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Idiopathic pulmonary fibrosis (IPF), known in Europe as cryptogenic fibrosing alveolitis, is a rare, progressive and usually fatal form of idiopathic interstitial pneumonia. IPF is characterized by failure of alveolar re-epithelization, persistence of fibroblasts, deposition of extracellular matrix, and distortion of lung architecture which ultimately results in respiratory failure. Current consensus statements reserve the term IPF to refer to a specific clinical entity associated with the histopatological pattern of usual interstitial pneumonia (UIP). UIP is characterized by temporal heterogeneity, with alternating areas of interstitial fibrosis, fibroblastic foci (areas of proliferating fibroblasts and myofibroblasts), inflammation, honeycomb lung, and normal parenchyma. Fibroblastic foci are associated with progressive disease. Treatment of IPF remains clinical problem. Currently, there is no conservative therapy improving the survival of patients. Lung transplantation, however, improves survival. Identification of pathways crucial to fibrogenesis might offer potentially novel therapeutic targets to slow or halt progression of IPF.

Background: Parasympatolytics are recommended as the first choice remedy in patients with the chronic obstructive lung disease. Though their side effects are rare, some physicians are afraid of they can in high doses influence the cardiovascular system. The aim of the work was to ascertain whether the inhalation of 0.12 mg of ipratropium bromide might affect the systemic and pulmonary circulation., Methods and Results: 15 patients (10 males, 5 females, average age 61.8 +/- 10.3 years) with chronic obstructive lung disease (13) and idiopathic pulmonary fibrosis (2) were examined during the period of disease stabilisation. Results of the right-side catheterization were not statistically changed (p < 0.91) 30 or 60 minutes after the inhaling of 0.12 of ipratropium. Also the value of the pick expiratory forced rate (PEFR) was not statistically increased (p < 0.25)., Conclusions: Inhaling of 0.12 mg of ipratropium in patients with serious chronic pneumopathies did not affect systemic or pulmonary hemodynamics. Such dose appears to be safe even for patients with the chronic ischaemic hart disease.