scholarly journals Abiotic dissolution rates of 24 (nano)forms of 6 substances compared to macrophage-assisted dissolution and in vivo pulmonary clearance: Grouping by biodissolution and transformation

NanoImpact ◽  
2018 ◽  
Vol 12 ◽  
pp. 29-41 ◽  
Author(s):  
Johanna Koltermann-Jülly ◽  
Johannes G. Keller ◽  
Antje Vennemann ◽  
Kai Werle ◽  
Philipp Müller ◽  
...  
1987 ◽  
Vol 33 (10) ◽  
pp. 923-927 ◽  
Author(s):  
B. Kournikakis ◽  
L. A. Babiuk

The synergistic interactions between Pseudomonas aeruginosa and virulent or attenuated murine cytomegalovirus (MCMV) were compared in vivo. Virulent MCMV challenge at a dose of 5 × 105 pfu/mouse intraperitioneally, followed by intranasal superinfection with 5 × 106 cfu/mouse of Pseudomonas aeruginosa after 48 h resulted in greater than 80% mortality, apparently owing to a failure of pulmonary clearance mechanisms. Single infections, or the use of attenuated MCMV in synergistic infections, did not result in significant morbidity or mortality. Infection with virulent MCMV in vivo resulted in the rapid spread of virus to the lung, liver, and spleen, followed later by spread to the salivary glands. Attenuated virus was detected in salivary glands only. Virulent MCMV was more effective in adsorbing to, or infecting, spleen cells in vitro than attenuated virus. Viral neutralization experiments using anti-viral serum, rabbit complement, and anti-mouse IgG confirmed the presence of a nonneutralizing antibody on the surface of the virulent virus. Our results suggest that the presence of the nonneutralizing antibody on virulent MCMV allows the virus to preferentially infect, or adsorb to, Fc+ cells in the peritoneum. These cells may then carry the virus, via the lymphatic circulation, to other areas of the body, resulting in the replication of virus in multiple organs. Virus replication in the lung may, in part, be the cause of the observed suppression of pulmonary clearance.


1983 ◽  
Vol 15 (2) ◽  
pp. 167-175 ◽  
Author(s):  
Hartmut Derendorf ◽  
Gertrude Drehsen ◽  
Peter Rohdewald

1997 ◽  
Vol 23 (10) ◽  
pp. 967-972
Author(s):  
Richard R. Schartman ◽  
Jens T. Carstensen

1996 ◽  
Vol 81 (4) ◽  
pp. 1510-1515 ◽  
Author(s):  
Jocelyn Dupuis ◽  
Carl A. Goresky ◽  
Alain Fournier

Dupuis, Jocelyn, Carl A. Goresky, and Alain Fournier.Pulmonary clearance of circulating endothelin-1 in dogs in vivo: exclusive role of ETB receptors. J. Appl. Physiol. 81(4): 1510–1515, 1996.—The pulmonary circulation plays an important role in the removal of circulating endothelin-1 (ET-1). Plasma ET-1 levels are increased in pulmonary hypertensive states of various etiologies (e.g., idiopathic, heart failure, and congenital anomalies) in proportion to the severity of pulmonary hypertension. It is possible that reduced pulmonary clearance of this peptide contributes to the hyperendothelinemia of those pathologies. The ETA and ETB receptors are abundant in lung tissues: on the vascular endothelium, the ETB receptor is predominant and may contribute to ET-1 extraction through receptor-mediated endocytosis. We designed experiments to determine and quantify the importance of the ETA and ETB receptors in the pulmonary extraction of circulating ET-1 in anesthetized dogs. The single-pass cumulative tracer ET-1 extraction by the lung was measured with the indicator-dilution technique before and 5 min after intrapulmonary injection of the specific ETAantagonist BQ-123 ( n = 5, 120–960 nmol) and the specific ETBantagonist BQ-788 ( n = 6, 1,000 nmol). The inhibitors had no significant effect on pulmonary and systemic hemodynamics. Mean cumulative pulmonary ET-1 extraction was not modified by BQ-123 [control (C): 36 ± 4%, antagonist (A): 34 ± 6%] but was completely abolished by BQ-788 (C: 34 ± 6%, A: 0 ± 2%, P < 0.001). The pulmonary rate constant ( K) for ET-1 removal was also unaffected by BQ-123 (C: 0.050 ± 0.0085 s−1, A: 0.047 ± 0.012 s−1) but significantly decreased and became close to zero after BQ-788 (C: 0.058 ± 0.014 s−1, A: 0.009 ± 0.007 s−1, P < 0.001). We conclude that the ETB receptor is completely and exclusively responsible for pulmonary ET-1 removal in vivo. Future studies are needed to show whether desensitization or downregulation of the ETB receptor may contribute to the increase in circulating ET-1 levels in conditions associated with pulmonary hypertension. This novel pulmonary endothelial cell function may play a protective role by modulating circulating ET-1 levels in the systemic circulation.


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