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Active oxygen forms (AOF) were measured in whole peripheral blood of 40 acute pneumonia patients using luminol-dependent spontaneous chemiluminescence (LDSC) and luminol-dependent zymosan-stimulated chemiluminescence (LDZSC) in the time course of the disease. Within week 1 of the disease both LDSC and LDZSC were increased in the majority of patients whereas low levels of AOF production served a predictor of poor prognosis in relation to acute pneumonia complications. If high intensity of LDSC and LDZSC persisted for 2 weeks pneumonia was likely to resolve completely though complications were possible. Protracted disease was associated with 3-week high AOF production. The data give evidence for possible application of LDSC and LDZSC of whole peripheral blood to predict complications and incomplete resolution of acute pneumonia.

A study was made of the production of active forms of oxygen (AFO) by liminol-dependent spontaneous chemiluminescence (LSC) of isolated polymorphonuclear leukocytes (PNL) and whole blood in 39 patients with acute pneumonias in different disease periods. The majority of the patients manifested activation of oxygen metabolism of PNL, with the intensity of LSC of whole blood appreciably exceeding LSC of neutrophils isolated from the given blood sample. If the production of AFO is insufficient, the acute period of pneumonia is characterized in most cases by the complicated disease course. Studies into LSC of whole blood is more informative for predicting complications within these times. The lack of the increment of the whole blood LSC intensity on the second week of the disease as compared to the first week as well as a rapid decrease of the initially high level of LSC to the level not differing from the donor's parameters is prognostically unfavourable as regards complete recovery. Inadequately high and long (during 3 weeks) generation of AFO detectable by both methods was associated with the lingering course of pneumonia. The monitoring of LSC of PNL and whole blood allows predicting complications of acute pneumonia together with administering corrective therapy with the aid of immunomodulators and antioxidants.

The presence of the lymphocyte migration inhibition factor consequent upon sensitization of the organism to the antigen of denaturalized protein of the heart muscle was studied in 72 patients with myocardial infarction and in 40 healthy individuals. It was established that the migration inhibition factor appears in the blood 6 hours after the occurrence of myocardial infarction. The migration index is 52 +/- 2% in such patients and no less than 90% in the controls.

Humoral and cellular immunological paramaters were studied in 3 groups of patients with ischemic heart disease. A distinct correlation was revealed between these parameters and clinical symptoms of the disease. It was shown that an immunological reconstruction took place already in the ischemic stage of coronarosclerosis. This reconstruction is expressed by the growth of hemagglutinating and precipitating antibody titers, as well as by the emergence of sensitized lymphocytes and excretion of the lymphocyte migration inhibiting factor. The use of various homogenates (a normal or atherosclerotic aorta, an infarctial myocardium) or the nonspecific mitogen PHA showed the presence of a specific antigenoactive complex in the blood of patients with ischemic heart disease. The complex was capable of penetrating and affecting the vascular wall as well as of producing antitissular (antivascular) antibodies which, together with the other factors, can help lipoprotein penetration through the arterial wall to form atheromatous plaques.