Effect of Dobutamine on Lung Microvascular Fluid Flux in Sheep with “Sepsis Syndrome”: Lungs microvascular

Mar-4-2015

Effect of Dobutamine on Lung Microvascular Fluid Flux in Sheep with “Sepsis Syndrome”: Lungs microvascularSince dobutamine has been recommended as an adrenergic receptor agonist which might be used in preference to dopamine when systemic flows require pharmacologic support in ARDS, we studied its effects on fluid flux in an animal model of peritonitis which is characterized by lung microvascular injury. This model seems more representative of early clinical sepsis than are endotoxic models, since it is characterized by a high systemic flow and low peripheral resistance state, with maintenance of systemic pressures. We evaluated the effects of dobutamine on microvascular fluid exchange in the lung of chronically cannulated sheep by using changes in the magnitude of Ql to reflect changes in water flux and using changes in the CLP to represent changes in protein flux. cipro tablets

The remote effects of surgically induced peritonitis on the lungs microvascular exchanging membrane were seen as an increase in QL, without a significant depression in [L/P]TP ratios. Hence, CLP, or protein flux, was also increased with the onset of “sepsis syndrome.” Concurrently, both the cardiac output and the mean pulmonary artery pressure were greater than was observed in the nonseptic studies. An increase in Ql, with unchanged [L/P]TP ratios, must represent the effects of an increase in either endothelial permeability or in the surface area of the lungs exchanging membrane on lung microvascular fluid flux. Although an increase in QL secondary to intraperitoneal contamination may arguably have been the consequence of an increase in the lungs perfused surface area, previous morphologic examination of this model has documented that a permeability lesion is the primary explanation for an observed increase in QL with the onset of sepsis. The lack of any demonstrable correlation between changes in QL and cardiac output during the septic studies would lend further support to our contention that an increase in QL with unchanged [L/P]TP ratios was not primarily the consequence of an alteration in the lungs perfused surface area. Therefore, bacterial peritonitis in this animal model was associated with an increase in CLP secondary to an increase in pulmonary microvascular permeability. Undoubtedly, an increase in microvascular surface area or the Pmv (or both) may also contribute to the augmented QL documented, as has been demonstrated in endotoxic models of lung injury.