Effects of chronic hypoxia on fetal coronary responses.
This review examines the effect of high altitude and/or chronic hypoxia on cardiac mechanisms that influence perfusion of the fetal heart (e.g., tissue metabolism, coronary vessel growth, and coronary blood flow and vessel responsiveness). In response to intrauterine hypoxia, the fetal heart may either reduce its energy demand or increase its substrate and oxygen delivery as a means of sustaining cardiac function. Cardiac glycolysis predominates as a metabolic pathway of ATP synthesis in the fetal heart under both normoxic and hypoxic conditions. During prolonged oxygen insufficiency, normal cardiac function is sustained by anaerobic glycolysis relying primarily on high levels of stored glycogen in the heart. Chronic hypoxia increases coronary vessel growth and myocardial vascularization in fetal hearts, although the response may depend on the presence of ventricular hypertrophy. Recent studies demonstrate that high altitude hypoxia increases both resting fetal coronary flow and coronary flow reserve as an adaptive response toward increasing oxygen delivery. Hypoxia may also directly effect local vascular smooth muscle mechanisms, resulting in altered coronary artery reactivity to circulating vasoactive substances and contributing to enhanced perfusion. Further study is needed to understand the relative importance of each of these cardiac adaptations in contributing to fetal survival. It is likely that differences in fetal coronary responses to intrauterine hypoxia are highly dependent on the gestational age and relative maturity of the animal species.
Thompson
Loren P
LP
Department of Obstetrics, Gynecology, and Reproductive Sciences, University of Maryland School of Medicine, Baltimore, MD, USA. Ithompson1@umm.edu
D000222:Adaptation, Physiological / Q000502:physiology; D001783:Blood Flow Velocity / Q000502:physiology; D002908:Chronic Disease; D003326:Coronary Circulation / Q000502:physiology; D003331:Coronary Vessels / Q000196:embryology / Q000503:physiopathology; D004734:Energy Metabolism / Q000502:physiology; D006321:Heart / Q000196:embryology* / Q000503:physiopathology; D006801:Humans; D000860:Hypoxia / Q000196:embryology* / Q000503:physiopathology