HEMODYNAMIC PATTERN AND SOMATIC SURVIVAL OF POTENTIAL ORGAN DONORS IN THE BRAIN DEATH ANIMAL MODEL

Highlights

The article deepens the understanding of the pathogenesis of brain death in potential organ donors and, in particular, clarifies information on the dynamics of hemodynamic disorders and their contribution to the somatic survival of potential donors, which constitutes the scientific novelty of the study.

Abstract

Aim. To study the development of early central hemodynamic disturbances and evaluate the somatic survival of experimental organ donor animals using an experimental model of brain death

Methods. The experiments were carried out on mature outbred male rats (n = 50). The experimental animals of experimental group №1 (n = 20, normotensive individuals, optimal donors) were anesthetized, invasive mean arterial pressure (MAP) and heart rate (HR) were recorded. Brain death was modeled by creating intracranial pneumopression. For conditioning the potential donor with brain death mean BP and HR were recorded for 3 hours; when mean BP dropped below 75 mm Hg, Gelofusin solution (B. Braun medical, AG, Switzerland) was infused. Animals from experimental group №2 (n = 20, hypotensive individuals, “marginal” donors) were anesthetized, then brain death was modeled in them, and mean BP and HR were monitored in the same way as in experimental group №1, but without correction of developing hemodynamic disorders. Intact anesthetized intubated animals (n = 10), whose hemodynamic parameters were recorded, served as controls.

Results. After 30 minutes from the beginning of the experiment and further at all observation periods, a decrease in mean BP and HR was observed in the groups of normotensive and hypotensive animals compared to the control. By the end of the third hour of the experiment, despite volemic support, in normotensive animals, mean BP decreased to 60 [61; 67] mm Hg (p = 0.01 compared to the control), HR to 250 [248; 260] beats/min (p = 0.03 compared to the control). In the group of hypotensive animals, the dynamics of the decrease in mean BP was more pronounced and by the end of the third hour of the experiment, mean BP was 45 [41; 46] mm Hg (p = 0.01 compared to the control and normotensive animals), HR – 230 [224; 237] beats/min (p = 0.03 compared to the control and normotensive animals). In the normotensive group of animals, death due to progression of circulatory failure occurred in 8 individuals, the mortality rate was 40%, p = 0.02 compared with the control. In the hypotensive group of animals, death occurred in 14 individuals, the mortality rate was 60%, p = 0.01 compared with the control and normotensive animals.

Conclusion. The results of the study of early central hemodynamic disturbances in an experiment on a brain death model indicate the development of more pronounced circulatory failure in marginal donors, which is accompanied by an increase in their mortality within 3 hours after the induction of brain death in comparison with optimal donors. Correction of systemic perfusion disturbances by volemic loading leads to an improvement in hemodynamic parameters and somatic survival of potential donors.

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