prostaglandin-d2 and Persistent-Fetal-Circulation-Syndrome

It is clear that prostaglandins and related compounds are important in the physiology and pathophysiology of the perinatal pulmonary circulation. This article focuses on what is known about prostaglandin-related compounds (PRC) in the pulmonary circulation of the developing and newly born mammal. Also included is a discussion of the effects of PRC on the ductus arteriosus and on the systemic circulation.

Topics: Animals; Animals, Newborn; Arachidonic Acids; Blood Pressure; Epoprostenol; Female; Fetus; Humans; Hydroxyeicosatetraenoic Acids; Hypertension, Pulmonary; Infant, Newborn; Lung; Persistent Fetal Circulation Syndrome; Pregnancy; Prostaglandin Antagonists; Prostaglandin D2; Prostaglandins; Prostaglandins D; Prostaglandins E; Prostaglandins F; Pulmonary Circulation; Sheep; SRS-A; Thromboxanes; Vascular Resistance; Vasoconstriction

This 15-year-old disease has been clearly described anatomically. Some understanding of possible in utero predisposing conditions has emerged from clinical and animal studies. However, we have very little understanding of the cellular processes that trigger and/or prolong the abnormal medial smooth muscle hypertrophy underlying the condition. Empiric observation has resulted in the development of hyperventilation as a fairly successful treatment modality, although the underlying mechanism of this salubrious effect is unknown. Drugs, a major focus of clinical and laboratory investigations, sometimes are marginally successful (and sometimes are utter failures). Translated into the neonatal intensive care unit, the disease is more frequently accurately diagnosed than in the past, but it remains frustratingly difficult to manage, and thus far is impossible to prevent. The research foundations laid in the past decade provide impetus for accelerated search into the fundamental cellular and biochemical derangements that cause persistent pulmonary hypertension. It is to be hoped that the next decade will yield major advances in both mechanistic understanding and in treatment.

Topics: Acetylcholine; Calcium; Catecholamines; Epoprostenol; Homeostasis; Humans; Hypertension, Pulmonary; Infant, Newborn; Muscle Contraction; Muscle, Smooth, Vascular; Nifedipine; Nitroglycerin; Nitroprusside; Oxygen; Persistent Fetal Circulation Syndrome; Prostaglandin D2; Prostaglandins D; Pulmonary Artery; Pulmonary Veins; Tolazoline; Verapamil

We studied the effects of prostaglandin D2 (PGD2) in six newborn infants, 1 to 2 days of age, who had persistent pulmonary hypertension syndrome and a PaO2 less than 75 torr during mechanical hyperventilation with an inspired oxygen concentration of 100%. Tolazoline and dopamine were used to treat some of the patients. No patients had congenital heart disease or sepsis. Catheters were placed to measure pulmonary and systemic arterial blood pressures. PGD2 was infused intravenously at doses of 1 to 25 micrograms/kg/min. Pulmonary and systemic arterial blood pressures, heart rate, and descending aortic blood gas values were measured before each dose change. Only two of six patients had a transient increase in PaO2. All had an increase in heart rate. Two of six patients had an increase in pulmonary arterial blood pressure. No deleterious effects occurred during the infusion. Four of six patients subsequently died. Although PGD2 is a specific pulmonary vasodilator in fetal and newborn animals, it did not lower pulmonary arterial blood pressure nor improve oxygenation in newborn infants with persistent pulmonary hypertension syndrome.

Topics: Blood Pressure; Heart Rate; Humans; Infant, Newborn; Persistent Fetal Circulation Syndrome; Prostaglandin D2; Prostaglandins D; Pulmonary Artery; Respiration, Artificial

Topics: Animals; Blood Pressure; Drug Industry; Female; Fetal Hypoxia; Humans; Infant, Newborn; Persistent Fetal Circulation Syndrome; Pregnancy; Prostaglandin D2; Prostaglandins; Prostaglandins D; Tolazoline