Intestinal oxygen exchange at condition of anemia

Abstract

Relevance. Although disorders of oxygen delivery is one of the main factors in the development of intestinal dysfunction and bacterial translocation, the critical level of anemia and possibilities of it lowering remain unclear. Aim. Тo study changes of the system as well as the regional mesenterial oxygen exchange in conditions of normovolemic anemia of different severity. Material and methods. In experiment on 60 white rats under the general anaesthesia by ketamine 50 mg/kg stage-by-stage blood donation and it normovolemic replacement by hydroxyethyl starch were performed, gradually reducing haematocrit to 0,30, 0,25 and 0,20 l/l. Arterial, mixed venous, and mesenteric venous PO2, PCO2, and pH were measured. Systemic and intestinal oxygen transports and consumptions (DO2 and VO2) were calculated by standard equations. The content of lactic acid in the intestinal tissues is additionally determined to assess the degree of activity of local anaerobic metabolism. Results. At mild anemia reduction СаО2 by third of initial size essentially did not influence on system and regional DО2 to tissues. Compensation of oxygen deficiency at haematocrit 0,30 л/л was carried out by rising of a cardiac index due to reduction of viscosity of blood. At moderated anemia concentration hemoglobin and СаО2 decreased twice, changes in system DО2 to tissues led to reduction of Са-vО2 by 32,1 % (р < 0,05). Physiological adaptation was carried out through the increasing of О2ЕR by tissues and was effective. In experimental animals with severe degree of anemia (Hb 58,8 ± 2,4 g/l) СаО2 decreased in 2,5 times what led to occurrence of haemic hypoxia according to level of gases contents of blood. The concentration of lactic acid in intestinal tissues increased on 36.1 % (p = 0.05), deficiency of buffer bases till -8,2 ± 1,7 (p = 0.05). Conclusions. In case of severe anaemia, hypoxia of the intestinal tissues develops, which is accompanied by an increase in the local levels of lactic acid and deficiency of base buffers with the development of subcompensated metabolic acidosis.