Effects of Long-Term High-Altitude Hypoxia and Troponin I Phosphorylation on Cardiac Myofilament Calcium Responses in Fetal and Nonpregnant Sheep

2004 ◽  
Vol 11 (1) ◽  
pp. 1-8 ◽  
Author(s):  
Junji Onishi ◽  
Vaughn A. Browne ◽  
Satoshi Kono ◽  
Virginia M. Stiffel ◽  
Raymond D. Gilbert
Keyword(s):  
High Altitude ◽  
Troponin I ◽  
Altitude Hypoxia ◽  
High Altitude Hypoxia ◽  
Cardiac Myofilament

scholarly journals Long-Term High-Altitude Hypoxia and Alpha Adrenoceptor-Dependent Pulmonary Arterial Contractions in Fetal and Adult Sheep

2019 ◽  
Vol 10 ◽  
Author(s):  
Dafne Moretta ◽  
Demosthenes G. Papamatheakis ◽  
Daniel P. Morris ◽  
Paresh C. Giri ◽  
Quintin Blood ◽  
...  
Keyword(s):  
High Altitude ◽  
Altitude Hypoxia ◽  
Adult Sheep ◽  
Alpha Adrenoceptor ◽  
High Altitude Hypoxia ◽  
Pulmonary Arterial

Ca2+ Sensitivity of Fetal Coronary Arteries Exposed to Long-Term, High-Altitude Hypoxia

2000 ◽  
Vol 7 (3) ◽  
pp. 161-166 ◽  
Author(s):  
Felizabel C. Garcia ◽  
Virginia M. Stiffel ◽  
William J. Pearce ◽  
Lubo Zhang ◽  
Raymond D. Gilbert
Keyword(s):  
High Altitude ◽  
Coronary Arteries ◽  
Altitude Hypoxia ◽  
High Altitude Hypoxia

Effect of long-term high-altitude hypoxia on fetal pulmonary vascular contractility

2008 ◽  
Vol 104 (6) ◽  
pp. 1786-1792 ◽  
Author(s):  
Qin Xue ◽  
Charles A. Ducsay ◽  
Lawrence D. Longo ◽  
Lubo Zhang
Keyword(s):  
High Altitude ◽  
Pulmonary Arteries ◽  
Common Mechanism ◽  
Maximal Response ◽  
Pulmonary Vessel ◽  
Altitude Hypoxia ◽  
Protein Levels ◽  
High Altitude Hypoxia ◽  
Increased Risk

Hypoxia in the fetus and/or newborn is associated with an increased risk of pulmonary hypertension. The present study tested the hypothesis that long-term high-altitude hypoxemia differentially regulates contractility of fetal pulmonary arteries (PA) and veins (PV) mediated by differences in endothelial NO synthase (eNOS). PA and PV were isolated from near-term fetuses of pregnant ewes maintained at sea level (300 m) or high altitude of 3,801 m for 110 days (arterial Po2 of 60 Torr). Hypoxia had no effect on the medial wall thickness of pulmonary vessels and did not alter KCl-induced contractions. In PA, hypoxia significantly increased norepinephrine (NE)-induced contractions, which were not affected by eNOS inhibitor NG-nitro-l-arginine (l-NNA). In PV, hypoxia had no effect on NE-induced contractions in the absence of l-NNA. l-NNA significantly increased NE-induced contractions in both control and hypoxic PV. In the presence of l-NNA, NE-induced contractions of PV were significantly decreased in hypoxic lambs compared with normoxic animals. Acetylcholine caused relaxations of PV but not PA, and hypoxia significantly decreased both pD2 and the maximal response of acetylcholine-induced relaxation in PV. Additionally, hypoxia significantly decreased the maximal response of sodium nitroprusside-induced relaxations of both PA and PV. eNOS was detected in the endothelium of both PA and PV, and eNOS protein levels were significantly higher in PV than in PA in normoxic lambs. Hypoxia had no significant effect on eNOS levels in either PA or PV. The results demonstrate heterogeneity of fetal pulmonary arteries and veins in response to long-term high-altitude hypoxia and suggest a likely common mechanism downstream of NO in fetal pulmonary vessel response to chronic hypoxia in utero.

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