An increasing body of experimental evidence suggests that lung/kidney interactions are involved both in AKI-associated acute lung injury (ALI) and renal consequences of acute respiratory failure. Positive pressure ventilation, changes in PaCO2 and PaO2 levels along with systemic inflammation participate in the renal response to acute respiratory failure.
Positive pressure ventilation may modify venous return, cardiac after-load and may decrease cardiac output along with decreased renal blood flow, in glomerular filtration rate (GFR), and in osmolar and water clearance [1, 2]. Beyond hemodynamic consequences of mechanical ventilation, these effects were partly ascribable to an activation of the sympathetic and renin-angiotensin systems, suppress the atrial natriuretic peptide release, while anti-diuretic hormone concentration was demonstrated to play little role [1, 3–5]
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Changes in PaCO2 and PaO2 levels were shown to influence renal perfusion or sodium and water clearance. Hence diuretic impact of both hypobaric and isobaric hypoxemia was demonstrated several decades ago [4–6]. Hypoxic ventilatory response, including increased minute ventilation and subsequent negative inspiratory pressure [2], along with respiratory alkalosis and therefore sodium bicarbonate …show more content…
Although fluid overload and subsequent pulmonary edema are the most obvious mechanisms, renal ischemia-reperfusion was found, in experimental model, to induce intra-alveolar damage, leukocyte infiltration, increased capillary permeability, and distinct lung transcriptional changes when compared to bilateral nephrectomy [15]. This finding strongly suggest that mechanism of lung injury may be promoted by acute renal injury independently from mere fluid overload or theoritical deleterious effects of
Positive pressure ventilation may modify venous return, cardiac after-load and may decrease cardiac output along with decreased renal blood flow, in glomerular filtration rate (GFR), and in osmolar and water clearance [1, 2]. Beyond hemodynamic consequences of mechanical ventilation, these effects were partly ascribable to an activation of the sympathetic and renin-angiotensin systems, suppress the atrial natriuretic peptide release, while anti-diuretic hormone concentration was demonstrated to play little role [1, 3–5]
.
Changes in PaCO2 and PaO2 levels were shown to influence renal perfusion or sodium and water clearance. Hence diuretic impact of both hypobaric and isobaric hypoxemia was demonstrated several decades ago [4–6]. Hypoxic ventilatory response, including increased minute ventilation and subsequent negative inspiratory pressure [2], along with respiratory alkalosis and therefore sodium bicarbonate …show more content…
Although fluid overload and subsequent pulmonary edema are the most obvious mechanisms, renal ischemia-reperfusion was found, in experimental model, to induce intra-alveolar damage, leukocyte infiltration, increased capillary permeability, and distinct lung transcriptional changes when compared to bilateral nephrectomy [15]. This finding strongly suggest that mechanism of lung injury may be promoted by acute renal injury independently from mere fluid overload or theoritical deleterious effects of