Structural basis of impairment of the external respiratory function in the post-resuscitation period

External enhancement of free-radical processes followed by considerable tissue accumulation of toxic lipid peroxidation products in an early postresuscitation period is the main pathochemical mechanism which causes lung air-blood barrier disturbance. The basis of animal respiratory insufficiency morphogenesis after clinical death is ventilation failure (dis- and atelectasis), circulation disorder (edema, hemorrhage) being secondary. However, morphological examination of lungs of animals after four-minutes clinical death from an acute blood loss and resuscitation showed that it is the severity of circulation disorders that determines the animals condition in the postresuscitation period.     

Synthesis and Pharmacological Activity of the Oxidized Fractions of Arabinogalactan from Siberian Larch (<Emphasis Type="Italic">Larix sibirica L.</Emphasis>)

Aqueous solutions of arabinogalactan from Siberian larch (Larix sibirica L.) were subjected to oxidative destruction by a hydrogen peroxide – molecular oxygen system. The obtained high- and low-molecular-weight fractions of oxidation products were characterized by chemical and spectral methods and tested for pharmacological activity. The results of experiments on animals showed evidence for significant antiulcer and antiinflammatory properties of the preparations studied. __________ Translated from Khimiko-Farmatsevticheskii Zhurnal, Vol. 39, No. 8, pp. 23 – 26, August, 2005.     

Diagnosis of formaldehyde allergy

Exposure to small-dose environmental agents is a risk factor of immunopathological reactions. The levels of formaldehyde-specific IgE were comparatively analyzed in 50 children of whom 25 live in the area exposed to formaldehyde. Children with varying respiratory allergic reactions comprised a study group. To identify allergen-specific IgE, the authors used a method that determined formaldehyde antibodies by using the tested allergen (formaldehyde on the paper). There were significant group-specific differences in the levels of formaldehyde antibodies (3.8 times higher in the study group than in the controls). Combined therapy substantially reduced specific IgE whose levels returned to the levels observed in the controls. The findings may recommend the use of this test for the diagnosis of immune-depended abnormalities and the evaluation of their effective treatment.     

Platelet adhesion and thrombus formation on subendothelium in platelets deficient in glycoproteins IIb-IIIa, Ib, and storage granules

Patients whose platelets are deficient in glycoprotein (GP) Ib, IIb- IIIa (thrombasthenia), or granule substances (storage pool deficiency, SPD) were studied to define further the properties of platelets that mediate platelet adhesion and thrombus formation on subendothelium. Both nonanticoagulated and citrated blood were exposed to everted, de- endothelialized rabbit vessel segments under controlled flow conditions and shear rates varying from 650 to 3,300 sec-1. Morphometry was used to measure platelet thrombus dimensions and the percentage of the subendothelial surface covered with contact (C) or spread (S) platelets. Adhesion was defined as C + S. The results in SPD demonstrated (1) reduced thrombus dimensions in delta-SPD (pure dense granule deficiency) in proportion to the magnitude of the dense granule defect; (2) an even greater reduction in thrombus dimensions in patients with combined deficiencies of alpha and dense granules (alpha delta-SPD); and (3) impaired platelet adhesion at several conditions in alpha delta-SPD and, in delta-SPD, a hematocrit-dependent impairment of adhesion in citrated blood at 2,600 sec-1. In thrombasthenia, platelets were present as a monolayer on the subendothelial surface in both nonanticoagulated and citrated blood, indicating an absolute requirement for GPIIb-IIIa in promoting platelet-platelet interaction at all shear rates and perfusion times. Two types of abnormalities in platelet-vessel wall interactions were observed. In nonanticoagulated blood, the percentage of platelets in the C phase was consistently increased at all shear rates, but C + S values were normal. These observations indicate that platelets deficient in GPIIb-IIIa do not spread normally on the subendothelial surface exposed to nonanticoagulated blood. With citrated blood, the C + S value in thrombasthenia was reduced at both 800 and 2,600 sec-1, as in von Willebrand's disease, and a similar degree of reduction (about 50%) was observed in normal blood treated with a monoclonal antibody to GPIIb- IIIa. The findings, together with theoretical considerations, are consistent with an hypothesis that GPIIb-IIIa mediates the spreading of platelets on subendothelium following the initial attachment through GPIb and that GPIIb-IIIa may be considered an adhesion site on the platelet membrane. Abnormalities of GPIIb-IIIa may, depending on the conditions of study, result in either increased values of C platelets or decreased values of C + S. The results of the study further suggest that a complex interaction of platelet granule factors and membrane GP mediate platelet adhesion and thrombus formation.     

Toxic effect of the novel phenol antioxidant SO-3 in the subchronic experiment

Subchronic tests on rats showed that a new phenolic antioxidant bis[3,(3, 5-di-tert-butyl-4-hydroxyphenyl)propyl] sulfide (SO-3) exhibits low toxicity upon peroral administration. Neither significant variations in the hematological and integral indices, nor pathological shifts in the activity of serum enzymes or pathomorphological changes in the internal organs were observed. Simultaneous administration of a sunflower oil with SO-3 led to a significant decrease in the blood cholesterol level, produced a hepatoprotector effect, and exhibited a protective action with respect to the mucous membranes of the gastrointestinal tract. Animals receiving large doses of SO-3 showed no signs of a prelipid stage of the arteriosclerosis typically observed in the control group.     

Amylolytic Activity of Small Intestinal Brush-Border Membrane in the Late Postresuscitation Period

Functional changes in the small intestinal brush-border membrane were studied in the late recovery period after acute fatal blood loss. Delayed recovery of enzyme activity in the small intestinal brush-border membrane was due to impaired functional topography of the digestive transport system. It was manifested in a shift of the proximodistal gradient toward reserve zones of the ileum.