The Experts below are selected from a list of 288 Experts worldwide ranked by ideXlab platform
Ola Didrik Saugstad - One of the best experts on this subject based on the ideXlab platform.
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Release of xanthine oxidase to the Systemic Circulation during resuscitation from severe hypoxemia in newborn pigs
Acta paediatrica (Oslo Norway : 1992), 1995Co-Authors: Terje Rootwelt, Runar Almaas, Stephanie Øyasæter, Atle Moen, Ola Didrik SaugstadAbstract:Xanthine oxidase may contribute to oxygen free radical formation during reoxygenation after hypoxia, but in humans the enzyme is present in substantial amounts only in the liver and intestine. We developed a sensitive assay for xanthine oxidase using 14C-xanthine as substrate and investigated whether xanthine oxidase was released into the Systemic Circulation when 19 newborn pigs were resuscitated after severe hypoxemia. In five piglets plasma xanthine oxidase concentrations increased from undetectable levels to a median value of 8 (range 4-18) microU/ml after 30 min of reoxygenation. In these pigs serum aspartate aminotransferase increased from 45 to 148 U/l, while alanine aminotransferase was unchanged (28-31 U/l). The release of xanthine oxidase did not seem to correlate with the severity of the histological brain damage after 4 days. We conclude that only low levels of xanthine oxidase are released to the Systemic Circulation after severe hypoxemia in newborn pigs.
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RELEASE OF XANTHINE OXIDASE (XO) TO THE Systemic Circulation DURING RESUSCITATION AFTER SEVERE HYPOXEMIA
Pediatric Research, 1994Co-Authors: Terje Rootwelt, Runar Almaas, Stephanie Øyasæter, Atle Moen, Ola Didrik SaugstadAbstract:XO may contribute to oxygen free radical production during reoxygenation after hypoxia, but in humans XO is present in substantial amounts only in liver and intestine and possibly to a smaller extent in vascular endothelium. We wanted to determine whether XO is released to the Systemic Circulation during reoxygenation after general hypoxia and thus possibly contributes to oxygen radical production in other organs also. Plasma levels of XO were determined in 19 newborn pigs resuscitated from severe hypoxemia (8% O2 until systolic blood pressure had fallen to 20 mmhg). 14C-xanthine was used as substrate, and the 14C-uric acid product was isolated with an HPLC technique and counted Plasma XO was below 2.5 μU/ml in all piglets before hypoxemia and in 4 control piglets throughout the experiment. In 5 of 19 piglets plasma XO rose during reoxygenation to a mean value of 10 {range 4 - 18) μU/ml after 30 min. In these piglets plasma aspartate aminotransferase increased also (from 20 to 94 U/l), but not alanine aminotransferase (36 to 39 U/ml). We conclude that XO may be released to the Systemic Circulation after severe hypoxia although in the present experiment XO was only elevated in 5 out of 19 piglets.
Marja-liisa Vuori - One of the best experts on this subject based on the ideXlab platform.
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ß1‐ and ß2‐antagonist activity of topically applied betaxolol and timolol in the Systemic Circulation
Acta Ophthalmologica, 2009Co-Authors: Marja-liisa Vuori, Esko Lisalo, Timo Kaila, Timo Ali‐melkkilä, K. Matti SaariAbstract:The beta 1- and beta 2-antagonist activity of betaxolol and timolol in the Systemic Circulation was studied ex-vivo after their ocular administration in thirty patients during cataract surgery. The patients received 40 microliters of 0.5% betaxolol or 0.25% timolol into the lower cul-de-sacs of both eyes. Blood samples were collected up to four h after instillation of the doses. Plasma concentrations of betaxolol and timolol were analyzed using a radioreceptor assay. The ex-vivo-beta 1-and beta 2-receptor occupancies corresponding drug plasma levels were calculated using radioligand binding techniques. The extent of beta 1-receptor occupancy of betaxolol in the Systemic Circulation was less than 20% and its beta 2-receptor occupancy was negligible. The extent of beta 1-receptor occupancy of timolol was about 65% and its beta 2-receptor occupancy about 80%. Because receptor occupancy is the basis of antagonist activity of beta-blocking agents, this study shows that the beta 1-antagonist activity of betaxolol in the Systemic Circulation is much less than that of timolol, and that its beta 2-antagonist activity is negligible. The study suggests that the reported side effects of betaxolol in patients with obstructive pulmonary diseases are not mediated via its beta 2-receptor blocking properties.
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s1 and s2 antagonist activity of topically applied betaxolol and timolol in the Systemic Circulation
Acta Ophthalmologica, 2009Co-Authors: Marja-liisa Vuori, Esko Lisalo, Timo Kaila, Timo Alimelkkila, Matti K. SaariAbstract:The beta 1- and beta 2-antagonist activity of betaxolol and timolol in the Systemic Circulation was studied ex-vivo after their ocular administration in thirty patients during cataract surgery. The patients received 40 microliters of 0.5% betaxolol or 0.25% timolol into the lower cul-de-sacs of both eyes. Blood samples were collected up to four h after instillation of the doses. Plasma concentrations of betaxolol and timolol were analyzed using a radioreceptor assay. The ex-vivo-beta 1-and beta 2-receptor occupancies corresponding drug plasma levels were calculated using radioligand binding techniques. The extent of beta 1-receptor occupancy of betaxolol in the Systemic Circulation was less than 20% and its beta 2-receptor occupancy was negligible. The extent of beta 1-receptor occupancy of timolol was about 65% and its beta 2-receptor occupancy about 80%. Because receptor occupancy is the basis of antagonist activity of beta-blocking agents, this study shows that the beta 1-antagonist activity of betaxolol in the Systemic Circulation is much less than that of timolol, and that its beta 2-antagonist activity is negligible. The study suggests that the reported side effects of betaxolol in patients with obstructive pulmonary diseases are not mediated via its beta 2-receptor blocking properties.
Terje Rootwelt - One of the best experts on this subject based on the ideXlab platform.
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Release of xanthine oxidase to the Systemic Circulation during resuscitation from severe hypoxemia in newborn pigs
Acta paediatrica (Oslo Norway : 1992), 1995Co-Authors: Terje Rootwelt, Runar Almaas, Stephanie Øyasæter, Atle Moen, Ola Didrik SaugstadAbstract:Xanthine oxidase may contribute to oxygen free radical formation during reoxygenation after hypoxia, but in humans the enzyme is present in substantial amounts only in the liver and intestine. We developed a sensitive assay for xanthine oxidase using 14C-xanthine as substrate and investigated whether xanthine oxidase was released into the Systemic Circulation when 19 newborn pigs were resuscitated after severe hypoxemia. In five piglets plasma xanthine oxidase concentrations increased from undetectable levels to a median value of 8 (range 4-18) microU/ml after 30 min of reoxygenation. In these pigs serum aspartate aminotransferase increased from 45 to 148 U/l, while alanine aminotransferase was unchanged (28-31 U/l). The release of xanthine oxidase did not seem to correlate with the severity of the histological brain damage after 4 days. We conclude that only low levels of xanthine oxidase are released to the Systemic Circulation after severe hypoxemia in newborn pigs.
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RELEASE OF XANTHINE OXIDASE (XO) TO THE Systemic Circulation DURING RESUSCITATION AFTER SEVERE HYPOXEMIA
Pediatric Research, 1994Co-Authors: Terje Rootwelt, Runar Almaas, Stephanie Øyasæter, Atle Moen, Ola Didrik SaugstadAbstract:XO may contribute to oxygen free radical production during reoxygenation after hypoxia, but in humans XO is present in substantial amounts only in liver and intestine and possibly to a smaller extent in vascular endothelium. We wanted to determine whether XO is released to the Systemic Circulation during reoxygenation after general hypoxia and thus possibly contributes to oxygen radical production in other organs also. Plasma levels of XO were determined in 19 newborn pigs resuscitated from severe hypoxemia (8% O2 until systolic blood pressure had fallen to 20 mmhg). 14C-xanthine was used as substrate, and the 14C-uric acid product was isolated with an HPLC technique and counted Plasma XO was below 2.5 μU/ml in all piglets before hypoxemia and in 4 control piglets throughout the experiment. In 5 of 19 piglets plasma XO rose during reoxygenation to a mean value of 10 {range 4 - 18) μU/ml after 30 min. In these piglets plasma aspartate aminotransferase increased also (from 20 to 94 U/l), but not alanine aminotransferase (36 to 39 U/ml). We conclude that XO may be released to the Systemic Circulation after severe hypoxia although in the present experiment XO was only elevated in 5 out of 19 piglets.
Matti K. Saari - One of the best experts on this subject based on the ideXlab platform.
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s1 and s2 antagonist activity of topically applied betaxolol and timolol in the Systemic Circulation
Acta Ophthalmologica, 2009Co-Authors: Marja-liisa Vuori, Esko Lisalo, Timo Kaila, Timo Alimelkkila, Matti K. SaariAbstract:The beta 1- and beta 2-antagonist activity of betaxolol and timolol in the Systemic Circulation was studied ex-vivo after their ocular administration in thirty patients during cataract surgery. The patients received 40 microliters of 0.5% betaxolol or 0.25% timolol into the lower cul-de-sacs of both eyes. Blood samples were collected up to four h after instillation of the doses. Plasma concentrations of betaxolol and timolol were analyzed using a radioreceptor assay. The ex-vivo-beta 1-and beta 2-receptor occupancies corresponding drug plasma levels were calculated using radioligand binding techniques. The extent of beta 1-receptor occupancy of betaxolol in the Systemic Circulation was less than 20% and its beta 2-receptor occupancy was negligible. The extent of beta 1-receptor occupancy of timolol was about 65% and its beta 2-receptor occupancy about 80%. Because receptor occupancy is the basis of antagonist activity of beta-blocking agents, this study shows that the beta 1-antagonist activity of betaxolol in the Systemic Circulation is much less than that of timolol, and that its beta 2-antagonist activity is negligible. The study suggests that the reported side effects of betaxolol in patients with obstructive pulmonary diseases are not mediated via its beta 2-receptor blocking properties.
David S Celermajer - One of the best experts on this subject based on the ideXlab platform.
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treatment of obstructive sleep apnoea leads to improved microvascular endothelial function in the Systemic Circulation
Thorax, 2006Co-Authors: Jodee Lattimore, Ian Wilcox, Michael R Skilton, M R Langenfeld, David S CelermajerAbstract:Background: Obstructive sleep apnoea (OSA) is a common and potentially reversible cause of Systemic hypertension. The mechanisms whereby OSA leads to hypertension and the effects of treatment on arterial function, however, are not well established. Microvascular arterial endothelial and smooth muscle function was assessed in subjects with OSA before and after treatment with continuous positive airways pressure (CPAP). Methods: Ten subjects of mean (SE) age 49 (8) years with at least moderately severe OSA had detailed forearm vascular reactivity studies before and after 3 months of CPAP treatment. The Systemic Circulation was assessed by measuring brachial artery pressure, flow and resistance responses to intra-arterial infusions of acetylcholine (ACh; an endothelium dependent vasodilator), sodium nitroprusside (SNP; an endothelium independent vasodilator), l-NMMA (a nitric oxide (NO) antagonist), and l-arginine (the substrate for NO). Results: Before CPAP, ACh and SNP infusions increased forearm blood flow in a dose dependent manner (p<0.01). After CPAP, endothelium dependent dilation to ACh was significantly increased (434 (23)% of baseline after CPAP v 278 (20)% before CPAP, p<0.001), whereas SNP induced dilation was unchanged. Resting NO production was higher after CPAP, evidenced by a significantly greater reduction in basal flow by l-NMMA (p = 0.05). l-Arginine reversed the effect of l-NMMA in all cases. Conclusion: In patients with OSA, treatment with CPAP improves baseline endothelial NO release and stimulates endothelium dependent vasorelaxation in the Systemic Circulation. This is a potential mechanism for improving Systemic and vascular function in patients with OSA treated with CPAP.
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Treatment of obstructive sleep apnoea leads to improved microvascular endothelial function in the Systemic Circulation.
Thorax, 2006Co-Authors: Jodee Lattimore, Ian Wilcox, Michael R Skilton, M R Langenfeld, David S CelermajerAbstract:Background: Obstructive sleep apnoea (OSA) is a common and potentially reversible cause of Systemic hypertension. The mechanisms whereby OSA leads to hypertension and the effects of treatment on arterial function, however, are not well established. Microvascular arterial endothelial and smooth muscle function was assessed in subjects with OSA before and after treatment with continuous positive airways pressure (CPAP). Methods: Ten subjects of mean (SE) age 49 (8) years with at least moderately severe OSA had detailed forearm vascular reactivity studies before and after 3 months of CPAP treatment. The Systemic Circulation was assessed by measuring brachial artery pressure, flow and resistance responses to intra-arterial infusions of acetylcholine (ACh; an endothelium dependent vasodilator), sodium nitroprusside (SNP; an endothelium independent vasodilator), l-NMMA (a nitric oxide (NO) antagonist), and l-arginine (the substrate for NO). Results: Before CPAP, ACh and SNP infusions increased forearm blood flow in a dose dependent manner (p
