Premium
Hemodynamic vulnerability to acute hypoxia in day 10.5–16.5 murine embryos
Author(s) -
Furukawa Seishi,
Tinney Joseph P.,
Tobita Kimimasa,
Keller Bradley B.
Publication year - 2007
Publication title -
journal of obstetrics and gynaecology research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.597
H-Index - 50
eISSN - 1447-0756
pISSN - 1341-8076
DOI - 10.1111/j.1447-0756.2007.00499.x
Subject(s) - hypoxia (environmental) , medicine , gestation , bradycardia , heart rate , embryo , ventilation (architecture) , gestational age , hemodynamics , anesthesia , andrology , oxygenation , cardiology , blood pressure , pregnancy , biology , oxygen , chemistry , engineering , genetics , microbiology and biotechnology , mechanical engineering , organic chemistry
Aim: We tested the hypothesis that murine embryonic cardiovascular (CV) function is vulnerable to transient changes in maternal transplacental oxygen support during the critical period of CV morphogenesis. Methods: We measured maternal heart rate (MHR), maternal blood pressure (MBP), and embryonic heart rate (EHR) during mechanical ventilatory support, then induced transient maternal hypoxia daily from gestation day (ED) 10.5 to ED16.5 in pregnant ICR mice. Hypoxia was induced by suspending mechanical ventilation for 30 s or by the replacement of inspired oxygen with nitrogen (75% or 100%) for 30 s while maintaining ventilation. Results: We noted a rapid onset of maternal hypotension in response to hypoxia that quickly recovered following reoxygenation. Following a brief lag time that was not gestation specific, EHR decreased in response to hypoxia. The magnitude of embryo bradycardia and the rate of EHR decline and recovery displayed gestation specific patterns. The magnitude of embryo bradycardia was similar from ED10.5 to ED13.5 and then increased with gestation. Before ED13.5, only 40% of embryos recovered to the baseline EHR following transient maternal hypoxia (vs 80% of embryos after ED 13.5). EHR following recovery exceeded baseline EHR after ED15.5. Nitrogen inhalation (75% or 100%) produced changes in maternal and embryonic hemodynamics similar to suspended ventilation induced hypoxia. Conclusions: The mammalian embryo is vulnerable to transient decreases in maternal oxygenation during the critical period of organogenesis and the gestational specific EHR response to hypoxia may reflect both increased embryonic oxygen demand and the maturation of neurohumoral heart rate regulation.