In a rat model of 5-min clinical death caused by massive blood loss actovegin prevented the development of metabolic disorders induced by hypoxia and reoxygenation as well as the damage to the central nervous system in the early postresuscitation period. Intmcarotid administration of actovegin increased the activity of reduction-oxidation enzymes, intensified aerobic metabolism of glucose, prevented lactate accumulation in the brain, reduced structural disorders in the central nervous system, and provided lhster restoration of the major reflexes after a 5-min total ischemia. Key Words: central nervous system; postresuscitation period; actoveginFast and adequate restoration of the central nervous system (CNS) activity is an important resuscitation measure. Since the energy metabolism disorders are the major cause of postischemic damage to the brain [6,7], their timely normalization determines the course of postresuscitation period.In the present study we examined the effect of actovegin (AV), a deproteinated hemolysate which enhances aerobic metabolisln by intensifying the utilization of oxygen and glucose and stimulating ATP formation [9,10], on functional, metabolic, and morphological changes in the brain during postresuscitation period. MATERIALS AND METHODSExperiments were performed on outbred albino male rats (body weight 220-350 g) using a model of 5-rain clinical death caused by massive blood loss [81. Tracheostomy and catheterization of the common carotid artery were performed under Nembutal anesthesia (35 lng/kg intraperitoneally). The maximum possible volume of blood was relnoved through the catheter until cessation of respiration and heart beat and zero blood pressure in the carotid a1"te13r, which was considered as the beginning of clinical death. Resuscitation by the standard scheme was started after 5 rain. Artificial ventilation was performed throughout the entire postresuscitation period (40 min). Adrenomimetics were not administered.The rats were divided into 4 groups. Group I consisted of intact animals (n=14). Group 2 rots were subjected to 5-rain clinical death (n =14) without administering AV in postresuscitation period. Group 3 rats (n=Ig) were given AV in a total dose of 30 mg. In order to prevent sharp increase in energy metabolism the preparation was injected into the carotid m"tery in three equal doses on the 5th, 15th, and 30th rain of the postresuscitation period. Group 4 rats were administered an equivalent volume of normal saline (control, n=21).Arterial pressure and heart and respiratory rates were recorded before and on the 5th, 10th, 20th,

No abstract

One of the prerequisites for the correct assessment of the function of external respiration is the comparison of the indicators obtained during its study with the corresponding proper values, that is, the values that should be in a perfectly healthy person of the same sex, age and height.

The morbidity and character of acute pneumonia are influenced by such factors as temperature fluctuations, dustiness of air, presence of harmful impurities in it, but information about the nature of this influence is rather contradictory. Some authors believe that contact with elevated concentrations of sulfur dioxide, nitrogen oxides, chromium and other irritants leads to an increased incidence of acute respiratory disease and pneumonia. Other researchers have shown that the incidence of acute pneumonia among workers in the chemical industry is lower than in the general adult population. The question about peculiarities of course and outcomes of acute pneumonia in persons working in contact with respiratory irritating chemicals remains practically unstudied. Meanwhile, such substances as chlorine, sulfur dioxide, ammonia, nitrogen oxides and others are widely used in chemical industry when performing various types of work.

Currently, the role of bronchospasm in the development of respiratory insufficiency in pulmonary patients has been fully proven [1, 4, 8, 9, etc.]. The severity of bronchospasm is usually determined using a pneumotachometer of the power (maximum volumetric velocity) of the air jet during exhalation [3, 4, 10, 12). However, a pneumotachometrically recorded decrease in the absolute figures of the maximum volume expiratory velocity, apparently, is not always a criterion of bronchospasm. G. O. Badalyan (1962), proposing to express the actual expiratory power as a percentage of the proper value, found that with normal bronchial patency, this ratio is at least 85%. For the proper amount of exhalation power, they took the actual WEL multiplied by 1.2.