Abstract
The aim of this study was to evaluate whether possible preglomerular arterial-to-venous oxygen shunting is affected by the interaction between renal preglomerular carbon dioxide and oxygen transport. We hypothesized that a reverse (venous-to-arterial) shunting of carbon dioxide will increase partial pressure of carbon dioxide and decrease pH in the arteries and thereby lead to increased oxygen offloading and consequent oxygen shunting. To test this hypothesis, we employed a segment-wise three-dimensional computational model of coupled renal oxygen and carbon dioxide transport, wherein coupling is achieved by shifting the oxygen-hemoglobin dissociation curve in dependence of local changes in partial pressure of carbon dioxide and pH. The model suggests that primarily due to the high buffering capacity of blood, there is only marginally increased acidity in the preglomerular vasculature compared to systemic arterial blood caused by carbon dioxide shunting. Furthermore, effects of carbon dioxide transport do not promote but rather impair preglomerular oxygen shunting, as the increase in acidity is higher in the veins compared to that in the arteries. We conclude that while substantial arterial-to-venous oxygen shunting might take place in the postglomerular vasculature, the net amount of oxygen shunted at the preglomerular vasculature appears to be marginal.
Highlights
Hypoxic conditions in the renal cortex or in the medulla may induce tissue damage and contribute to the pathogenesis of acute and chronic kidney diseases (Evans et al, 2008)
We have shown previously that preglomerular arterial-to-venous (AV) oxygen shunting—a mechanism hypothesized to contribute to the regulation of renal oxygenation (Leong et al, 2007; Evans et al, 2008)—is unlikely to be significant (Olgac and Kurtcuoglu, 2015a,b)
We first present the output of the model employing two different boundary conditions on the venous return
Summary
Hypoxic conditions in the renal cortex or in the medulla may induce tissue damage and contribute to the pathogenesis of acute and chronic kidney diseases (Evans et al, 2008). It is essential to understand the mechanisms that are involved in the regulation of renal oxygenation. We have shown previously that preglomerular arterial-to-venous (AV) oxygen shunting—a mechanism hypothesized to contribute to the regulation of renal oxygenation (Leong et al, 2007; Evans et al, 2008)—is unlikely to be significant (Olgac and Kurtcuoglu, 2015a,b). Since the question has arisen whether substantial shunting may exist, enabled by the influence of preglomerular carbon dioxide dynamics on oxygen transport. We hypothesize that reverse, venous-to-arterial (VA) shunting of carbon dioxide will increase arterial partial pressure of carbon dioxide, decrease pH, and thereby lead to augmented oxygen offloading through the Bohr effect (Kilmartin and Rossi-Bernardi, 1973; Dash et al, 2016) and consequent AV oxygen shunting.
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