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

Mar-3-2015

The flow-dependency of systemic Vo2, which is frequently demonstrable when ARDS complicates the “sepsis syndrome,” may clinically dictate the use of P-adrenergic receptor agonists when cardiac output (hence systemic oxygen transport) is not deemed sufficient to satisfy peripheral oxygen needs. Theoretically, the administration of (3-adrenergic receptor agonists could increase pulmonary microvascular fluid flux in ARDS and thereby lead to further edema; however, we found in this study that dobutamine did not substantially increase QL in an animal model of sepsis-induced microvascular pulmonary injury when infused at a dose of 10μg/kg/min, although a modest increase (+ 24 percent) was demonstrable when dobutamine was infused at a lower dose.

To augment central flows and systemic oxygen transport in ARDS, the use of (3-adrenergic receptor agonists may represent a presumed advantage when compared to intravascular volume loading. An increase in the Pmv, which might well accompany an increase in ventricular preload following volume loading, should augment QL2 and extravascular lung water accumulation to a greater degree in ARDS than when the normal permeability characteristics of the lungs microvascular membrane remain unaffected by underlying disease. Nevertheless, it could be argued that the administration of (3-adrenergic receptor agonists might increase extravascular lung water accumulation in ARDS by independently affecting any of the major determinants of pulmonary microvascular fluid flux which are defined within the Starling equation, specifically the following: pulmonary microvascular permeability; the Pmv; and the perfused surface area of the lungs exchanging microvasculature. Studies from which the effects of (3-adrenergic receptor agonists on lung microvascular fluid flux might be related to the clinical correlate have either been performed in healthy animals or were designed as a pretreatment protocol; conclusions therein derived may well not characterize the effects of exogenous catecholamines on both lung microvascular fluid flux and systemic hemodynamics in the “sepsis syndrome” is also critically important; for example, endotoxin models of on both lung microvascular fluid flux and systemic hemodynamics in the “sepsis syndrome” is also critically important; for example, endotoxin models of lung microvascular injury may only reflect a later period in a progression of the “sepsis syndrome” because of the marked dissimilarities noted in both flow and pressure characteristics (among others) between this model and early human sepsis. Therefore, when administered to an endotoxic model, conclusions about the effects of (3-adrenergic receptor agonists on lung fluid balance may also not represent their real effects during the early phases of ARDS complicating human sepsis.