Development of pulmonary vascular response to oxygen

Morin, Frederick C.; Egan, Edmund A.; Ferguson, Wayne W.; Lundgren, Ceg

doi:10.1152/ajpheart.1988.254.3.h542

Cited by 83 publications

(97 citation statements)

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“…The pulmonary vasodilator response to oxygen (mediated by NO) improves with advancing GA in animal studies. [24][25][26] Reactivity of the human fetal pulmonary circulation to maternal hyperoxygenation also increases with advancing gestation. 27 Our data support the experimental evidence that the iNO signaling pathways may be intact in near term lambs and infants, but not in the very preterm.…”

Section: Discussionmentioning

confidence: 99%

Characteristics of pulmonary hypertension in preterm neonates

et al. 2007

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Objective: Characteristics of preterm infants who develop pulmonary hypertension (PHT) and their response to inhaled nitric oxide (iNO) are not well described. Our objective was to identify risk factors for PHT in infants <37 weeks gestational age (GA) and to evaluate their response to iNO.Study design: A retrospective chart review was conducted in infants <37 weeks GA born from July/2000 to October/2005 who had an echocardiographic diagnosis of PHT in the first 4 weeks of life. A comparison non-PHT group was generated matched for GA and birth date. Data on prenatal and postnatal characteristics, response to iNO and mortality were collected.Results: Low Apgar scores, preterm premature rupture of membranes, oligohydramnios, pulmonary hypoplasia and sepsis were independently predictive of PHT. Mortality was significantly higher in the PHT group (26.2% versus 4.1%; P<0.0001) compared to the control group. Low birth weight, severe intraventricular hemorrhage and male sex were significantly associated with death in infants with PHT. Thirty-seven percent (23/61) of infants with PHT were treated with inhaled NO. Infants <29-week GA had poor response to iNO and the response to iNO increased with GA (P<0.02).Conclusions: Low Apgar scores, oligohydramnios and pulmonary hypoplasia are associated with the development of PHT in premature infants. The percentage of infants responding to iNO increases with advancing GA.

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Section: Discussionmentioning

confidence: 99%

Characteristics of pulmonary hypertension in preterm neonates

et al. 2007

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“…In fetal lambs in the third trimester of pregnancy, pulmonary blood flow did not change relative to lung weight and right ventricular output at the normal low oxygen tension of the fetus despite an increase in pulmonary vessel density. 27,28 In near-term fetuses, pulmonary blood flow was 35 to 40 mL · min Ϫ1 · kg Ϫ1 fetal weight. 27 It has been demonstrated in animal experiments that volumetric blood flow through the aortic and pulmonary valves can be accurately determined through sonographic measurements of vessel diameter and the time-velocity integral.…”

Section: Discussionmentioning

confidence: 99%

“…27,28 In near-term fetuses, pulmonary blood flow was 35 to 40 mL · min Ϫ1 · kg Ϫ1 fetal weight. 27 It has been demonstrated in animal experiments that volumetric blood flow through the aortic and pulmonary valves can be accurately determined through sonographic measurements of vessel diameter and the time-velocity integral. 8 However, previous Doppler studies in human fetuses have resulted in conflicting data concerning fetal cardiac …”

Section: Discussionmentioning

confidence: 99%

Cardiac Output and Central Distribution of Blood Flow in the Human Fetus

2001

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Background-The objectives of this study were to establish reference ranges for left and right cardiac output and to investigate blood flow distribution through the foramen ovale, ductus arteriosus, and pulmonary bed in human fetuses. Methods and Results-A prospective study was performed in 222 normal fetuses from 13 to 41 weeks of gestation with high-resolution color Doppler ultrasound. Cardiac output and ductal flow were calculated by use of vessel diameter and the time-velocity integral. Pulmonary blood flow was expressed as the difference between right cardiac output and ductal flow. Foramen ovale flow was estimated as the difference between pulmonary flow and left cardiac output. Gestational age-specific reference ranges are given for left, right, and biventricular output and volume of ductal blood flow, showing an exponential increase with gestational age. Median ratio of right to left cardiac output was 1.42 and was not associated with gestational age. Right cardiac output was 59% and left cardiac output was 41% of biventricular cardiac output. Median biventricular cardiac output was estimated to be 425 mL · min Ϫ1 · kg Ϫ1 fetal weight. Ductal blood flow was 46%, estimated pulmonary flow was 11%, and estimated foramen ovale flow was 33% of biventricular output. Conclusions-The study establishes reference ranges for fetal cardiac output and offers insights into the central blood flow distribution in human fetuses from 13 weeks to term. There is a clear right heart dominance. The estimated ratio of pulmonary blood flow to cardiac output is higher than in fetal lamb studies. (Circulation. 2001;103:1662-1668.)

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“…Inasmuch as high circulating levels of vasoconstrictors such as catecholamines a i d angiotens;n I1 are elevated and contribute to the increase in systemic vascular resistance at birth (17,18), EDRF could play a counterbalancing role in the pulmonary circulation. Attention is now turning to the relief of hypoxic pulmonary vasoconstriction as the principal process involved in the decrease in pulmonary vascular resistance at birth (19). The role of endothelial cell and EDRF production during hypoxia appears to be a new avenue for research (20).…”

Section: Discussionmentioning

confidence: 99%

Endothelium-Derived Relaxing Factor: Presence in Pulmonary and Systemic Arteries of the Newborn Guinea Pig

Davidson

Eldemerdash

1990

Pediatr Res

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ABSTRACT. Endothelium-derived relaxing factor (EDRF), believed to be nitric oxide or a compound that releases nitric oxide, is a potent vasodilator produced by some arteries in response to acetylcholine (ACh) and bradykinin (BK). ACh and BK are potent dilators of perinatal pulmonary and systemic arteries. The objectives of this study were to determine if EDRF is present in newborn vessels and if EDRF mediates the vasodilator actions of ACh and BK. Arterial rings from newborn guinea pigs, 1 to 3 d old, were obtained from a branch of the main pulmonary artery and the descending aorta for isometric force bioassays. At their optimal resting tension, the rings were preconstricted with phenylephrine lo-' M in KrebsHenseleit solution before adding incremental doses of ACh or BK. If the endothelium was intact, ACh (lo-' M) relaxed pulmonary arteries and aortas (64 f 7%, 72 f 9% relaxation, respectively, mean f SE). ACh-induced relaxation (ACh lo-' M) in the pulmonary artery and aorta, respectively, was significantly (p < 0.05) attenuated by 1 ) endothelial removal (11 f 9%, 28 f 10%) by rubbing the ring lumen; 2) methylene blue, 10" M, (6 f 8%, 7 f 3%) that inhibits EDRF-associated cGMP production in smooth muscle; and 3) methemoglobin, lo-' M, (13 f 9%, 17 f 7%) that binds EDRF. The results for BK were similar to ACh for the pulmonary artery but BK did not relax the aorta. Indomethacin diminished relaxation of the pulmonary artery and aorta to the submaximal dose (lo-' M) of ACh but indomethacin did not effect the relaxation to ACh lo4 M or BK. We conclude that EDRF is produced in the guinea pig pulmonary artery and descending aorta at birth and that EDRF is a mediator of the vasodilator actions of ACh and BK. Vasodilation by ACh may also involve activation of the cyclooxygenase pathway. (Pediatr Res 27: 128-132,1990) Abbreviations EDRF, endothelium-derived relaxing factor ACh, acetylcholine BK, bradykinin EDRF, now believed to be nitric oxide or a compound that releases nitric oxide, was discovered in 1980 when acetycholine was found to relax preconstricted rabbit artery strips in vitro only if the luminal endothelial cell lining was intact (1). Subsequently, EDRF has been identified by bioassay techniques in pulmonary and systemic arteries of many mammalian species and substances other than ACh (e.g. BK and calcium ionophore) have been shown to stimulate EDRF production. Based on a rapidly expanding body of work (2) that followed the discovery of EDRF, certain bioassay criteria have evolved for attributing vasodilatation to EDRF. These include inhibition of vascular relaxation: 1 ) after removal of or injury to luminal endothelium of the blood vessel (1); 2) by pretreatment with methylene blue that inhibits the increase in cGMP in smooth muscle cells associated with EDRF production (3); and 3) by pretreatment with methemoglobin or Hb that binds EDRF (4).EDRF has not previously been described in pulmonary and systemic blood vessels at birth. It is known that ACh (5) and BK are potent dilators of the perinatal pulm...

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Development of pulmonary vascular response to oxygen

Cited by 83 publications

References 0 publications

Characteristics of pulmonary hypertension in preterm neonates

Characteristics of pulmonary hypertension in preterm neonates

Cardiac Output and Central Distribution of Blood Flow in the Human Fetus

Endothelium-Derived Relaxing Factor: Presence in Pulmonary and Systemic Arteries of the Newborn Guinea Pig

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