Strength of hypoxic vasoconstriction determines shunt fraction in dogs with atelectasis

Abstract

We investigated the degree to which strength of pulmonary hypoxic vasoconstriction affects perfusion of pulmonary shunt pathways in acute atelectasis. In 17 intact supine dogs (anesthetized, paralyzed, and ventilated) we produced left lower lobe atelectasis by occluding the lobar bronchus during oxygen inhalation. Subsequently, shunt fraction (reflecting perfusion of that lobe) was measured using an SF6 infusion while the dogs breathed room air; the mean was 26% (range 14-40%). Pulmonary pressor response to hypoxia was assessed in 13 dogs using the increase in pulmonary end-diastolic gradient (PDG) produced by inhalation of 10% oxygen. Those animals with the largest increase in pulmonary diastolic gradient had the smallest shunt fraction while breathing room air, whereas those with the smallest response had the largest shunt fraction. The contribution of local hypoxia to vasoconstriction in the shunt pathway was assessed in 13 dogs breathing room air by measuring the increase in shunt fraction produced by infusing prostaglandin E1 (PGE1). Those with the largest increase in shunt fraction had the smallest pre-PGE1 shunt fraction. Thus the strength of pulmonary vascular reactivity to hypoxia markedly influences the degree of vasoconstriction in shunt pathways and is a major determinant of shunt pathway perfusion.

Alterations in Gas Exchange Associated with Lobar Atelectasis in Young Piglets

“…DISCUSSION This study demonstrates that infant animals with lobar atelectasis effectively minimize intrapulmonary shunt by reducing pulmonary blood flow to the atelectatic region. The results are similar to those reported in normal adult dogs with lobar atelec- tasis (5,6). In these previous studies, regional hypoxic pulmonary vasoconstriction was found to be the primary mechanism responsible for minimizing gas exchange abnormalities associated with lobar atelectasis (6).…”

“…The results are similar to those reported in normal adult dogs with lobar atelec- tasis (5,6). In these previous studies, regional hypoxic pulmonary vasoconstriction was found to be the primary mechanism responsible for minimizing gas exchange abnormalities associated with lobar atelectasis (6). The consistent rise in total pulmonary resistance in piglets following lobar collapse suggested that this mechanism of redistributing pulmonary blood flow is also operative in infant animals.…”

“…These findings suggest that pulmonary vessels can constrict more effectively in newborns compared to older animals and that shunt during lobar atelectasis might be more effectively minimized in infants compared to adults. In this report, the average shunt following lobar collapse was 5.9 t 4.2%; among adult dogs left lower lobe atelectasis produced a 10-25% shunt fraction (5,6). In piglets lobar blood flow was reduced to an average value of 9% of total pulmonary blood flow.…”

“…In piglets lobar blood flow was reduced to an average value of 9% of total pulmonary blood flow. Similar measurements in adult dogs revealed that 13-2 1 % pulmonary blood flow perfused the atelectatic areas (5,6). It is unclear whether these differences may reflect a species-related or an age-related difference in pulmonary vasoconstriction capabilities (1 8).…”

“…However, the effect of lobar collapse in the presence of diffuse lung disease on gas exchange in the pediatric age group has not been described. Previous studies in adult dogs with atelectasis demonstrate that intrapulmonary shunt is minimized as a result of regional hypoxic pulmonary vasoconstriction and reduction in blood flow to the atelectatic region (5,6). It is unclear to what extent this compensatory mechanism occurs in young animals.…”