Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034069 (pulmonary fibrosis)
 7,050 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors investigated the influence of some vasodilatory drugs on pulmonary and systemic haemodynamic parameters in 69 patients with pulmonary hypertension secondary to chronic obstructive pulmonary disease (with the exception of two patients with diffuse pulmonary fibrosis and one patient with recurrent pulmonary thromboembolism). The investigated vasodilatory drugs were as follows: Dihydralazine Spofa--8 patients, Corinfar--10 patients, Ketanserin--13 patients, Nit-Ret 7 patients, Nitroglycerin Spofa--10 patients, Nitro-Mack--11 patients, Iso-Mack retard--10 patients. The haemodynamic parameters were measured before and at various time intervals after the administration of the vasodilatory agent (Dihydralazine 50 mg perorally--30th and 60th minute, Corinfar--20 mg sublingually--60th minute, and in 7 patients following a 6 months period of 30-60 mg Corinfar daily dose, Ketanserin--10 mg intravenously--10th, 20th and 40th minute, Nit-Ret--2.5 mg perorally--30th and 60th minute, Nitroglycerin Spofa--0.5 mg sublingually--10th and 30th minute, Nitro-Mack--1 mg intravenously--immediately following the end of a slow i. v. infusion for 20 minutes, Iso-Mack retard--20 mg perorally, 60th minute). The blood gases were measured at the same time intervals, too. The results in various groups were as follows: Dihydralazine administration was not followed by any significant change in PAP, CO, PVR, while a significant decrease in AOP and SVR was ascertained. A significant decrease of PaCO2 and no change in PaO2 were measured. Following Corinfar administration, no change in PAP, CO or PVR and a significant decrease of PaCO2 and no change in PaO2 were measured. Following Corinfar administration, no change in PAP, CO or PVR and a significant decrease in AOP were determined. No significant changes in blood gases were measured. Following a 6 month Corinfar treatment period in 7 subjects, no significant changes in pulmonary haemodynamics or blood gases values were found. No clinical benefit of this drug could be estimated. Ketanserin administration was not followed by any changes in pulmonary haemodynamics, whereas a significant decrease in AOP and SVR were found. The administration of Nit-Ret was followed by a significant decrease of CO, whereas no changes in PAP, AOP or PVR and SVR were found. No significant changes in the blood gas tenses values were measured. The administration of Nitroglycerin Spofa was followed by a significant decrease in RAP, PAP, AOP, RVEDP as well as in CO. No significant changes in blood gases were observed. The application of 1 mg Nitro-Mack intravenously was followed by a significant decrease in RAP, PAP, AOP and CO.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Changes in pulmonary and systemic haemodynamics after the administration of various vasodilators in patients with pulmonary hypertension. 208 23

We studied the effect of ketanserin on hemopoietic progenitor cells (Lin(-)Sca-1(+)c-Kit(+)CD34- and Lin(-)Sca-1(+)c-Kit(+)CD34(+)), progenitor hemopoietic cells (Lin(-)Sca-1(+)c-kit(+)), and multipotent mesenchymal stromal cells (CD45(-)CD73(+)CD106(+)) in C57Bl/6 mice during pulmonary fibrosis. It was shown that the blocker of 5-HT2A receptors lowers the activity of bleomycin-induced inflammation in the lungs and prevents the infiltration of alveolar interstitium and alveolar ducts by hemopoietic stem and hemopoietic progenitor cells; in this case, they are more numerous in the bone marrow of sick animals. Ketanserin reduces the capacity for self-renewal of lung multipotent mesenchymal stromal cells in the fibrotic phase of the disease and inhibits their differentiation into stromal cell lines (adipocytes, chondrocytes, and fibroblasts) simultaneously with the decrease in the percentage of connective tissue in the lung parenchyma.
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PMID:Response of hemopoietic, progenitor, and multipotent mesenchymal stromal cells to administration of ketanserin during pulmonary fibrosis. 2540 89