Hemorrhagic shock (HS) is a life-threatening condition that leads to multiple organ failure due to centralization of blood flow and impaired blood clotting. In this study, we investigated the acute and delayed effects of HS on the brain, kidneys, and liver of rats to identify molecular targets for therapy of the consequences of shock. Blood acid-base balance and electrocardiography (ECG) parameters were studied in rats in the acute phase of HS. Gene expression of antioxidant enzymes (Gpx1, Sod1, Cat, Nfe2l2) and inflammatory markers (Ptprc, Cxcl1, Cd86, Itgal, Il1b, Il6, Tnf, Tlr2, Cox2, Cst7, Ccl3, Il10) in brain, kidney, and liver tissues was analyzed, as well as the amount of protein markers for kidney damage (NGAL, KIM-1) in urine 24 h after HS. In addition, markers for the activation of astrocytes (Gfap) and microglia (Aif1) as well as neuronal markers (Eno2, Tubb3) in brain tissue were analyzed. Biochemical markers for liver and kidney damage and total antioxidant activity were determined in blood serum. Acute HS caused decompensated lactic acidosis, arterial hypotension and characteristic changes in the ECG. Although no pronounced inflammatory response was detected in brain, kidney and liver tissue in the late phase after acute blood loss, the brain and liver tissue were more susceptible to the adverse effects of acute blood loss than the kidneys according to a number of indicators. This points to the need to develop targeted strategies to protect organs in the post-resuscitation period by targeting specific molecular targets in specific tissues.
Andrianova et al. (2026) studied this question.