.6%+/-3.5% (P < 0.05). Concomitantly, the number of "old-appearing" RBCs with small visible surface area (20-30 microm2) significantly decreased from 5.3%+/-2.7% to 2.7%+/-2.3% (P < 0.01). At the stage of decompensated blood loss, the opposite phenomenon was observed. The number of "old-appearing" RBCs increased to 8.2%+/-1.1% (P < 0.01), whereas the number of "young-appearing" RBCs decreased to 12.3%+/-4.2% (P< 0.01). The changes in visible surface area of RBCs was accompanied by significant alterations in their shape. The percentage of abnormal shaped RBCs increased from 8.9%+/-1.1% before the hemorrhage to 36.4%+/-5.8% at the stage of decompensated hemorragic shock (P < 0.01). Thus, during the late decompensated stage of hemorrhagic shock, RBCs assume shape and surface area changes that are similar to those seen in aging. These changes in RBC size and shape may be due to the effects of shock-induced oxidative stress.
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Effect of low-intensity laser exposure of the blood on the central hemodynamics, oxygen transporting function of the blood, oxygen balance of the organism, and surface configuration of erythrocyte membranes was studied in dogs exposed to 2-h arterial hypotension (arterial pressure 40 mm Hg). Blood exposure was started from the tenth min of hypotension and went on for 45 min (group 2) or 120 min (group 3); group 1 was control. The best results were attained after 45-min laser exposure. A longer exposure creates prerequisites for complications, such as dysadaptation of the vascular tone and delayed decrease of hemoglobin concentration.
Hemostatic system function was studied in dogs dying of acute blood loss and restoring to life after 4-min clinical death. Phasic changes in hemostatic system of two and three types occurred in the blood loss and reanimation, respectively. Dogs with favorable postresuscitation period exhibited hypercoagulation when dying, hypocoagulation 1 hour after reanimation and normal coagulation 3-6 hours after clinical death.
Effects of intravascular low-intensive laser exposure of the blood on the hemostasis during acute blood loss and the early postresuscitation period after 4-min clinical death were studied on narcotized dogs (8-17 kg) of both sexes with different initial levels of heparin. During the preagonal period laser exposure caused hypercoagulation in animals with initial heparin content below 60 micrograms/ml. This acceleration of blood clotting prevented a drop in the activity of antithrombin III and hypercoagulation by the third hour of postresuscitation period. In animals with initial heparin content more than 60 micrograms/ml laser exposure caused hypocoagulation in the presence of reduced activity of antithrombin III by the third hour of the resuscitation period.
To evaluate the body's compensatory reserves, experiments were made on anesthetized (with heparine) mongrel dogs of both sexes weighing 8-25 kg. The experiments have indicated that early monitoring of physiological parameters (external respiration, cardiovascular performance, hemostasis, red blood cell morphometry) in the first 5-10 minutes of acute massive hemorrhage is of high informative value. The generalization of vasoconstriction resulting in higher overall blood volume, the maintenance of venous return, tachypnea, active spontaneous hemodilution, and increased heart rate are the leading mechanisms of perfusion pressure maintenance in early acute hemorrhage. The severity of acute damage to the membranes of red blood cells and endotheliocytes and hence changes occurring in the suspension structure of blood, which drastically impairs its rheological parameters and fluidity, can play the key role in the pathogenesis of decompensatory cardiovascular and visceral functions in prolonged arterial hypotension. The findings open up new possibilities for early evaluation and prediction of the ensurina course of delayed massive hemorrhage.
The earliest significant unfavourable signs of shock are as follows: an increase in total pulmonary resistance, reduced pulmonary blood flow and tachypnea. Ventilation-perfusion disturbances in the lungs precede the onset of circulation decompensation, which in the pulmonary flow manifests as enhanced pulmonary blood content and elevated pressure in the pulmonary artery. Pulmonary flow damage in the early postresuscitation period is to a great extent predetermined by the degree of circulation disturbances in the lungs, developing during hypotension period, the leading among them being congestive processes in the lungs (increased blood content, hypertension) which progressed in case of unfavourable outcome of resuscitation and reduction of the microvascular bed.
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The elevated cross-shaped labyrinth test carried out on highly, moderately, and low active experimental animals revealed significant differences in the baseline density and composition of neuroglial populations of numerous formations of the brain, as well as in the early structural and functional sequels of experienced clinical death. The most pronounced postresuscitation abnormal changes were observed in highly active animals and the least marked ones were seen in moderately active animals.
Different forms of water content were studied in myocardium and liver of male rats at 2-h hypotension and during the early postreanimation period. The phenomenon of redistribution of free and bound water was found. Comparison of water balance during the postreanimation period in the myocardium and liver revealed that normalization of different forms of water occured in myocardium. In hepatocytes oedema remained over the whole period studied.
Male white rats divided in three groups on the basis of their behavior in the elevated plus-maze were subjected to 10-min cardiac arrest. Analysis of the results of their subsequent food and active avoidance conditioning revealed the effects of the following factors: (1) a factor of initial typological features of the higher nervous activity, (2) a factor of general brain mechanisms of postresuscitation, and (3) a factor of postresuscitation features in rats with different behaviors, which represented changes in different mechanisms of conditioned reflex performance in these animals.
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The use of caffeine or diazepam in experiments on dogs recovered after a 12-min circulatory arrest has no significant effect on the end points of resuscitation, as compared to the control. Diazepam has a more favourable effect on the recovery of central nervous system functions than caffeine. Combined use of caffeine and diazepam or lidocaine at certain stages of the early postresuscitation period accelerates the recovery of the neurological status and improves the outcome of resuscitation.
Alterations in activity of lysosomal acid phosphatase and cathepsin D, as well as of hepatocyte ultrastructure were studied in rat liver tissue after experimental heart arrest within 10 and 30 min and during the early post-resuscitation period. Cathepsin D free activity in a supernatant fraction as well as both enzymatic activities in lysosomal fraction were increased after 30 min heart arrest. Activity of acid phosphatase and cathepsin D in lysosomes was decreased, while the activity of the free enzymes was increased within 1 and 4 hrs after resuscitation. Triton X-100 (0.025%) caused labilization of lysosomal membranes. Alterations in ultrastructure of hepatocytes were observed within 30 min of the heart arrest and within first hour of the post-resuscitation period. The lysosomal membranes tended to normalization within 24 hrs after the post-resuscitation period, whereas the enzymatic activity remained elevated. Role of lysosomes in regulation of intracellular metabolism is discussed.
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