Development of pulmonary vascular response to oxygen

1988 ◽  
Vol 254 (3) ◽  
pp. H542-H546 ◽  
Author(s):  
F. C. Morin ◽  
E. A. Egan ◽  
W. Ferguson ◽  
C. E. Lundgren

The ability of the pulmonary circulation of the fetal lamb to respond to a rise in oxygen tension was studied from 94 to 146 days of gestation. The unanesthetized ewe breathed room air at normal atmospheric pressure, followed by 100% oxygen at three atmospheres absolute pressure in a hyperbaric chamber. In eleven near-term lambs (132 to 146 days of gestation), fetal arterial oxygen tension (PaO2) increased from 25 +/- 1 to 55 +/- 6 Torr (mean +/- SE), which increased the proportion of right ventricular output distributed to the fetal lungs from 8 +/- 1 to 59 +/- 5%. In five very immature lambs (94 to 101 days of gestation), fetal PaO2 increased from 27 +/- 1 to 174 +/- 70 Torr, but the proportion of right ventricular output distributed to the lung did not change, 8 +/- 1 to 9 +/- 1%. In five of the near-term lambs, pulmonary blood flow was measured. It increased from 34 +/- 3 to 298 +/- 35 ml.kg fetal wt-1.min-1, an 8.8-fold increase. We conclude that the pulmonary circulation of the fetal lamb does not respond to an increase in oxygen tension before 101 days of gestation; however, near term an increase in oxygen tension alone can induce the entire increase in pulmonary blood flow that normally occurs after the onset of breathing at birth.

1993 ◽  
Vol 265 (1) ◽  
pp. H376-H380 ◽  
Author(s):  
M. H. Tiktinsky ◽  
F. C. Morin

We examined the role of endothelium-derived relaxing factor (EDRF) in the increase in pulmonary blood flow caused by increasing oxygen tension in the lungs of the fetus. Fetal lambs at 133 days of gestation were instrumented for intrauterine measurement of pulmonary arterial, left atrial, and amniotic fluid pressure and pulmonary blood flow. Three days later oxygen tension in the pulmonary arterial blood of the fetus was doubled by having the ewe breathe 100% oxygen at 3 atm absolute pressure. In the control fetuses (n = 5), hyperbaric oxygenation increased pulmonary blood flow eightfold. Blocking EDRF production by infusing 45 mg of NG-monomethyl-L-arginine into the superior vena cava of the fetus over 5 min starting 30 min after the beginning of hyperbaric oxygen reversed the increase in pulmonary blood flow (n = 5). Blocking EDRF production by infusing NG-nitro-L-arginine at 1 mg/min for 60 min starting 30 min before hyperbaric oxygen blunted the initial increase in pulmonary blood flow and eliminated it by the end of the experiment (n = 5). As hyperbaric oxygen did not significantly alter pulmonary arterial or left atrial pressure, changes in pulmonary vascular conductance paralleled those in pulmonary blood flow. We conclude that the majority of the vasodilation of the fetal pulmonary circulation caused by increasing oxygen tension is mediated by EDRF. We speculate that EDRF is involved in maintaining low vascular tone at the relatively high oxygen tension of the postnatal lung.


Children ◽  
2020 ◽  
Vol 7 (9) ◽  
pp. 137
Author(s):  
Amy Lesneski ◽  
Morgan Hardie ◽  
William Ferrier ◽  
Satyan Lakshminrusimha ◽  
Payam Vali

Background: The aim was to evaluate the relationship between the direction of the patent ductus arteriosus (PDA) shunt and the pre- and postductal gradient for arterial blood gas (ABG) parameters in a lamb model of meconium aspiration syndrome (MAS) with persistent pulmonary hypertension of the newborn (PPHN). Methods: PPHN was induced by intermittent umbilical cord occlusion and the aspiration of meconium through the tracheal tube. After delivery, 13 lambs were ventilated and simultaneous 129 pairs of pre- and postductal ABG were drawn (right carotid and umbilical artery, respectively) while recording the PDA and the carotid and pulmonary blood flow. Results: Meconium aspiration resulted in hypoxemia. The bidirectional ductal shunt had a lower postductal partial arterial oxygen tension ([PaO2] with lower PaO2/FiO2 ratio—97 ± 36 vs. 130 ± 65 mmHg) and left pulmonary flow (81 ± 52 vs. 133 ± 82 mL/kg/min). However, 56% of the samples with a bidirectional shunt had a pre- and postductal saturation gradient of < 3%. Conclusions: The presence of a bidirectional ductal shunt is associated with hypoxemia and low pulmonary blood flow. The absence of a pre- and postductal saturation difference is frequently observed with bidirectional right-to-left shunting through the PDA, and does not exclude a diagnosis of PPHN in this model.


Circulation ◽  
1992 ◽  
Vol 85 (2) ◽  
pp. 828-838 ◽  
Author(s):  
B A Cason ◽  
J A Wisneski ◽  
R A Neese ◽  
W C Stanley ◽  
R F Hickey ◽  
...  

1989 ◽  
Vol 17 (12) ◽  
pp. 1328-1332 ◽  
Author(s):  
WILLIAM F. RUTHERFORD ◽  
EDWARD A. PANACEK ◽  
J. KEYEN GRIFFITH ◽  
JEFFREY A. GREEN ◽  
MARK MUNGER ◽  
...  

1992 ◽  
Vol 262 (2) ◽  
pp. H406-H410 ◽  
Author(s):  
M. H. Tiktinsky ◽  
J. J. Cummings ◽  
F. C. Morin

In vitro, acetylcholine causes vasodilation by releasing endothelium-derived relaxing factor (EDRF) from endothelial cells. EDRF may be nitric oxide, derived from the amino acid L-arginine (L-Arg), by a process that is inhibited by NG-monomethyl-L-arginine (L-NMMA) and restored by L-Arg. We studied the effect of L-NMMA and L-Arg on the increase in pulmonary blood flow caused by acetylcholine in unanesthetized intrauterine near-term fetal lambs. Three protocols were employed. In each protocol, acetylcholine (0.48 +/- 0.15 micrograms/kg) was injected at 15-min intervals for 120 min. In the control protocol, nothing else was given. In the second protocol, L-NMMA (14 +/- 5 mg/kg) was given at 35 min. In the third protocol, L-NMMA was given at 35 min followed by L-Arg (138 +/- 73 mg/kg) at 80 min. In the control protocol, acetylcholine increased pulmonary blood flow 179 +/- 17% while it decreased pulmonary arterial pressure 15 +/- 1% and did not affect left atrial pressure. The response to each injection lasted less than 1 min and did not change throughout the experiment. L-NMMA completely blocked, whereas L-Arg completely restored, the effect of acetylcholine on pulmonary blood flow. We conclude that acetylcholine increases pulmonary blood flow in the fetal lamb via the release of EDRF derived from L-Arg. We speculate that endothelium-dependent vasodilation may play a role in the increase in pulmonary blood flow at birth.


Neonatology ◽  
1980 ◽  
Vol 38 (1-2) ◽  
pp. 49-60 ◽  
Author(s):  
J.G. Aarnoudse ◽  
B. Oeseburg ◽  
G. Kwant ◽  
H.J. Huisjes ◽  
W.G. Zijlstra

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