Failure to produce germinal matrix or intraventricular hemorrhage by hypoxia, hypo-, or hypervolemia.
Our study with midgestational sheep fetuses failed to support a cause-and-effect relation between marked hypoxia with or without hypo- or hypervolemia and rapid surges of blood pressure and the development of germinal matrix or intraventricular hemorrhage. Twenty-nine percent of fetuses exposed to marked hypoxia concomitantly with manipulations of their blood volume and blood pressure developed widespread cerebral necrosis. However, despite this marked anoxic-ischemic brain injury, none developed any germinal matrix or intraventricular hemorrhage. Rapidly and markedly elevating the blood pressure in these fetuses despite the presumed presence of an impaired autoregulation and a probable elevation of their central venous pressure also failed to cause germinal matrix or intraventricular hemorrhage. Marked hypoxia accompanied by reductions in blood pressure brought about by blood withdrawal produced an 80% delayed fetal mortality but not a single instance of germinal matrix or intraventricular hemorrhage.
D000818:Animals; D001794:Blood Pressure; D002552:Cerebral Ventricles / Q000098:blood supply*; D002560:Cerebrovascular Circulation; D005260:Female; D005313:Fetal Death; D005333:Fetus / Q000502:physiology; D006470:Hemorrhage / Q000209:etiology / Q000503:physiopathology*; D000860:Hypoxia / Q000503:physiopathology*; D010953:Plasma Volume; D011247:Pregnancy; D012756:Sheep