The Experts below are selected from a list of 36444 Experts worldwide ranked by ideXlab platform
John W. Hammon - One of the best experts on this subject based on the ideXlab platform.
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Attenuation of the pulmonary vascular response to endotoxin by a thromboxane synthesis inhibitor (UK-38485) in unanesthetized sheep.
The Journal of surgical research, 1991Co-Authors: Clarke L. Henry, Kenneth L. Brigham, Martin L. Ogletree, John W. HammonAbstract:Abstract Previous studies have documented the phasic pulmonary vascular response to infused Eschericha coli endotoxin in unanesthetized sheep. Cyclooxygenase inhibition attenuates the initial vasoconstrictive phase (phase I) but not the late phase of increased microvascular permeability (phase II). We undertook to selectively inhibit thromboxane A2 synthesis and assess the pulmonary microvascular response to endotoxin. Twelve paired studies were carried out in six sheep prepared with chronic lung Lymph fistulas and pressure monitoring catheters. Each sheep received E. coli endotoxin (0.5 μg/kg) at time 0, both alone (control group) and 1 hr after pretreatment with a thromboxane synthetase inhibitor (UK-38485, 2 mg/kg). The animals were monitored for 1–2 hr prior to and 5 hr following endotoxin infusion to ensure a steady-state baseline and a complete late response. The pairs of studies were done in random order. In the presence of UK-38485, endotoxin caused significantly less pulmonary hypertension and shorter duration of leukopenia and lower lung Lymph flow and Lymph Protein clearance rates than did endotoxin alone. The differences in Lymph Protein clearance were more pronounced in phase II. These data suggest that both the vasoconstrictive and permeability phases of the pulmonary vascular response to endotoxin may be modified on endogenous thromboxane A2.
Robert A Brace - One of the best experts on this subject based on the ideXlab platform.
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Changes in left thoracic duct Lymph flow during progressive anemia in the ovine fetus
American Journal of Obstetrics and Gynecology, 1996Co-Authors: Lowell Davis, A. Roger Hohimer, Robert A BraceAbstract:Abstract OBJECTIVE: The purpose of this study was to evaluate the extent to which increased Lymph flow can return fluid and Protein to the circulation in the chronically anemic fetus. STUDY DESIGN: Thoracic duct Lymph flow rate over a range of outflow pressures was measured in 8 near-term fetal sheep 4 to 5 days after surgery and daily thereafter for 5 days. After each day's study 60 to 150 ml of blood was withdrawn at a rate of 1 ml per minute. Regression analysis was used to establish the Lymph flow function curve. Lymph and plasma Protein concentrations and Lymph flow rate were compared by analysis of variance for repeated measures. RESULTS: As the hematocrit was reduced from 34.6% ± 1.3% (mean ± SE) to 14.4% ± 1.0%, thoracic duct Lymph flow increased from 0.12 ± 0.01 to 0.28 ± 0.02 ml/min/kg. Plasma total Protein concentration did not change, Lymph Protein concentration fell (2.6 ± 0.1 to 2.4 ± 0.1 gm/dl), and the difference between plasma and Lymph Protein concentrations increased (1.04 ± 0.05 to 1.34 ± 0.10 gm/dl). Protein returned to the circulation increased from 11.5 ± 0.3 to 23.7 ± 1.5 mg per minute. Central venous pressure did not change and remained less than the breakpoint pressure. Although the plateau Lymph flow rate increased, neither the breakpoint or stopflow pressures of the Lymph flow function curve were altered. CONCLUSIONS: Fetal Lymph flow and thereby capillary filtration increased progressively as anemia became more severe. The increase in Lymph flow did not appear to be limited by outflow pressure. By returning Protein to the circulation, an increase in thoracic duct Lymph flow helped to limit expansion of extravascular fluid volume during chronic fetal anemia. (AM J OBSTET GYNECOL 1996;174:1469-76.)
Donald R. Bell - One of the best experts on this subject based on the ideXlab platform.
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Transvascular albumin and IgG flux in skin after a continuous 3-h bradykinin infusion
American Journal of Physiology-Heart and Circulatory Physiology, 1992Co-Authors: J. R. Wallace, Donald R. BellAbstract:Bradykinin (1 microgram/min) was infused into the femoral artery of one hindleg of anesthetized rabbits for 3 h. Measurements of the initial extravascular uptake for labeled albumin and immunoglobulin (Ig) G were compared with measurements of the Lymph Protein flux for endogenous albumin and IgG. With bradykinin, the initial extravascular uptake for both albumin and IgG, calculated as the 1-h extravascular distribution space at plasma concentration divided by time and expressed as a plasma clearance, was 12 times the control values. For both Proteins, the Lymph fluxes were not significantly greater than the values for extravascular uptake, indicating that the sustained increase in Lymph Protein flux was not due to washout of interstitial Protein. The extravascular uptake for IgG was approximately 80% of that for albumin in both control and bradykinin animals, suggesting that the sustained response did not change the selectivity between the two Proteins. Changes in the extravascular masses of endogenous albumin and IgG suggest that the initial response to bradykinin was a transient formation of endothelial gaps that did not restrict transvascular IgG transport more than albumin.
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Comparison of Protein Lymph flux and extravascular uptake in skin during increased venous pressure.
American Journal of Physiology-Heart and Circulatory Physiology, 1992Co-Authors: J. R. Wallace, Donald R. BellAbstract:The hypothesis that the albumin reflection coefficient is underestimated from measurements of Lymph Protein flux because of a prolonged interstitial washout was tested in the hindleg of anesthetized rabbits. In heel skin, the initial extravascular uptake for labeled albumin and immunoglobulin G (IgG) was compared with prenodal Lymph flux for native albumin and IgG. Venous pressure was increased in one leg for 4 h, while the contralateral leg was the control. The extravascular uptake for labeled albumin was 67% greater than control during the fourth hour of increased venous pressure. Lymph albumin flux was 2.3 times control, indicating a small but significant washout of interstitial albumin. The magnitude of the interstitial washout for IgG was less than that for albumin. Using the relationship between the change in extravascular uptake and the change in Lymph flow, the reflection coefficients for albumin and IgG were both 0.91. The reflection coefficient for albumin using Lymph Protein flux was lower because of a continued interstitial washout.
Clarke L. Henry - One of the best experts on this subject based on the ideXlab platform.
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Attenuation of the pulmonary vascular response to endotoxin by a thromboxane synthesis inhibitor (UK-38485) in unanesthetized sheep.
The Journal of surgical research, 1991Co-Authors: Clarke L. Henry, Kenneth L. Brigham, Martin L. Ogletree, John W. HammonAbstract:Abstract Previous studies have documented the phasic pulmonary vascular response to infused Eschericha coli endotoxin in unanesthetized sheep. Cyclooxygenase inhibition attenuates the initial vasoconstrictive phase (phase I) but not the late phase of increased microvascular permeability (phase II). We undertook to selectively inhibit thromboxane A2 synthesis and assess the pulmonary microvascular response to endotoxin. Twelve paired studies were carried out in six sheep prepared with chronic lung Lymph fistulas and pressure monitoring catheters. Each sheep received E. coli endotoxin (0.5 μg/kg) at time 0, both alone (control group) and 1 hr after pretreatment with a thromboxane synthetase inhibitor (UK-38485, 2 mg/kg). The animals were monitored for 1–2 hr prior to and 5 hr following endotoxin infusion to ensure a steady-state baseline and a complete late response. The pairs of studies were done in random order. In the presence of UK-38485, endotoxin caused significantly less pulmonary hypertension and shorter duration of leukopenia and lower lung Lymph flow and Lymph Protein clearance rates than did endotoxin alone. The differences in Lymph Protein clearance were more pronounced in phase II. These data suggest that both the vasoconstrictive and permeability phases of the pulmonary vascular response to endotoxin may be modified on endogenous thromboxane A2.
Lowell Davis - One of the best experts on this subject based on the ideXlab platform.
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Changes in left thoracic duct Lymph flow during progressive anemia in the ovine fetus
American Journal of Obstetrics and Gynecology, 1996Co-Authors: Lowell Davis, A. Roger Hohimer, Robert A BraceAbstract:Abstract OBJECTIVE: The purpose of this study was to evaluate the extent to which increased Lymph flow can return fluid and Protein to the circulation in the chronically anemic fetus. STUDY DESIGN: Thoracic duct Lymph flow rate over a range of outflow pressures was measured in 8 near-term fetal sheep 4 to 5 days after surgery and daily thereafter for 5 days. After each day's study 60 to 150 ml of blood was withdrawn at a rate of 1 ml per minute. Regression analysis was used to establish the Lymph flow function curve. Lymph and plasma Protein concentrations and Lymph flow rate were compared by analysis of variance for repeated measures. RESULTS: As the hematocrit was reduced from 34.6% ± 1.3% (mean ± SE) to 14.4% ± 1.0%, thoracic duct Lymph flow increased from 0.12 ± 0.01 to 0.28 ± 0.02 ml/min/kg. Plasma total Protein concentration did not change, Lymph Protein concentration fell (2.6 ± 0.1 to 2.4 ± 0.1 gm/dl), and the difference between plasma and Lymph Protein concentrations increased (1.04 ± 0.05 to 1.34 ± 0.10 gm/dl). Protein returned to the circulation increased from 11.5 ± 0.3 to 23.7 ± 1.5 mg per minute. Central venous pressure did not change and remained less than the breakpoint pressure. Although the plateau Lymph flow rate increased, neither the breakpoint or stopflow pressures of the Lymph flow function curve were altered. CONCLUSIONS: Fetal Lymph flow and thereby capillary filtration increased progressively as anemia became more severe. The increase in Lymph flow did not appear to be limited by outflow pressure. By returning Protein to the circulation, an increase in thoracic duct Lymph flow helped to limit expansion of extravascular fluid volume during chronic fetal anemia. (AM J OBSTET GYNECOL 1996;174:1469-76.)
