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The authors studied changes in beta- and alpha 1-adrenoceptors (beta-AC, alpha 1-AC) as well as in m-cholinoceptors in tuberculosis, pneumonia and cancer. Specimens of the lung parenchyma were obtained at thoracic surgery from 43 patients. Relevant ligands binding to the receptors was evaluated by incubation of the membrane proteins with radioligands varying in concentrations. Irrespective of the inflammation variant, beta-AC and alpha 1-AC levels were found decreased this being an correlation with the scope of fibrous and destructive involvement. The degree of the process chronicity and advance was judged from a decline in the binding parameters for beta-AC and alpha 1 AC. A dramatic fall in alpha 1 AC occurred in tuberculosis. This may be related to microcirculatory failure and vascular deformity. The levels of m-cholinoceptors underwent insignificant changes in pulmonary inflammation, whereas lung cancer displayed their sharp rise.

In the present study alpha 1-adrenergic receptors have been investigated in liver parenchyma, obtained at the resection of prehepatic portal hypertension children without parenchymal affection (control group, n = 7) and the resection of children in parenchymal affection (group of cirrhosis, n = 8). It has been shown, that the binding of alpha 1-adrenergic antagonist 3H-prasozin (3H-PRZ) in liver parenchyma membranes of both control and cirrhosis groups is saturable and shows a high affinity. The Scatchard analysis of the binding data indicated that the binding site is characterized by Kd and Bmax of 0.6 +/- 0.12 nM, 92.8 +/- 8.0 fmol/mg, respectively, for the control group; and 1.5 +/- 0.4 nM, 254.1 +/- 28.4 fmol/mg, respectively, for the group of cirrhosis; (mean +/- SEM). It has been found that the number of binding sites of 3H-PRZ significantly increases in cirrhosis liver parenchyma in comparison with the control group. The results obtained suggest that alpha 1-adrenergic receptors play an important role in cirrhosis formation in children, showing liver parenchyma affection severity and its regenerative properties.

In the present study adrenergic receptors have been investigated in liver parenchyma, obtained at the resection of extrahepatic portal hypertension children without parenchymal affection (control group, n-7) and the resection of children in parenchymal affection (group of chronic hepatitis children, n-6). It has been shown, that the binding of beta-adrenergic radioligand 3H-dihydroalprenolol (3H-DHA) in liver parenchyma membranes of both control and chronic hepatitis groups was saturable and showed high affinity. The Scatchard analysis of the binding data indicated that the binding site was characterized by Kd and Bmax of 1.2 +/- 0.5 nM, 261.2 +/- 50 fmol/mg, respectively, for the control group; and 0.9 +/- 0.15 nM, 68.5 +/- 18.8 fmol/mg, respectively, for the group of chronic hepatitis patients; (mean+SEM). The binding of alpha 1-adrenergic antagonist 3H-prazosin (3H-PRZ) in liver parenchyma was also saturable and showed high affinity. The binding site is characterized by Kd = 0.6 +/- 0.12 nM, Bmax = 92.8 +/- 8.0 fmol/mg, for the control group; and Kd = 0.8 +/- 0.15 nM, Bmax = 195.0 +/- 22.0 fmol/mg, for the group of chronic hepatitis. It has been found that the number of binding sites of 3H-DHA significantly decreased and the number of binding sites of 3H-PRZ did not change in chronic hepatitis liver parenchyma in comparison with the control group. The results obtained suggest the important role of beta-adrenergic receptors in the pathogenesis of chronic hepatitis and in liver regeneration in children.

Adrenergic receptors were studied in human lung parenchyma obtained from 10 patients with tuberculoma after segmental resection within the limits of surrounding normal tissues (controls) as well as from 10 patients with destructive pulmonary tuberculosis. Binding of alpha-adrenergic radioligand 3H-prazosin was saturable with high rate of affinity in lung parenchymal membranes of both normal tissues and tissues impaired with tuberculosis. The Scatchard analysis indicated that the affinity of 3H-prazosin binding was not altered in patients with tuberculosis, while amount of the ligand binding sites was significantly decreased as compared with control preparations (KD = 0.5 +/- 0.9 nM, Bmax = 273.5 +/- 59.9 fmol/mg in controls; KD = 0.5 +/- 0.07 nM, Bmax = 51.7 +/- 7.5 fmol/mg in tuberculous lung parenchyma). beta-Adrenergic and muscarinic acetylcholinergic receptors were studied in lung parenchyma of patients with tuberculosis. Binding parameters of beta-adrenergic ligand 3H-dihydroalprenolol and muscarinic antagonist 3H-quinuclidinyl benzylate were similar to those of control values. Amount of 3H-dihydroalprenolol binding sites was not markedly altered while content of 3H-prazosin binding sites was considerably decreased in lung parenchyma of patients with tuberculosis as compared with normal state. The data obtained suggest that population of alpha-adrenergic receptors was decreased in human lung parenchyma under conditions of destructive tuberculosis.

beta-Adrenergic and muscarinic cholinergic receptors have been investigated in human lung parenchyma during cancer and chronic pneumonia as compared with normal tissue, obtained after segmental resection of tuberculoma from surrounding normal tissues. Binding of beta-adrenergic radioligand 3H-dihydroalprenolol (3H-DHA) and muscarinic antagonist 3H-quinuclidinyl benzylate (3H-QNB) was saturating with high rate of affinity in lung parenchyma membranes of both controls and patients with cancer and chronic pneumonia. Amount of binding sites of 3H-QNB was significantly increased in cancer (Bmax = 377.5 +/- 65.5 fmole/mg) and did not change in chronic pneumonia (Bmax = 97.7 +/- 14.7 fmole/mg) as compared with normal tissues (Bmax = 108.9 +/- 12.1 fmole/mg); a number of binding sites of 3H-DHA was significantly decreased both in lung parenchyma under conditions of cancer (Bmax = 84.1 +/- 14.5 fmole/mg) and chronic pneumonia (Bmax = 113.8 +/- 10.3 fmole/mg) as compared with normal tissue (Bmax = 456.7 +/- 73.7 fmole/mg). The affinity of 3H-DHA and 3H-QNB binding was practically unaltered. The results obtained suggest the important role of beta-adrenergic receptors in formation of lung cancer in the patients with pneumonia.

beta-Adrenergic and muscarine acetylcholinergic receptors were studied in human lung parenchyma obtained from patients with tuberculoma (after segmental resection of tuberculoma surrounding normal tissues were performed to obtain control samples) as well as from patients with pulmonary adenocarcinoma. Assays of binding of beta-adrenergic radioligand 3H-dihydroalprenolol (3H-DHA) exhibited high affinity in lung parenchyma membranes in both control samples and in that of patients with tumors. Binding of muscarine antagonist 3H-quinuclidinyl benzylate (3H-QNB) also showed high rate of affinity in lung parenchyma. High number of 3H-DHA binding sites was distinctly decreased and 3H-QNB--was increased in lung malignant tumors as compared with normal tissue. Considerable decrease of beta-adrenergic and increase of muscarine receptors were found in patients with pulmonary adenocarcinoma. beta-Adrenergic and muscarine receptors appear to be of importance in pathogenesis of human lung malignant tumors.

Application of biochemical parameters of blood, reflecting disturbances in lipid, protein, carbohydrate, pigment and water-saline metabolism for diagnostics for internal organs diseases is discussed. Methods of clinical biochemistry in combination with subsequent automatic processing of the data obtained on the basis of probability theory and mathematical statistics methods can be used for preliminary computer diagnosis and further examination of a patient, as well as for construction of specific complexes of symptoms for some diseases. Due to their mobility, the preliminary computer diagnostics data can be successfully applied to different pathologies and groups of population.