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By Nicholas S. Assali (Eds.)

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M a y also play a role. These anatomic characteristics of the fetal circulation dampen the increase or decrease in the systemic vascular resistance necessary to increase or decrease the arterial pressure in response to a variety of stimuli. 2 m g / k g of endotoxin into the mother produces a marked fall in t h e arterial pressure and cardiac output. I n the fetus, the injection of 1 m g / k g produces a minor fall in the systemic arterial pressure. T h e same occurs with hemorrhage. T h e withdrawal of 2 0 % of the maternal blood volume elicits hypovolemic shock in the mother.

These communications are in the form of multiple hemangiomata, hemangioendotheliomata, or hemangioepitheliomata. M u l tiple enlarging cutaneous hemangiomata m a y be associated with hepatic angiomata resulting in hepatomegaly and heart failure. Congeni- 1. DISORDERS OF CIRCULATION 31 tal communications between the hepatic artery and ductus venosus have also been reported (112). Arteriovenous fistulae have been described in peripheral vessels, including communications between the left subclavian artery and innominate vein (187) and left internal m a m m a r y artery and portal vein (70).

I t is well established now t h a t during strong uterine contractions, a transitory fetal bradycardia m a y appear (for more information on this subject, see Chapter 3, Vol. I ) . T h e bradycardia caused by uterine contraction m a y be due to (1) compression of the fetal head by the contracting u t e r u s ; (2) compression of the umbilical cord, particularly the umbilical veins by the contracting u t e r u s ; (3) decreased uterine blood flow and oxygen transfer subsequent to increased i n t r a m u r a l resistance; (4) increased pressure in t h e intervillous space with altered hemodynamics on both the m a t e r n a l and fetal sides; and (5) a combination of several of these factors.

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