scholarly journals Physiological gas exchange mapping of hyperpolarized 129 Xe using spiral-IDEAL and MOXE in a model of regional radiation-induced lung injury

2018 ◽  
Vol 45 (2) ◽  
pp. 803-816 ◽  
Author(s):  
Brandon Zanette ◽  
Elaine Stirrat ◽  
Salomeh Jelveh ◽  
Andrew Hope ◽  
Giles Santyr
2016 ◽  
Vol 43 (5) ◽  
pp. 2410-2420 ◽  
Author(s):  
Ozkan Doganay ◽  
Elaine Stirrat ◽  
Charles McKenzie ◽  
Rolf F. Schulte ◽  
Giles E. Santyr

2003 ◽  
Vol 79 (3) ◽  
pp. 159-167 ◽  
Author(s):  
Ji-Hong Hong ◽  
Shih-Ming Jung ◽  
Thomas Chang Yao Tsao ◽  
Chi-Jung Wu ◽  
Chin-Yi Lee ◽  
...  

CHEST Journal ◽  
2008 ◽  
Vol 134 (4) ◽  
pp. 127P ◽  
Author(s):  
Rade Tomic ◽  
Elizabeth Jacobs ◽  
Metha Medhora ◽  
Andreea Antonescu-Turcu ◽  
Ghosh Swarajit

2001 ◽  
Vol 95 (6) ◽  
pp. 1414-1421 ◽  
Author(s):  
Matthias Hübler ◽  
Jennifer E. Souders ◽  
Erin D. Shade ◽  
Nayak L. Polissar ◽  
Carmel Schimmel ◽  
...  

Background Perfluorocarbon (PFC) liquids are known to improve gas exchange and pulmonary function in various models of acute respiratory failure. Vaporization has been recently reported as a new method of delivering PFC to the lung. Our aim was to study the effect of PFC vapor on the ventilation/perfusion (VA/Q) matching and relative pulmonary blood flow (Qrel) distribution. Methods In nine sheep, lung injury was induced using oleic acid. Four sheep were treated with vaporized perfluorohexane (PFX) for 30 min, whereas the remaining sheep served as control animals. Vaporization was achieved using a modified isoflurane vaporizer. The animals were studied for 90 min after vaporization. VA/Q distributions were estimated using the multiple inert gas elimination technique. Change in Qrel distribution was assessed using fluorescent-labeled microspheres. Results Treatment with PFX vapor improved oxygenation significantly and led to significantly lower shunt values (P < 0.05, repeated-measures analysis of covariance). Analysis of the multiple inert gas elimination technique data showed that animals treated with PFX vapor demonstrated a higher VA/Q heterogeneity than the control animals (P < 0.05, repeated-measures analysis of covariance). Microsphere data showed a redistribution of Qrel attributable to oleic acid injury. Qrel shifted from areas that were initially high-flow to areas that were initially low-flow, with no difference in redistribution between the groups. After established injury, Qrel was redistributed to the nondependent lung areas in control animals, whereas Qrel distribution did not change in treatment animals. Conclusion In oleic acid lung injury, treatment with PFX vapor improves gas exchange by increasing VA/Q heterogeneity in the whole lung without a significant change in gravitational gradient.


1990 ◽  
Vol 11 (1) ◽  
pp. 65-71
Author(s):  
Richard A. Rosiello ◽  
William W. Merrill

2018 ◽  
Vol 41 (3) ◽  
pp. 370-379 ◽  
Author(s):  
Sunil Gowda S. N. ◽  
Raghavi Raviraj ◽  
Devipriya Nagarajan ◽  
Weiling Zhao

2017 ◽  
Vol 23 ◽  
pp. 3446-3450 ◽  
Author(s):  
Yijuan Huang ◽  
Weiqiang Zhang ◽  
Fangrong Yu ◽  
Fu Gao

2000 ◽  
Vol 278 (4) ◽  
pp. L719-L725 ◽  
Author(s):  
Chizuko Tsuji ◽  
Sumie Shioya ◽  
Yuki Hirota ◽  
Naoto Fukuyama ◽  
Daisaku Kurita ◽  
...  

The purposes of this study were 1) to identify the nitric oxide (NO) synthase (NOS) isoform responsible for NO-mediated radiation-induced lung injury, 2) to examine the formation of nitrotyrosine, and 3) to see whether nitrotyrosine formation and lung injury are reduced by an inducible NOS (iNOS) inhibitor, aminoguanidine. The left hemithorax of rats was irradiated (20 Gy), and the degree of lung injury, the expression of NOS isoforms, and the formation of nitrotyrosine and superoxide were examined after 2 wk. iNOS mRNA was induced, and endothelial NOS mRNA was markedly increased in the irradiated lung. Nitrotyrosine was detected biochemically and immunohistochemically. Aminoguanidine prevented acute lung injury as indicated by decreased protein concentration and lactate dehydrogenase activity in bronchoalveolar lavage fluid and improved NMR parameters and histology. Furthermore, the formation of nitrotyrosine was significantly reduced in the aminoguanidine group. We conclude that iNOS induction is a major factor in radiation-induced lung injury and that nitrotyrosine formation may participate in the NO-induced pathogenesis.


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