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Part of the book series: Nitric Oxide in Biology and Medicine ((NOBM,volume 1))

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Abstract

In fetal sheep close to term, pulmonary blood flow is approximately 35–40 ml/min/kg body weight (approximately 8%–10% of the total combined ventricular output), as measured by microsphere techniques in unanesthetized fetal sheep with indwelling catheters (Rudolph and Heymann 1970). The pulmonary arterial pressure is suprasystemic. The elevated vascular resistance to pulmonary blood flow in fetal lungs may be due to (a) arterioles that may have a very thick smooth muscle layer; (b) relative hypoxia in utero (normal PO2 in pulmonary arteries is 18–22 mmHg); (c) vessels that are extremely reactive to changes in pH, PO2, and PCO2; and (d) circulating vasoactive substances. Since the postnatal survival of the fetus depends on a very rapid and appropriate establishment of pulmonary blood flow and alveolar ventilation, a remarkable adaptation of the pulmonary circulation must occur with the initiation of respiration. The circulatory pattern must change toward the adult pattern, in which the ventricles work in series rather than in parallel, and the lungs become for the first time organs of gaseous exchange. During the transition from an in utero liquid-breathing fetus to an air-breathing newborn, pulmonary blood flow increases approximately fivefold when measured in the lamb or kid. The factors responsible for this change in pulmonary blood flow have been studied in detail (Tod and Cassin 1997).

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Cassin, S. (2000). Nitric Oxide and the Perinatal Pulmonary Circulation. In: Kadowitz, P.J., McNamara, D.B. (eds) Nitric Oxide and the Regulation of the Peripheral Circulation. Nitric Oxide in Biology and Medicine, vol 1. Birkhäuser, Boston, MA. https://doi.org/10.1007/978-1-4612-1326-0_12

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