AIM: To specify formation of systemic compensatory-adaptive processes and analysis of their characteristics in cardiac failure (CF) of various genesis. MATERIALS AND METHODS: 101 patients with CF functional class II (53 patients with IHD without blood hypertension and 48 patients with blood hypertension without IHD) were examined for lactate, 2,3-diphosphate dehydrogenase (DPG), activity of lactate dehydrogenase (LDG), G-6-PDG in red cells, succinate dehydrogenase (SDG) in leukocytes. 47 patients received treatment including inhibitors of angiotensin-converting enzyme (ACEI). RESULTS: IHD patients demonstrated after treatment drop in the levels of lactate, 2,3-DPG, LDG, SDG activation. Hypertensive patients continued with latent hypoxia (high activity of SDG, G-6-PDG, 2,3-PDG, low lactate concentration). LDG and G-6-PDG rose more in patients given ACEI. CONCLUSION: At initial stages of CF blood system compensatory reactions form differently depending on the mechanism of decompensation development. This is confirmed by changes of blood oxygen-transport function and cell metabolism.
AIM: To specify formation of systemic compensatory-adaptive processes and analysis of their characteristics in cardiac failure (CF) of various genesis. MATERIALS AND METHODS: 101 patients with CF functional class II (53 patients with IHD without blood hypertension and 48 patients with blood hypertension without IHD) were examined for lactate, 2,3-diphosphate dehydrogenase (DPG), activity of lactate dehydrogenase (LDG), G-6-PDG in red cells, succinate dehydrogenase (SDG) in leukocytes. 47 patients received treatment including inhibitors of angiotensin-converting enzyme (ACEI). RESULTS: IHD patients demonstrated after treatment drop in the levels of lactate, 2,3-DPG, LDG, SDG activation. Hypertensivepatients continued with latent hypoxia (high activity of SDG, G-6-PDG, 2,3-PDG, low lactate concentration). LDG and G-6-PDG rose more in patients given ACEI. CONCLUSION: At initial stages of CF blood system compensatory reactions form differently depending on the mechanism of decompensation development. This is confirmed by changes of blood oxygen-transport function and cell metabolism.