Experimental model of DIC syndrome

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Experimental model of DIC syndrome

Boiarchuk Olena D. Candidate of Biological Sciences, Associate Professor, Head of Department of Anatomy, Physiology, Human and Animals, Luhansk Taras Shevchenko National University

Summary

Experiments were performed on 30 rabbits. DIC-syndrome was modeled with the drug "Efa-2", made on the basis of the poison of the multi-scaled snake Efa. The obtained experimental model corresponds to the subacute form of the course of DIC-syndrome, which lasts an average of 19 days and in which four stages of the development of the latter can be clearly traced. At the same time, changes developed in the internal organs of the experimental animals, which make it possible to state a violation of microcirculation, which is typical for DIC syndrome.

Keywords: DIC, experimental model, hemostasis, histology

Disseminated intravascular coagulation syndrome (DIC) has attracted the close attention of scientists in recent years, since in modern clinics it occurs in a variety of human pathologies, often being the direct cause of death.

DIC syndrome is a complex pathological process in which simultaneous or sequential activation of blood coagulation factors, activation of fibrinolysis, formation of microthrombi and bleeding occurs [1 ]

The simplest and most widespread models of DIC syndrome are artificially created ones, in which DIC syndrome was caused by massive blood loss, irreversible shock, burns, and hemocoagulating poisons [2, 3].

However, the current models of DIC syndrome are short-term, occur in an acute form and do not allow a more detailed study of the clinic of the DIC syndrome itself, and to study new preventive and therapeutic methods.

The goal of the work was to create a new experimental model of DIC syndrome, which would characterize the subacute form of the latter.

Disseminated intravascular coagulation syndrome was modeled with the drug "Efa-2," which is made from the venom of the epha snake (Echis multisguamatus). It is known that epha poison has coagulating properties and when it enters the body, one of the forms of DIC syndrome develops [4]. Therefore, to simulate DIC syndrome, a drug containing efa snake venom was used.

To create a model of DIC syndrome, various doses of the drug "Efa-2" were used. It was noted that, depending on its dose, acute, subacute and chronic forms of DIC syndrome developed.

To study all phases of DIC syndrome, the most appropriate is the subacute form of the course. At the same time, changes develop in the internal organs that make it possible to detect microcirculation disorders characteristic of DIC syndrome.

The experiments were carried out on 30 rabbits of both sexes weighing 2.53.0 kg [5]. DIC syndrome was modeled with the drug "Efa-2", which was administered orally on an empty stomach at a dose of 8.3-8.4 g/kg.

The state of the hemostatic system was assessed by plasma recalcification time, thrombin time, fibrinogen amount, factor XIII activity, ethanol test and protamine sulfate test for fibrin/fibrinogen degradation products (PDF) [6].

All indicators were studied before modeling DIC and after administration of the drug until hemostatic indicators were restored to their original level.

To morphologically confirm DIC syndrome in the hypocoagulation stage, the lungs, kidneys, adrenal glands and liver were examined.

After the administration of the drug "Efa-2", the study made it possible to identify 4 successive phases of the development of DIC syndrome: I - hypercoagulation, II - consumption coagulopathy, III - hypocoagulation and IV - recovery (Table 1).

During the first four days after administration of the drug, the animals showed a shortening of the plasma recalcification time and thrombin time, an increase in fibrinogen content and factor XIII activity, positive ethanol test samples were observed and early products of PDP degradation were determined, which indicated the development of hypercoagulation (stage I).

Table 1. Indicators of the hemostatic system after administration of the drug "Efa-2" (M±m)

Over the next four days, the stage of consumption coagulopathy developed, in which the activity of blood coagulation factors began to decrease, and positive ethanol test samples were determined for PDP (stage II).

From the 9th to the 14th day, the state of hemostasis was characterized by a sharp decrease in the activity of blood coagulation factors, up to the complete loss of the latter's ability to clot. Ethanol test samples were noted as negative, which was explained by the high level of PDP in the plasma, and which in turn characterized pronounced hypocoagulation (stage III).

The values returned to normal on average on the 19th day.

The resulting picture of DIC syndrome corresponds to the data of other authors [1,7].

It is known that an important evidence of the development of DIC is the presence of microthrombi and aggregates of blood cells in the vessels of internal organs [8].

The morphological study showed that in animals the lung tissue in certain fields of view is enphysematous with areas of dysatelectasis. Sharp congestion of the microcirculatory bed. No total vascular occlusion was noted. In small vessels, agglutiation of erythrocytes and erythrocyte thrombi were determined, and in some vessels - typical thrombi with the presence of fibrin and leukocytes (Fig. 1).

Moderate parenchymal degeneration was observed in the kidneys. Congestion of the microcirculatory bed. In the capillaries of the glomeruli and the vessels of the medulla, aggregation of erythrocytes was determined, and in some cases, erythrocyte thrombi (Fig. 2).

Dystrophic and necrobiotic changes in cells were observed in the zona glomerulosa and zona fasciculata of the adrenal cortex. There are focal hemorrhages in the cortex and capsule. Partial occlusion of the microvasculature in the form of erythrocyte aggregation was noted (Fig. 3).

In the liver, parenchymal degeneration of hepatocytes with areas of necrobiosis and necrosis was observed. The interbeam capillaries are dilated and full of blood. In some of them, erythrocyte aggregation was determined. Focal hemorrhages were noted in the parenchyma (Fig. 4).

Thus, we have developed a new experimental model of DIC syndrome, in which the successive stages of development of this pathology are clearly traced and which corresponds to the clinical picture of the subacute form of DIC syndrome.

Fig. 1. Lung. Erythrocyte thrombus. Hematoxylin and eosin, x400.

Fig. 2. Kidney. Aggregation in glomeruli. Hematoxylin and eosin, x400.

Fig. 3. Adrenal gland. Focal hemorrhage. Hematoxylin and eosin, x400.

Fig. 4. Liver. Necrobiosis and necrosis of hepatocytes. Hematoxylin and eosin, x400.

disseminated intravascular coagulation snake efa

References

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2. Yoshikawa T., Furukawa Y., Murakami M., Takemura S., Kondo M. (1981). Experimental model of disseminated intravascular coagulation induced by sustained infusion of endotoxin. Research in experimental medicine. Zeitschrift fur die gesamte experimented Medizin einschliesslich experimenteller Chirurgie, 179(3), 223-228.

3. Berthelesen L.O., Kristensen A.T., Tranholm M. (2011). Animal models of DIC and their relevance to human DIC: A systematic review. Thrombossis research, 128(2), 103-116.

4. Jeon Y.J., Kim J.W., Park S., Shin D.W. (2019). Risk factor, monitoring, and treatment for snakebite induced coagulopathy: a multicenter retrospective study. Acute and critical care, 34(4), 269-275.

5. European convention for the protection of vertebrate animals used for experimental and other scientific purpose (1986). Council of Europe 18.03.1986. Strasbourg, 52.

6. Levi M., Toh C.H., Thachil J., Watson H.G. (2009). Guidelines for the diagnosis and management of disseminated intravascular coagulation. British Committee for Standards in Haematology. British journal of haematology, 145(1), 24-33.

7. Maly J., Pecka M., Pidrman V., Blaha M., Siroky O., Jebavy L. (1994). Poznamky k diagnostice a lecbe diseminovane intravaskularni koagulace [Diagnosis and therapy of disseminated intravascular coagulation]. Casopis lekaru ceskych, 133(23), 719-722.

8. Dalainas I. (2008). Pathogenesis, diagnosis, and management of disseminated intravascular coagulation: a literature review. European review for medical and pharmacological sciences, 12(1), 19-31.

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