To study the effects of inflation pressure and tidal volume (VT) on protein permeability in the neonatal pulmonary microcirculation, we measured lung vascular pressures, blood flow, lymph flow (QL), and concentrations of protein in lymph (L) and plasma (P) of 22 chronically catheterized lambs that received mechanical ventilation at various peak inflation pressures (PIP) and VT. Nine lambs were ventilated initially with a PIP of 19 +/- 1 cmH2O and a VT of 10 +/- 1 ml/kg for 2-4 h (base line), after which we overexpanded their lungs with a PIP of 58 +/- 3 cmH2O and a VT of 48 +/- 4 ml/kg for 4-8 h. QL increased from 2.1 +/- 0.4 to 13.9 +/- 5.0 ml/h. L/P did not change, but the ratio of albumin to globulin in lymph relative to the same ratio in plasma decreased, indicating altered protein sieving in the pulmonary microcirculation. Seven other lambs were mechanically ventilated for 2-4 h at a PIP of 34 +/- 1 cmH2O and a VT of 23 +/- 2 ml/kg (base line), after which their chest and abdomen were bound so that PIP increased to 54 +/- 1 cmH2O for 4-6 h without a change in VT. QL decreased on average from 2.8 +/- 0.6 to 1.9 +/- 0.3 ml/h (P = 0.08), and L/P was unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)
ABSTRACT. Previous studies showed that increased pul-The DA is a fetal vascular channel that normally closes soon monary blood flow from a patent ductus arteriosus had after birth. If it remains patent, as it often does after premature little or no effect on the amount of fluid in the lungs of birth, blood flow from the aorta into the pulmonary artery mechanically ventilated preterm lambs. The purpose of increases as pulmonary vascular resistance decreases postnatally. this study was to examine the effect of a patent ductus A PDA is thus associated with increased pulmonary blood flow, arteriosus on lung vascular permeability and to see whether pulmonary blood pressure, and PLvED (1, 2). The presence of a increased pulmonary lymph flow might compensate for the PDA may cause pulmonary edema in premature infants with increased rate of fluid filtration. Using a model that allows respiratory distress (3,4). However, little information is available mechanical control of ductus patency, we studied the effects to demonstrate how the PDA adversely affects pulmonary fluid of increased pulmonary blood flow on lung vascular pres-balance. sures in six mechanically ventilated premature lambs at Several studies have examined the effects of increased pulmo-We nary blood flow on lung fluid balance in adult and mature measured lung lymph flow and protein concentrations in newborn animals (5-1 1). In some of these studies, the increase lymph and plasma to assess pulmonary vascular fluid in microvascular fluid filtration associated with increased pulfiltration and protein permeability. We studied each lamb monary blood flow was attributed to increased microvascular during sequential steady state periods, first with the ductus filtration pressure (5, 6, 1 1); in other studies, the increased open and then with it closed. When the ductus was open, filtration was thought to be the result of lung vascular recruitment pulmonary blood flow was twice what it was when the (7-10). There is some evidence that the capacity for vascular ductus was closed. Mean pulmonary artery pressure and recruitment and increased fluid filtration in the pulmonary cirleft ventricular end-diastolic pressure were greater with culation may be age dependent (10-13). Little information is the ductus open [40 +. 5 torr (5.3 f 0.7 kPa) and 8 f 3 available regarding the influence of increased perfusion on lung torr (1.1 f 0.4 kPa), respectively] than when it was closed fluid filtration in the presence of underlying pulmonary pathol-124 f 3 torr (3.2 f 0.4 kPa) and 4 f 2 torr (0.5 f 0.3 ogy (9, 14), and the relationship between blood flow and fluid kPa), respectively]. When the ductus was open, lymph flow dynamics in the immature lung is even more obscure. was 68% greater and lymph protein concentration was 17%We used an animal model of the PDA that enables us to study lower than when the ductus was closed. Lymph protein the effects of increased pulmonary blood flow on lung fluid clearance (lymph flow % lymph protein concentration/ balance in newborn sheep (1,2,15). Pr...
The purpose of this study was
To study the effects of furosemide on the neonatal pulmonary circulation in the presence of lung injury, we measured pulmonary arterial and left atrial pressures, cardiac output, lung lymph flow, and concentrations of protein in lymph and plasma of nine lambs that received furosemide, 2 mg/kg iv, during a continuous 8-h intravenous infusion of air. Air embolism increased pulmonary vascular resistance by 71% and nearly tripled steady-state lung lymph flow, with no change in lymph-to-plasma protein ratio. These findings reflect an increase in lung vascular protein permeability. During sustained lung endothelial injury, diuresis from furosemide led to a rapid reduction in cardiac output (average 29%) and a 2-Torr decrease in left atrial pressure. Diuresis also led to hemoconcentration, with a 15% increase in both plasma and lymph protein concentrations. These changes were associated with a 27% reduction in lung lymph flow. In a second set of studies, we prevented the reduction in left atrial pressure after furosemide by inflating a balloon catheter in the left atrium. Nevertheless, lymph flow decreased by 25%, commensurate with the reduction in cardiac output that occurred after furosemide. In a third series of experiments, we minimized the furosemide-related decrease in cardiac output by opening an external fistula between the carotid artery and jugular vein immediately after injection of furosemide. In these studies, the reduction in lung lymph flow (average 17%) paralleled the smaller (17%) decrease in cardiac output. These results suggest that changes in lung vascular filtration pressure probably do not account for the reduction in lung lymph flow after furosemide in the presence of lung vascular injury.(ABSTRACT TRUNCATED AT 250 WORDS)
The purpose of this study was to see whether there are developmental differences in the protein permeability of the pulmonary circulation that might contribute to the abnormal lung fluid balance seen in premature lambs with respiratory failure. In one series of experiments, we measured albumin turnover time, which reflects the escape rate of radiolabeled albumin from the pulmonary circulation, of five preterm fetal lambs (125 +/- 1 days gestation) and five newborn lambs (19 +/- 9 days old). Turnover time was not significantly different in fetuses (160 +/- 38 min) and newborns (141 +/- 54 min), implying a similar protein permeability of the pulmonary circulation. In additional experiments, we measured pulmonary hemodynamic and lung lymph flow responses to intravenous saline infusion in seven preterm fetal lambs (130 +/- 3 days gestation) and seven newborn lambs (14 +/- 3 days old). During saline infusion, calculated fluid filtration pressure increased by a similar amount in fetuses and newborns (3.4 +/- 0.8 and 2.8 +/- 0.9 Torr, respectively), resulting in a similar change in lung lymph flow in fetuses and newborns (0.59 +/- 0.27 and 0.55 +/- 0.25 ml.h-1.kg body wt-1, respectively). The results of these studies indicate that protein permeability of the pulmonary circulation does not change significantly during late fetal and early postnatal development.
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