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{userid:"dunbar.ivy", "articletype":"article","pages":"L758-L765","author":"D D Ivy, T A Parker, S H Abman","year":"2000","title":"Prolonged endothelin B receptor blockade causes pulmonary hypertension in the ovine fetus.","month":"Oct","journal":"Am J Physiol Lung Cell Mol Physiol","publisher":"","volume":"279","number":"4","note":"","tags":"Animals,Antihypertensive Agents,Blood Pressure,Carbon Dioxide,Endothelin-1,Female,Gestational Age,Hemodynamics,Hypertension, Pulmonary,Oligopeptides,Oxygen,Piperidines,Pregnancy,Pulmonary Circulation,Receptor, Endothelin A,Receptor, Endothelin B,Receptors, Endothelin,Reference Values,Sheep,Vascular Resistance","booktitle":"","editor":"","abstract":"Endothelin (ET)-1 contributes to regulation of pulmonary vascular tone and structure in the normal ovine fetus and in models of perinatal pulmonary hypertension. The hemodynamic effects of ET-1 are due to activation of its receptors. The ET(A) receptor mediates vasoconstriction and smooth muscle cell proliferation, whereas the ET(B) receptor mediates vasodilation. In a lamb model of chronic intrauterine pulmonary hypertension, ET(B) receptor activity and gene expression are decreased. To determine whether prolonged ET(B) receptor blockade causes pulmonary hypertension, we studied the hemodynamic effects of selective ET(B) receptor blockade with BQ-788. Animals were treated with an infusion of either BQ-788 or vehicle for 7 days. Prolonged BQ-788 treatment increased pulmonary arterial pressure and pulmonary vascular resistance (P < 0.05). The pulmonary vasodilator response to sarafotoxin 6c, a selective ET(B) receptor agonist, was attenuated after 7 days of BQ-788 treatment, demonstrating pharmacological blockade of the ET(B) receptor. Animals treated with BQ-788 had greater right ventricular hypertrophy and muscularization of small pulmonary arteries (P < 0. 05). Lung ET-1 levels were threefold higher in the animals treated with BQ-788 (P < 0.05). We conclude that prolonged selective ET(B) receptor blockade causes severe pulmonary hypertension and pulmonary vascular remodeling in the late-gestation ovine fetus.","address":"","school":"","issn":"1040-0605","doi":"","isi":"","pubmed":"11000137","key":"Ivy2000","howpublished":"","urllink":"","refid":90}
,

{userid:"dunbar.ivy", "articletype":"article","pages":"2481-2487","author":"D D Ivy, J P Kinsella, S H Abman","year":"1996","title":"Endothelin blockade augments pulmonary vasodilation in the ovine fetus.","month":"Dec","journal":"J Appl Physiol","publisher":"","volume":"81","number":"6","note":"","tags":"Animals,Endothelin-1,Female,Pregnancy,Pulmonary Circulation,Sheep,Vasodilation","booktitle":"","editor":"","abstract":"The physiological role of endothelin-1 (ET-1) in regulation of vascular tone in the perinatal lung is controversial. Recent studies suggest that ET-1 contributes to high basal pulmonary vascular resistance in the normal fetus, but its role in the modulation of pulmonary vascular tone remains uncertain. We hypothesized that high ET-1 activity opposes the vasodilator response to some physiological stimuli such as increased pressure. To test the hypothesis that ET-1 modulates fetal pulmonary vascular responses to acute and prolonged physiological stimuli, we performed a series of experiments in the late-gestation ovine fetus. We studied the hemodynamic effects of two ET-1 antagonists, BQ-123 (a selective ETA-receptor antagonist) and phosphoramidon (a nonselective ET-1-converting enzyme inhibitor) during mechanical increases in pressure due to partial ductus arteriosus compression in chronically prepared late-gestation fetal lambs. In control studies, partial ductus arteriosus compression decreased the ratio of pulmonary arterial pressure to pulmonary artery flow in the left lung 34 +\/- 6% from baseline. Intrapulmonary infusions of BQ-123 (0.5 microgram\/min for 10 min; 0.025 microgram\/min for 2 h) or phosphoramidon (1.0 mg\/min for 10 min) augmented the peak vasodilator response during ductus arteriosus compression (52 +\/- 3 and 49 +\/- 6% from baseline, respectively, P < 0.05 vs. control). In addition, unlike the transient vasodilator response to ductus arteriosus compression in control studies, ET-1 blockade with BQ-123 or phosphoramidon prolonged the increase in flow caused by ductus arteriosus compression. In summary, ETA-receptor blockade and ET-1-converting enzyme inhibition augment and prolong fetal pulmonary vasodilation during partial compression of the ductus arteriosus. We conclude that ET-1 activity modulates acute and prolonged responses of the fetal pulmonary circulation to changes in vascular pressure. We speculate that ET-1 contributes to regulation and maintenance of high pulmonary vascular resistance in the normal ovine fetal lung.","address":"","school":"","issn":"8750-7587","doi":"","isi":"","pubmed":"9018495","key":"Ivy1996","howpublished":"","urllink":"","refid":109}
,

{userid:"dunbar.ivy", "articletype":"article","pages":"H1955-H1961","author":"J P Kinsella, D D Ivy, S H Abman","year":"1994","title":"Ontogeny of NO activity and response to inhaled NO in the developing ovine pulmonary circulation.","month":"Nov","journal":"Am J Physiol","publisher":"","volume":"267","number":"5 Pt 2","note":"","tags":"Administration, Inhalation,Analysis of Variance,Animals,Arginine,Embryonic and Fetal Development,Female,Gestational Age,Hemodynamics,Muscle, Smooth, Vascular,Nitric Oxide,Nitroarginine,Oxygen,Pregnancy,Pulmonary Artery,Pulmonary Circulation,Regional Blood Flow,Sheep,Vascular Resistance","booktitle":"","editor":"","abstract":"To determine maturation-related changes in nitric oxide (NO) activity in the developing pulmonary circulation, we studied the hemodynamic effects of endogenous NO inhibition under basal conditions in the premature ovine fetus and the response to birth-related stimuli and exogenous NO in 30 fetal sheep at three different gestational ages. At 0.95 term, pulmonary vasodilation during inhaled NO (20 parts per million) was equivalent to the dilator response to 100% O2, but at 0.86 term vasodilation during inhaled NO was greater than the dilator response to 100% O2 (P < 0.05). At 0.78 term, left pulmonary arterial flow (QLPA) did not increase with exposure to either NO or 100% O2. Intrapulmonary infusion of nitro-L-arginine (L-NA) increased basal pulmonary vascular resistance 38% in the premature fetus at 0.78 term. L-NA treatment decreased the ventilation-induced rise in QLPA by 60% compared with controls (P < 0.05). Inhaled NO but not 100% O2 increased QLPA after L-NA treatment to levels achieved with ventilation alone in the controls. We conclude that in the premature pulmonary circulation (0.78 term) 1) basal pulmonary vascular resistance is modulated by endogenous NO, 2) pulmonary vasodilation at birth is partly mediated by endogenous NO activity, and 3) inhaled NO causes potent vasodilation.","address":"","school":"","issn":"0002-9513","doi":"","isi":"","pubmed":"7977827","key":"Kinsella1994","howpublished":"","urllink":"","refid":114}
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{userid:"dunbar.ivy", "articletype":"article","pages":"647-648","author":"J P Kinsella, F Torielli, J W Ziegler, D D Ivy, S H Abman","year":"1995","title":"Dipyridamole augmentation of response to nitric oxide.","month":"Sep","journal":"Lancet","publisher":"","volume":"346","number":"8975","note":"","tags":"Dipyridamole,Drug Synergism,Hernia, Diaphragmatic,Humans,Infant, Newborn,Nitric Oxide,Persistent Fetal Circulation Syndrome,Phosphodiesterase Inhibitors","booktitle":"","editor":"","abstract":"","address":"","school":"","issn":"0140-6736","doi":"","isi":"","pubmed":"7651043","key":"Kinsella1995","howpublished":"","urllink":"","refid":104}
,

{userid:"dunbar.ivy", "articletype":"article","pages":"S18-S23","author":"S H Abman, D D Ivy, J W Ziegler, J P Kinsella","year":"1996","title":"Mechanisms of abnormal vasoreactivity in persistent pulmonary hypertension of the newborn infant.","month":"Mar\/Apr","journal":"J Perinatol","publisher":"","volume":"16","number":"2 Pt 2 Su","note":"","tags":"Humans,Infant, Newborn,Lung,Muscle, Smooth, Vascular,Persistent Fetal Circulation Syndrome,Pulmonary Artery,Pulmonary Circulation,Vascular Resistance,Vasoconstriction,Vasodilation","booktitle":"","editor":"","abstract":"","address":"","school":"","issn":"0743-8346","doi":"","isi":"","pubmed":"8732544","key":"Abman1996","howpublished":"","urllink":"","refid":106}
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{userid:"dunbar.ivy", "refid":"149","repocollections":"","attachment":"","_thumb":"","articletype":"article","sectionheading":"","title":"Chronic intrauterine pulmonary hypertension increases preproendothelin-1 and decreases endothelin B receptor mRNA expression in the ovine fetal lung.","year":"1998","author":"D D Ivy, T D Le Cras, M P Horan, S H Abman","journal":"Chest","volume":"114","number":"1 Suppl","pages":"","month":"Jul","doi":"","pubmed":"9676634","pdflink":"","urllink":"","abstract":"","note":"","tags":"Animals,Chronic Disease,Disease Models, Animal,Endothelin-1,Endothelins,Fetal Diseases,Hypertension, Pulmonary,Lung,Protein Precursors,RNA, Messenger,Receptors, Endothelin,Sheep,Vasoconstriction","publisher":"","booktitle":"","editor":"","address":"","school":"","issn":"0012-3692","isi":"","key":"Ivy1998","howpublished":""}
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{userid:"dunbar.ivy", "refid":"150","repocollections":"","attachment":"","_thumb":"","articletype":"article","sectionheading":"","title":"Hemodynamic effects of dipyridamole and inhaled nitric oxide in pediatric patients with pulmonary hypertension.","year":"1998","author":"D D Ivy, J W Ziegler, J P Kinsella, J W Wiggins, S H Abman","journal":"Chest","volume":"114","number":"1 Suppl","pages":"","month":"Jul","doi":"","pubmed":"9676605","pdflink":"","urllink":"","abstract":"","note":"","tags":"Administration, Inhalation,Child,Dipyridamole,Heart Defects, Congenital,Hemodynamics,Humans,Hypertension, Pulmonary,Nitric Oxide,Postoperative Period,Vasodilation","publisher":"","booktitle":"","editor":"","address":"","school":"","issn":"0012-3692","isi":"","key":"Ivy1998","howpublished":""}
,

{userid:"dunbar.ivy", "articletype":"article","pages":"291-291.e2","author":"Benjamin S Frank, Martin Runciman, William A Manning, D Dunbar Ivy, Steven H Abman, Lisa Howley","year":"2019","title":"Pulmonary Hypertension Secondary to Scurvy in a Developmentally Typical Child.","month":"May","journal":"The Journal of pediatrics","publisher":"","volume":"208","number":"","note":"","tags":"Adolescent,Ascorbic Acid,Chest Pain,Cholecalciferol,Dietary Supplements,Echocardiography,Gingiva,Hemorrhage,Humans,Hypertension, Pulmonary,Iron,Leg,Male,Pain,Scurvy,Wounds and Injuries","booktitle":"","editor":"","abstract":"","address":"","school":"","issn":"1097-6833","doi":"10.1016\/j.jpeds.2018.12.068","isi":"","pubmed":"30738657","key":"Frank2019","howpublished":"","urllink":"","refid":253,"weight":253}
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{userid:"dunbar.ivy", "articletype":"article","pages":"402-408","author":"J P Kinsella, D D Ivy, S H Abman","year":"1994","title":"Inhaled nitric oxide improves gas exchange and lowers pulmonary vascular resistance in severe experimental hyaline membrane disease.","month":"Sep","journal":"Pediatric research","publisher":"","volume":"36","number":"3","note":"","tags":"Administration, Inhalation,Animals,Animals, Newborn,Gestational Age,Hemodynamics,Humans,Hyaline Membrane Disease,Infant, Newborn,Lung,Nitric Oxide,Pulmonary Gas Exchange,Respiration, Artificial,Sheep,Survival Rate,Vascular Resistance","booktitle":"","editor":"","abstract":"To determine the effects of inhaled nitric oxide (NO) on pulmonary hemodynamics and gas exchange in experimental hyaline membrane disease (HMD), we studied 16 premature lambs (0.78 term) in two separate protocols. All animals were treated with exogenous surfactant before mechanical ventilation. In protocol 1, we measured the acute response to brief treatment with inhaled NO (20 ppm, 20 min) after 2 h of mechanical ventilation with fraction of inspired oxygen of 1.00 (n = 5). After 2 h, brief NO treatment lowered pulmonary vascular resistance from 0.26 +\/- 0.05 to 0.16 +\/- 0.03 mm Hg.(mL\/min)-1 (p < 0.01) and improved gas exchange (arterial PO2, 44 +\/- 9 mm Hg baseline to 168 +\/- 45 mm Hg NO, p < 0.01; arterial PCO2 45 +\/- 5 mm Hg baseline to 35 +\/- 4 mm Hg NO, p < 0.05). In protocol 2, to determine whether early and continuous treatment with inhaled NO could sustain improvement in gas exchange and pulmonary hemodynamics in severe HMD, we compared the physiologic effects of ventilation with high inspired oxygen concentrations for 3 h with NO (20 ppm, n = 6) and without NO (controls, n = 5). After 3 h, the NO treatment group had sustained reduction in pulmonary vascular resistance (0.10 +\/- 0.01 mm Hg.(mL\/min)-1 NO versus 0.25 +\/- 0.04 mm Hg.(mL\/min)-1 control, p < 0.05), increased left pulmonary artery blood flow (204 +\/- 24 mL\/min NO versus 109 +\/- 15 mL\/min control, p < 0.05), and increased arterial PO2 (114 +\/- 27 mm Hg NO versus 36 +\/- 11 mm Hg control, p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)","address":"","school":"","issn":"0031-3998","doi":"10.1203\/00006450-199409000-00022","isi":"","pubmed":"7808839","key":"Kinsella1994","howpublished":"","urllink":"","refid":115,"weight":115}
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{userid:"dunbar.ivy", "articletype":"article","pages":"2141-2148","author":"D D Ivy, J P Kinsella, S H Abman","year":"1994","title":"Physiologic characterization of endothelin A and B receptor activity in the ovine fetal pulmonary circulation.","month":"May","journal":"The Journal of clinical investigation","publisher":"","volume":"93","number":"5","note":"","tags":"Animals,Arginine,Blood Pressure,Endothelin-1,Endothelins,Fetus,Hypertension, Pulmonary,Muscle Tonus,Nitric Oxide,Nitroarginine,Peptides, Cyclic,Perfusion,Protein Precursors,Pulmonary Circulation,Receptor, Endothelin A,Receptor, Endothelin B,Receptors, Endothelin,Sheep,Vascular Resistance,Viper Venoms","booktitle":"","editor":"","abstract":"To determine the potential contribution of endothelin (ET) to modulation of high pulmonary vascular resistance in the normal fetus, we studied the effects of BQ 123, a selective ET-A receptor antagonist, and sarafoxotoxin S6c (SFX), a selective ET-B receptor agonist, in 31 chronically prepared late gestation fetal lambs. Brief intrapulmonary infusions of BQ 123 (0.1-1.0 mcg\/min for 10 min) caused sustained increases in left pulmonary artery flow (Qp) without changing main pulmonary artery (MPA) and aortic (Ao) pressures. In contrast, BQ 123 did not change vascular resistance in a regional systemic circulation (the fetal hindlimb). To determine whether big-endothelin-1 (big-ET-1)-induced pulmonary vasoconstriction is mediated by ET-A receptor stimulation, we studied the effects of big-ET-1 with or without pretreatment with BQ 123. BQ 123 (0.5 mcg\/min for 10 min) blocked the rise in total pulmonary resistance caused by big-ET-1. CGS 27830 (100 mcg\/min for 10 min), an ET-A and -B receptor antagonist, did not change basal tone but blocked big-ET-1-induced pulmonary vasoconstriction. Brief and prolonged intrapulmonary infusion of SFX (0.1 mcg\/min for 10 min) increased Qp twofold without changing MPA or Ao pressures. Nitro-L-arginine (L-NA), a selective endothelium-derived nitric oxide (EDNO) antagonist, blocked vasodilation caused by BQ 123 and SFX. We conclude that: (a) BQ 123 causes sustained fetal pulmonary vasodilation, but did not change vascular resistance in the fetal hindlimb; (b) Big-ET-1-induced pulmonary vasoconstriction may be mediated through ET-A receptor stimulation; and (c) ET-B receptor stimulation causes pulmonary vasodilation through EDNO release. These findings support the hypothesis that endothelin may play a role in modulation of high basal pulmonary vascular resistance in the normal fetus.","address":"","school":"","issn":"0021-9738","doi":"10.1172\/JCI117210","isi":"","pubmed":"8182146","key":"Ivy1994","howpublished":"","urllink":"","refid":117,"weight":117}
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