scholarly journals Glomerular filtration is reduced by high tidal volume ventilation in an in vivo healthy rat model

2009 ◽  
Vol 42 (11) ◽  
pp. 1104-1109 ◽  
Author(s):  
A. Luque ◽  
M.H.M. Shimizu ◽  
L. Andrade ◽  
T.R. Sanches ◽  
A.C. Seguro
2007 ◽  
Vol 103 (1) ◽  
pp. 148-155 ◽  
Author(s):  
Axel Kleinsasser ◽  
I. Mark Olfert ◽  
Alex Loeckinger ◽  
G. Kim Prisk ◽  
Susan R. Hopkins ◽  
...  

Independent of airway pressure, pulmonary resistance is known to fall with increasing tidal volumes, traditionally thought to result from radial traction on the airways. R. C. Anafi and T. A. Wilson ( J Appl Physiol 91: 1185–1192, 2001) recently presented a model of a single terminal airway that explains the tidal volume-associated fall in resistance with an additional mechanism pertinent to narrow airways: a stable, nearly closed airway that is challenged with an increase in tidal volume “pops open” to become a stable, well-opened airway, and thus resistance drops suddenly. To test this model in vivo, the effects of high (24 ml/kg) and low (9 ml/kg) tidal volume in bronchoconstricted lungs were assessed using 1) the multiple inert gas elimination technique (MIGET) and 2) a 15-breath multiple breath inert gas washout (MBW) technique in anesthetized pigs. With high tidal volume, ventilation/perfusion (V̇a/Q̇) mismatch was reduced (log SD Q̇ from 1.30 ± 0.11 to 1.09 ± 0.12, P < 0.05), and blood flow to lung units with V̇a/Q̇ ratios < 0.1 was significantly reduced (37 ± 4% of cardiac output to 7 ± 4%, P < 0.05). Dynamic compliance was twice as high during high-tidal-volume ventilation ( P = 0.002). MBW analysis revealed that, while heterogeneity of ventilation during bronchoconstriction was not significantly different between either low or high tidal volume (log SD V̇mbw = 1.39 ± 0.09 and 1.34 ± 0.02, respectively), preinspiratory lung volume (PILV) decreased by 42% with low-tidal-volume ventilation ( P < 0.05), whereas it did not change with high-tidal-volume ventilation. The higher PILV during high tidal volume is also consistent with Anafi and Wilson's model. In summary, the outcomes from MIGET, and to some extent the MBW, in our anesthetized and mechanically ventilated pigs are consistent with a bistable terminal airway model as proposed by Anafi and Wilson. However, our data do not allow exclusion of other mechanisms that may lead to improved ventilatory distribution when tidal volume is increased.


2012 ◽  
Vol 51 (1) ◽  
pp. 82-90 ◽  
Author(s):  
Juliana Monte Real ◽  
Graziela Machado Gruner Turco Spilborghs ◽  
Mariana Morato-Marques ◽  
Ricardo Pereira de Moura ◽  
Elnara Marcia Negri ◽  
...  

2003 ◽  
Vol 284 (5) ◽  
pp. L791-L798 ◽  
Author(s):  
James A. Frank ◽  
Jean-François Pittet ◽  
Hyon Lee ◽  
Micaela Godzich ◽  
Michael A. Matthay

Tidal volume reduction during mechanical ventilation reduces mortality in patients with acute lung injury and the acute respiratory distress syndrome. To determine the mechanisms underlying the protective effect of low tidal volume ventilation, we studied the time course and reversibility of ventilator-induced changes in permeability and distal air space edema fluid clearance in a rat model of ventilator-induced lung injury. Anesthetized rats were ventilated with a high tidal volume (30 ml/kg) or with a high tidal volume followed by ventilation with a low tidal volume of 6 ml/kg. Endothelial and epithelial protein permeability were significantly increased after high tidal volume ventilation but returned to baseline levels when tidal volume was reduced. The basal distal air space fluid clearance (AFC) rate decreased by 43% ( P < 0.05) after 1 h of high tidal volume but returned to the preventilation rate 2 h after tidal volume was reduced. Not all of the effects of high tidal volume ventilation were reversible. The cAMP-dependent AFC rate after 1 h of 30 ml/kg ventilation was significantly reduced and was not restored when tidal volume was reduced. High tidal volume ventilation also increased lung inducible nitric oxide synthase (NOS2) expression and air space total nitrite at 3 h. Inhibition of NOS2 activity preserved cAMP-dependent AFC. Because air space edema fluid inactivates surfactant and reduces ventilated lung volume, the reduction of cAMP-dependent AFC by reactive nitrogen species may be an important mechanism of clinical ventilator-associated lung injury.


2008 ◽  
Vol 21 (1) ◽  
pp. 54-60 ◽  
Author(s):  
Andrea Lessa ◽  
Cleide Suguihara ◽  
Shuming Xianyu ◽  
Dorothy Hehre ◽  
Carlos Devia ◽  
...  

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