The Experts below are selected from a list of 249 Experts worldwide ranked by ideXlab platform
Tom Saldeen - One of the best experts on this subject based on the ideXlab platform.
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A leukocyte elastase inhibitor reduces thrombin-induced pulmonary oedema in the rat: mechanisms of action.
Pulmonary Pharmacology & Therapeutics, 1998Co-Authors: Håkan Sandler, Tom SaldeenAbstract:Abstract The effect of a selective leukocyte elastase inhibitor, ICI 200,355, on thrombin-induced pulmonary oedema was studied in rats. Thrombin administration produced an increase in Lung Weight ( P P P P P P P P
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Beneficial effects of a leukotriene receptor antagonist on thrombin-induced pulmonary edema in the rat
Prostaglandins Leukotrienes and Essential Fatty Acids, 1995Co-Authors: Håkan Sandler, Tom SaldeenAbstract:Abstract The effect of a selective leukotriene receptor antagonist, the peptide ICI 198,615, on thrombin-induced pulmonary edema was studied in rats. Administration of thrombin produced a significant increase in Lung Weight ( p p p p
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Effect of a synthetic leukocyte elastase inhibitor on thrombin-induced pulmonary edema in the rat
Experimental Lung Research, 1993Co-Authors: Håkan Sandler, Mitchell Glass, Tom SaldeenAbstract:The effect of a synthetic leukocyte elastase inhibitor on thrombin-induced pulmonary edema was studied in rats. The chloromethylketone human neutrophil elastase inhibitor, ICI 200,355, blunted rat leukocyte elastase activity in rat Lung tissue. Administration of thrombin produced a significant increase (p < .01) in Lung Weight. The wet Weight to dry Weight ratio (WW/DW) and relative water contents were also significantly elevated (p < .01). Pretreatment with ICI 200,355 (200 μg/kg h−1) resulted in significant reductions (p < .05) in Lung Weight and a tendency to decrease WW/DW and water content compared with animals given thrombin alone. It is possible that the elastase inhibitor effectively reduced the rate of thrombin-induced pulmonary edema by attenuation of increased vascular permeability.
Håkan Sandler - One of the best experts on this subject based on the ideXlab platform.
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A leukocyte elastase inhibitor reduces thrombin-induced pulmonary oedema in the rat: mechanisms of action.
Pulmonary Pharmacology & Therapeutics, 1998Co-Authors: Håkan Sandler, Tom SaldeenAbstract:Abstract The effect of a selective leukocyte elastase inhibitor, ICI 200,355, on thrombin-induced pulmonary oedema was studied in rats. Thrombin administration produced an increase in Lung Weight ( P P P P P P P P
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Beneficial effects of a leukotriene receptor antagonist on thrombin-induced pulmonary edema in the rat
Prostaglandins Leukotrienes and Essential Fatty Acids, 1995Co-Authors: Håkan Sandler, Tom SaldeenAbstract:Abstract The effect of a selective leukotriene receptor antagonist, the peptide ICI 198,615, on thrombin-induced pulmonary edema was studied in rats. Administration of thrombin produced a significant increase in Lung Weight ( p p p p
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Effect of a synthetic leukocyte elastase inhibitor on thrombin-induced pulmonary edema in the rat
Experimental Lung Research, 1993Co-Authors: Håkan Sandler, Mitchell Glass, Tom SaldeenAbstract:The effect of a synthetic leukocyte elastase inhibitor on thrombin-induced pulmonary edema was studied in rats. The chloromethylketone human neutrophil elastase inhibitor, ICI 200,355, blunted rat leukocyte elastase activity in rat Lung tissue. Administration of thrombin produced a significant increase (p < .01) in Lung Weight. The wet Weight to dry Weight ratio (WW/DW) and relative water contents were also significantly elevated (p < .01). Pretreatment with ICI 200,355 (200 μg/kg h−1) resulted in significant reductions (p < .05) in Lung Weight and a tendency to decrease WW/DW and water content compared with animals given thrombin alone. It is possible that the elastase inhibitor effectively reduced the rate of thrombin-induced pulmonary edema by attenuation of increased vascular permeability.
Kenneth R. Mccurry - One of the best experts on this subject based on the ideXlab platform.
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Significance of Lung Weight in Cellular Ex Vivo Lung Perfusion.
The Journal of surgical research, 2020Co-Authors: Toshihiro Okamoto, Hiromichi Niikawa, David Wheeler, Basem Soliman, Kamal S. Ayyat, Yoshifumi Itoda, Carol Farver, Kenneth R. MccurryAbstract:Abstract Background Currently, pulmonary edema is evaluated via surgical inspection and palpation in donor Lungs, and there is no quantitative standard diagnostic tool for evaluating pulmonary edema in donor procurement and ex vivo Lung perfusion (EVLP). The purpose of this study was to investigate the significance of Lung Weight at the donor hospital and Lung Weight during EVLP as a complementary parameter of transplant suitability in EVLP. Materials and methods Twenty-one of rejected human Lungs were perfused in cellular EVLP. Transplant suitability was evaluated at 2 h as per standard criteria of Lund-protocol EVLP. Results Lung Weight at donor hospital was significantly correlated with PaO2/FiO2 (P/F) ratio in EVLP (r = −0.44). There was a significant difference in Lung Weight at donor hospital between suitable cases (n = 13) and nonsuitable cases (n = 8). Light Lung group (Lung Weight at donor hospital Conclusions Our findings demonstrate that Lung Weight at donor hospital, Lung Weight change, and Lung Weight at 2 h of EVLP might be a predictor of P/F ratio and transplant suitability in cellular EVLP.
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Real-Time Lung Weight Measurement: A Simple Predictor for Clinical Outcomes of Ex-Vivo Lung Perfusion
The Journal of Heart and Lung Transplantation, 2020Co-Authors: Ichiro Sakanoue, Toshihiro Okamoto, Kamal S. Ayyat, H. Niikawa, James Yun, Kenneth R. MccurryAbstract:Purpose Lung Weight (LW) gain is a typical characteristic of ischemia reperfusion injury in ex-vivo Lung perfusion (EVLP). However, LW gain data is available only at the end of EVLP. Additionally, objective physiological parameters useful in EVLP evaluation are limited. The study purpose was to investigate the usefulness of real-time LW measurement to assess pulmonary edema and to predict clinical outcomes. Methods LW at back table was measured before and after EVLP. During acellular EVLP, real-time LW was continuously measured by a scale attached under the organ chamber. The LW change (Weight change per time, g/min) was measured during the non-touching period at multiple time points and the estimated LW gain was calculated by LW change and its duration. Transplant suitability was judged based on the standard criteria including trend of physiological parameters and palpation findings. Results Ten Lungs were perfused at our institute and 8 Lungs were clinically transplanted. All patients survived and primary graft dysfunction (PGD) grade at 72 hours were Grade 0-1, n = 6; Grade 2, n = 2; Grade 3, n = 0. Estimated LW gain during the entire perfusion period significantly correlated with LW gain at the back table (n = 10, r = 0.95, p Conclusion The data suggest that LW gain calculated by real-time LW measurement might be useful to assess pulmonary edema during EVLP. Initial LW gain at 0-60 min of EVLP might be a predictor of transplant suitability and clinical outcomes.
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Donor Lung Weight at Lung Procurement; Predictive Value for Transplant Suitability during Ex Vivo Lung Perfusion
The Journal of Heart and Lung Transplantation, 2019Co-Authors: Toshihiro Okamoto, Hiromichi Niikawa, David Wheeler, Basem Soliman, Kamal S. Ayyat, Yoshifumi Itoda, Kenneth R. MccurryAbstract:Purpose Currently, pulmonary edema in donor Lungs is evaluated via surgical inspection and palpation at procurement with no quantitative, standard diagnostic tool in use. The purpose of this study was to investigate the significance of Lung Weight at the donor hospital (LW0) as an indicator of pulmonary edema and predictor of transplant suitability in ex vivo Lung perfusion (EVLP). Methods LW0 was recorded in standard donors (n = 53) and rejected donors (n = 69). Twenty-one rejected Lungs were perfused in cellular EVLP and transplant suitability evaluated at 2 hours. Results There was a significant difference in LW0 between standard and rejected donors (814.7 ± 185.9 vs. 956.1 ± 275.1 g, p Conclusion Our findings demonstrate that donor Lung Weight could be a predictor of P/F ratio and transplant suitability during EVLP. The prospect for recovery of EVLP treated rejected donor Lungs improved significantly if they weighed less than 1280 g.
Toshishige Shibamoto - One of the best experts on this subject based on the ideXlab platform.
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Effects of thromboxane A_2 analogue on vascular resistance distribution and permeability in isolated blood-perfused dog Lungs
Lung, 1995Co-Authors: Toshishige Shibamoto, H. -g. Wang, Y Saeki, Y Yamaguchi, S Tanaka, S KoyamaAbstract:This study was designed to determine the effects of thromboxane A_2 (TxA_2) on the distribution of vascular resistance, Lung Weight, and microvascular permeability in isolated dog Lungs perfused at a constant pressure with autologous blood. The stable TxA_2 analogue (STA_2; 30 μg, n = 5) caused an increase in pulmonary capillary pressure (Pc) assessed as double-occlusion pressure to 14.0 ± 0.4 mmHg from the baseline of 7.9 ± 0.3 mmHg with progressive Lung Weight gain. Pulmonary vascular resistance increased threefold exclusively due to pulmonary venoconstriction. Pulmonary venoconstriction was confirmed in Lungs perfused in a reverse direction from the pulmonary vein to the artery ( n = 5), as evidenced by marked precapillary vasoconstriction and a sustained Lung Weight loss. Furthermore, in Lungs perfused at a constant blood flow (n = 5), STA_2 also caused selective pulmonary venoconstriction. Vascular permeability measured by the capillary filtration coefficient and the isogravimetric Pc at 30 and 60 min after STA_2 infusion did not change significantly from baseline in any Lungs studied. Moreover, elevation of Pc by raising the venous reservoir of the intact lobes ( n = 5) to the same level as the STA_2 Lungs caused a greater or similar Weight gain compared with the STA_2 Lungs. Thus, we conclude that TxA_2 constricts selectively the pulmonary vein resulting in an increase in Pc and Lung Weight gain without significant changes in vascular permeability in isolated blood-perfused dog Lungs.
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Effects of thromboxane A2 analogue on vascular resistance distribution and permeability in isolated blood-perfused dog Lungs.
Lung, 1995Co-Authors: Toshishige Shibamoto, H. -g. Wang, Y Saeki, Y Yamaguchi, S Tanaka, T. Hayashi, Shozo KoyamaAbstract:This study was designed to determine the effects of thromboxane A2 (TxA2) on the distribution of vascular resistance, Lung Weight, and microvascular permeability in isolated dog Lungs perfused at a constant pressure with autologous blood. The stable TxA2 analogue (STA2; 30 μg, n = 5) caused an increase in pulmonary capillary pressure (Pc) assessed as double-occlusion pressure to 14.0 ± 0.4 mmHg from the baseline of 7.9 ± 0.3 mmHg with progressive Lung Weight gain. Pulmonary vascular resistance increased threefold exclusively due to pulmonary venoconstriction. Pulmonary venoconstriction was confirmed in Lungs perfused in a reverse direction from the pulmonary vein to the artery (n = 5), as evidenced by marked precapillary vasoconstriction and a sustained Lung Weight loss. Furthermore, in Lungs perfused at a constant blood flow (n = 5), STA2 also caused selective pulmonary venoconstriction. Vascular permeability measured by the capillary filtration coefficient and the isogravimetric Pc at 30 and 60 min after STA2 infusion did not change significantly from baseline in any Lungs studied. Moreover, elevation of Pc by raising the venous reservoir of the intact lobes (n = 5) to the same level as the STA2 Lungs caused a greater or similar Weight gain compared with the STA2 Lungs. Thus, we conclude that TxA2 constricts selectively the pulmonary vein resulting in an increase in Pc and Lung Weight gain without significant changes in vascular permeability in isolated blood-perfused dog Lungs.
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PAF increases capillary pressure but not vascular permeability in isolated blood-perfused canine Lungs.
American Journal of Physiology-heart and Circulatory Physiology, 1993Co-Authors: Toshishige Shibamoto, Y Saeki, Y Yamaguchi, T. Hayashi, M. Kawamoto, S KoyamaAbstract:We determined the effects of platelet-activating factor (PAF) on pulmonary vascular resistance, Lung Weight, and microvascular permeability in isolated canine Lungs perfused at constant pressure with autologous blood. PAF caused a dose-dependent increase in total pulmonary vascular resistance (Rt) and pulmonary capillary pressure assessed as double-occlusion pressure. PAF (33 micrograms; n = 7) caused a 10-fold increase in Rt and a decrease in precapillary-to-postcapillary vascular resistance ratio from 0.97 +/- 0.10 to 0.38 +/- 0.03, suggesting predominant pulmonary venoconstriction. Shortly after PAF, Lung Weight decreased transiently and then increased, reaching a plateau above baseline (112.5 +/- 1.6%) at 30 min. In Lungs perfused in the antidromic direction from the pulmonary vein to the artery (n = 5), PAF (33 micrograms) produced marked precapillary vasoconstriction, consistent with pulmonary venoconstriction, and a remarkable and sustained decrease in Lung Weight below baseline by 30 min. Vascular permeability, measured 30 min after PAF using the capillary filtration coefficient and isogravimetric capillary pressure, did not change significantly from baseline. Thus we conclude that PAF produces Lung Weight gain by means of an increase in capillary pressure predominantly due to pulmonary venoconstriction without significant changes in vascular permeability in isolated blood-perfused canine Lungs.
S Koyama - One of the best experts on this subject based on the ideXlab platform.
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Effects of thromboxane A_2 analogue on vascular resistance distribution and permeability in isolated blood-perfused dog Lungs
Lung, 1995Co-Authors: Toshishige Shibamoto, H. -g. Wang, Y Saeki, Y Yamaguchi, S Tanaka, S KoyamaAbstract:This study was designed to determine the effects of thromboxane A_2 (TxA_2) on the distribution of vascular resistance, Lung Weight, and microvascular permeability in isolated dog Lungs perfused at a constant pressure with autologous blood. The stable TxA_2 analogue (STA_2; 30 μg, n = 5) caused an increase in pulmonary capillary pressure (Pc) assessed as double-occlusion pressure to 14.0 ± 0.4 mmHg from the baseline of 7.9 ± 0.3 mmHg with progressive Lung Weight gain. Pulmonary vascular resistance increased threefold exclusively due to pulmonary venoconstriction. Pulmonary venoconstriction was confirmed in Lungs perfused in a reverse direction from the pulmonary vein to the artery ( n = 5), as evidenced by marked precapillary vasoconstriction and a sustained Lung Weight loss. Furthermore, in Lungs perfused at a constant blood flow (n = 5), STA_2 also caused selective pulmonary venoconstriction. Vascular permeability measured by the capillary filtration coefficient and the isogravimetric Pc at 30 and 60 min after STA_2 infusion did not change significantly from baseline in any Lungs studied. Moreover, elevation of Pc by raising the venous reservoir of the intact lobes ( n = 5) to the same level as the STA_2 Lungs caused a greater or similar Weight gain compared with the STA_2 Lungs. Thus, we conclude that TxA_2 constricts selectively the pulmonary vein resulting in an increase in Pc and Lung Weight gain without significant changes in vascular permeability in isolated blood-perfused dog Lungs.
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PAF increases capillary pressure but not vascular permeability in isolated blood-perfused canine Lungs.
American Journal of Physiology-heart and Circulatory Physiology, 1993Co-Authors: Toshishige Shibamoto, Y Saeki, Y Yamaguchi, T. Hayashi, M. Kawamoto, S KoyamaAbstract:We determined the effects of platelet-activating factor (PAF) on pulmonary vascular resistance, Lung Weight, and microvascular permeability in isolated canine Lungs perfused at constant pressure with autologous blood. PAF caused a dose-dependent increase in total pulmonary vascular resistance (Rt) and pulmonary capillary pressure assessed as double-occlusion pressure. PAF (33 micrograms; n = 7) caused a 10-fold increase in Rt and a decrease in precapillary-to-postcapillary vascular resistance ratio from 0.97 +/- 0.10 to 0.38 +/- 0.03, suggesting predominant pulmonary venoconstriction. Shortly after PAF, Lung Weight decreased transiently and then increased, reaching a plateau above baseline (112.5 +/- 1.6%) at 30 min. In Lungs perfused in the antidromic direction from the pulmonary vein to the artery (n = 5), PAF (33 micrograms) produced marked precapillary vasoconstriction, consistent with pulmonary venoconstriction, and a remarkable and sustained decrease in Lung Weight below baseline by 30 min. Vascular permeability, measured 30 min after PAF using the capillary filtration coefficient and isogravimetric capillary pressure, did not change significantly from baseline. Thus we conclude that PAF produces Lung Weight gain by means of an increase in capillary pressure predominantly due to pulmonary venoconstriction without significant changes in vascular permeability in isolated blood-perfused canine Lungs.
