Role of some neurohumoral factors in the development of pulmonary hypertension in patients with interstitial Jung diseases


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Aim. To ascertain the role of some neurohumoral factors - nitric oxide (NO), ACE, histamine - in development of pulmonary hypertension (PH) in patients with interstitial lung diseases (ILD). Material and methods. A total of 32 ILD patients were examined. Of them 14 had idiopathic fibrosing alveolitis (IFA), 6 had exogenous allergic alveolitis (EAA) and 12 patients had ILD in diffuse disease of the connective tissue (ILD-DDCT). In addition to routine tests, those for NO, ACE, histamine, serotonin in plasma were performed; Doppler echocardiography and high-resolution computed tomography were conducted. In 9 patients the diagnosis was verified at thoracoscopic biopsy of the lung. The control group consisted of 16 healthy subjects.
Results. The highest mean pressure in the pulmonary artery (PmPA) was registered in IFA vs EAA and ILD-DDCT patients (p < 0.001). NO concentration in plasma was higher in ILD-DDCT than in control patients. In IFA and EAA the level of NO was like in controls. Concentration of NO in plasma oflDL patients correlated with high activity of the process. No correlation was found between ACE in plasma and PmPA, ACE levels were much higher in controls than in the ILD patients (p < 0.05). Histamine levels were higher in ILD patients than in controls being the highest in ILD-DDCT. Serotonin was insignificantly higher in ILD patients than in controls.
Conclusion. Damage to the endothelium of the pulmonary arteries and imbalance of neurohumoral factors may be considered as a mechanism of development and stabilization of PH in ILD patients.

References

  1. Привалова Е. В. Легочная артериальная гипертензия при пороках сердца: Дис.... д-ра мед. наук. М.; 1998.
  2. Беленков Ю. Н., Чазова И. Е. Первичная легочная гипертензия. М.: Нолидж; 1999.
  3. Weitzenblum E., Hirth С. et al. Prognoctic value of pulmonary artery pressure in chronic obstructive pulmonary disease. Thorax 1981; 36: 752-758.
  4. Cailesl J., Winter S. et al. Defective endothelial^ mediated pulmonary vasodilatation in systemic sclerosis. Chest 1998' 144: 178-184.
  5. Schuster D. P., Crouch E. G. et al. Angiotensinconverting enzyme expression in primary pulmonary hypertension. Am. J. Respir. Crit. Care Med. 1996; 154: 1087-1091.
  6. Egermayer P., Town G. I., Peacock A. J. Role of serotonin in the pathogenesis of acute and chronic pulmonary hypertension. Occasional review. Thorax 1995; 54: 161 - 168.
  7. Tuder R. M., Voelkel N. F. Pulmonary hypertension and inflammation. J. Lab. Clin. Med. 1998; 132: 16-24.
  8. Curzen N., Archer S. Chronic lung disease and pulmonary hypertension: yes or no to NO? Thorax 1997; 52: 105-106.
  9. Singh S., Evans T. W. Nitric oxide, the biological mediator of the decade: fact or fiction? Eur. Respir. J. 1997; 10: 699-707.
  10. Pogorielska H., Korevwicki J., Zielinski T. et al. Prognostic significance of changes in complaince of the pulmonary venous system after isosorbiddinitrate in patients with mitral stenosis. Int. J. Cardiol. 1995; 49 (1): 9-15.
  11. Yoshihiko Katayama, Higenbottam T. W., de Atauri M. J. Diaz et al. Inhaled nitric oxide and arterial oxygen tension in patients with chronic obstructive pulmonary disease and severe pulmonary hypertension. Thorax 1997; 52: 120-124.
  12. Haas F., Bergofski E. H. Role of the mast cells in the pulmonary pressor response to hypoxia. J. Clin. Invest. 1972; 51: 154-162.
  13. Pogadaev V. I., Timin E. N., Khodorov B. I. Membrane mechanisms of activating depolarized smooth muscle contraction (guinea pig small intestine) during exposure to physiologically active compounds. Biofizika 1978; 23 (2): 290-295.
  14. Hales С. A., Kazemi H. Role of histamine in the hypoxic vascular response of the lungs. Respir. Physiol. 24: 81-88.
  15. Герасимов Н. М., Гулямов Д. С., Нам Л. Н. Роль эндогенных биологическиактивных веществ в регуляции легочного кровообращения у больных с гиперволемическими врожденными пороками сердца. Кардиология 1995; 31-33.
  16. Клиническое руководство по ультразвуковой диагностике. М.: ВИДАР; 1998; т. 5: 13.
  17. Reynolds T. The echocardiographer's pocket reference: Arizona Heart Institute Foundation; 1993. 160.
  18. Шахнович Р. М., Ефремов Е. Е., Игнашенкова Г. В. и др. Фенотип АПФ при различных формах ИБС. Кардиология 2000; 40 (6): 18-22.
  19. Герасимова Ц. И. Определение серотонина, триптофана, 5-окситриптофана, 5-оксииндолуксусной кислоты, гистамина и гистидина в одной пробе биологического материала. Лаб. дело. .1977; 1: 14-21.
  20. Ультразвуковая диагностика в кардиологии: Метод, пособие. М.: Международный центр авторских мед. технологий; 1992.
  21. Robbins. Pathologic basis of disease. 1999.
  22. Higenbottam T. Pathology of pulmonary hypertension. A role of endothelial dysfunction. Chest 1994; 105 (2, supple):
  23. Girod С. E. The lung in mixed connective tissue disease. Semin. Respir. Crit. Med. 1999; 20 (2): 99-108.
  24. Shen J. Y. et al. Pulmonary hypertension in systemic lupus erythematosus. Rheumatol. Int. 1999; 18: 147-151.
  25. Quismorio F. P. et al. Immunopathologic and clinical studies in pulmonary hypertension associated with SLE. Semin. Arthr. Rheum. 1984; 13: 349-359.
  26. Fahey P. et al. Raynaud's phenomenon of the lung. Am. J. Med. 1984; 76: 263-269.
  27. Gomez-Reino J. J. Pulmonary hypertension in connective tissue diseases. Br. J. Rheum. 1994; 33 (9): 796-797.
  28. Murata I. et al. Clinical evaluation of p. h. in systemic sclerosis and related disorders. A Doppler EchoCG. Study of 135 Japanese patients. Chest 1997; 111: 36-43.
  29. Bunch T. W., Tancredi R. G., Lie J. T. Pulmonary hypertension in polymyositis. Ibid. 1981; 79: 105-107.
  30. Шаталов Н. Н., Гусейнов С. Н. Легочная гипертензия при идиопатическом фиброзирующем альвеолите. Пробл. туб. 1984; 12: 29-33.
  31. Архипова Д. В., Мухин Н. А., Корнев Б. М. Легочная гипертензия при интерстициальных болезнях легких. Клин. мед. 2002; 6: 13-20.
  32. Adnot S., Raffestin В. Pulmonary hypertension: NO-therapy? Thorax 1996; 51: 762-764.
  33. Попова Е. Н. Клинико-морфологическая характеристика альвеолита при идиопатическом фиброзирующем альвеолите и саркоидозе. Дис. ... канд. мед. наук. М., 1996.
  34. Ozavwa Т. et al. Increased serum angiotensin I-converting enzyme activity in patients with mixed connective tissue disease and pulmonary hypertension. Scand. J. Reumatol. 1995; 24 (1): 38-43.
  35. Morrell N. W. et al. Angiotensin converting enzyme expression is increased in small pulmonary arteries of rats with hypoxia-induced p. h. J. Clin-Invest. 1995; 96 (4): 1823-1833.
  36. Mancini G. B. J., Henry G. C. et al. Angiotensin-converting enzyme inhibition with quinapril improves endothelial vasomotor dysfunction in patients with coronary artery disease. The TREND (Trial on Reversing Endothelial Dysfunction) study. Circulation 1996; 94: 258-265.
  37. Anderson T. J., Elstein E., Haber H. et al. Comparative study of ACE-inhibition, angeotensin II antagonism, and calcium channel blockade on flow mediated vasodilatation in patients with coronary disease (BANFF Study). J. Am. Coll. Cardiol. 2000; 35: 60-66.
  38. Goldberg N. D., О'Dean W. C., Haddox M. K. In: Advances in cyclic nucleotide research. New York; 1973; 3: 155-223.

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