Intrapulmonary Venous Admixture in the Respiratory Distress Syndrome

Murdock, A. I.; Kidd, Brent; Llewellyn, M; Reid, M; Swyer, Paul R.

doi:10.1159/000240204

Cited by 21 publications

(8 citation statements)

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“…The presence of right-to-left shunting of blood in association with neonatal RDS is well documented (22)(23)(24)(25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35). Several investigators have suggested that the right-to-left shunting in infants with RDS occurs predominantly within the lungs (29,46,47).…”

Section: Discussionmentioning

confidence: 99%

“…Several investigators have suggested that the right-to-left shunting in infants with RDS occurs predominantly within the lungs (29,46,47). What remains unclear is whether human premature infants have a reactive pulmonary vascular bed that can respond to nitric oxide inhalation.…”

Section: Discussionmentioning

confidence: 99%

“…They suggested that large right-to-left shunts predict an early death of infants with RDS. RDS is also complicated by intrapulmonary shunting of blood (28)(29)(30)(31)(32)(33)(34)(35). Regional atelectasis and hyaline membrane formations probably contribute greatly to the pathophysiology of the intrapulmonary shunting associated with RDS.…”

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confidence: 99%

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The Effects of Nitric Oxide Inhalation on the Pulmonary Circulation of Preterm Lambs

1995

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This study was designed to test the hypothesis that inhalation of nitric oxide by lambs delivered prematurely would result in increased systemic arterial blood oxygen tension and decreased pulmonary vascular resistance. Eleven premature fetal lambs were delivered by cesarean section at 126-127 d gestation. One hundred min after the onset of ventilation, nitric oxide gas was added to the lambs' breathing mixture. The animals were exposed in random order to 5 pprn for 10 min, 20 pprn for 10 min, and 20 pprn for 20 min. Each treatment period was preceded by and followed by a 10-min washout period. When compared with the washout (control) periods, all three treatment periods resulted in an improvement in both the systemic arterial blood oxygen tension and the physiologic intrapulmonary shunt. Inhalation of nitric oxide also resulted in a selective decrease in pulmonary arterial blood pressure. Comparisons between the different treatment groups revealed a further improvement in blood oxygenation and pulmonary hemodynamics when using the higher concentration of nitric oxide. Interestingly, the rise in arterial blood oxygenation continued after inhaling 20 pprn nitric oxide for more than 10 min. (Pediatr Res 37: [35][36][37][38][39][40] 1995) Abbreviations QsIQt, physiologic intrapulmonary shunt PAP, mean pulmonary arterial pressure ppm, parts per million RDS, respiratory distress syndrome SAP, mean systemic arterial pressure LAP, left atrial pressure RAP, right atrial pressure Qp, pulmonary blood flow PVR, pulmonary vascular resistance Pao,, arterial oxygen partial pressure Nitric oxide, an inorganic gas formed by combustion processes, has been recognized for many years as an industrial pollutant. In fact, cigarette smoke contains nitric oxide gas in concentrations up to 1000 pprn (1). In both dogs (2, 3) and humans (4-6), inhalation of concentrations of more than 15 000 pprn rapidly causes a fatal condition involving severe alveolar edema, methemoglobinemia, and hypoxemia. Ironically, inhalation of concentrations less than 100 pprn has been used in an attempt to facilitate the management of several cardiopulmonary diseases such as persistent pulmonary hypertension of the newborn (7,8), primary pulmonary hypertension (9, lo), and adult RDS (11).Treatment of pulmonary hypertension with i.v. administered vasodilator agents has been limited because of the inability to localize the effects of these drugs to the pulmonary circulation. Nitric oxide gas seems to be an ideal drug to obviate this problem. Experience in animals (12-16) and humans (9,17) Received March 18, 1994; accepted June 5, 1994. Supported by grants from the American Heart Association, Florida Affiliate (AHA Awards 93CRFl6, 92Fl2, and 91GIAn16), and the National Institute of Health Grant HL10834.suggests that inhaled nitric oxide can cause a decrease in PVR without causing significant systemic hypotension. The mechanisms of this selective pulmonary vasodilation are not entirely understood; however, the short half-life of nitric oxide (18,19) and its rapi...

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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The Effects of Nitric Oxide Inhalation on the Pulmonary Circulation of Preterm Lambs

1995

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“…Shunting, which is the principal cause of hypoxaemia during the acute phase of hyaline membrane disease, is thought to occur 4 mainly because interference with pulmonary gas exchange and atelectasis cause constriction of pulmonary blood vessels and an increase in pulmonary vascular resistance: as Pao2 falls and pulmonary vascular resistance rises the foramen ovale and ductus arteriosus reopen and blood passes from the right side of the heart to the aorta without traversing the lungs (Cook et al, 1963;Reynolds and Strang, 1966;Strang, 1966). Intrapulmonary shunts, in which blood flows past atelectatic air-spaces, may also be present (Wallgren et al, 1967;Murdock et al, 1970). The increasing PaO2 and decreasing right-to-left shunt found in this investigation caused by increasing the I : E ratio can be ascribed to the release of pulmonary vasoconstrictor tone, to the mechanical effects of alveolar inflation in dilating pulmonary blood vessels (Howell et al, 1961;Cassin et al, 1964), and to the oxygenation of blood passing through intrapulmonary shunts.…”

Section: Resultsmentioning

confidence: 99%

Effect of Alterations in Mechanical Ventilator Settings on Pulmonary Gas Exchange in Hyaline Membrane Disease

Reynolds¹

1971

Archives of Disease in Childhood

144

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“…On any one day the samples were all drawn from the same site so that a change in arterial oxygen saturation due to a patent ductus arteriosus within one day's profile was taken into account. It has been shown that a patent ductus arteriosus may account for roughly one-tenth of the total cardiopulmonary shunt seen in respiratory distress syndrome (Murdock et al, 1970), although it has recently been suggested that the standard shunt equation may underestimate large ductal shunts (Gersony et al, 1972).…”

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confidence: 99%