The effect of adenosine triphosphate on the functional status of the ductus arteriosus.
J Pediatr Surg
; 24(7): 649-53, 1989 Jul.
Article
em En
| MEDLINE
| ID: mdl-2754581
ABSTRACT
We investigated whether a low-dose infusion of ATP-MgCl2 could affect the functional status of the ductus arteriosus during hypoxia-induced pulmonary vasoconstriction. Three-day-old piglets were made hypoxic by ventilation with a mixture containing 10% oxygen, 4% CO2, and balance nitrogen. Serial infusions of ATP-MgCl2 at 0.1, 0.5, and 1.0 mg/kg/min were compared with preinfusion hypoxia baselines. The functional status of the ductus arteriosus was determined by change in transit time of a bolus of iced saline between thermistor probes in the pulmonary artery and aorta. The method was validated using a Blalock-Taussing shunt (subclavian to pulmonary artery) in 3-week-old piglets instrumented in a similar manner. In these three-day-old piglets, hypoxia alone produced a significant elevation in pulmonary artery pressure and reduction in PO2. All dose rates of ATP-MgCl2 produced a significant decrease in mean pulmonary artery pressure. Systemic pressure was significantly decreased only during the 1.0-mg/kg/min infusion. Transit times of a bolus of iced saline during the validation were definitive for characterizing a situation of "shunt open" or "shunt closed." Infusion of ATP-MgCl2 produced no change in the status of the ductus arteriosus in 45 (94%) of the determinations. In only three cases was the effect of ATP-MgCl2 sufficient to result in a functional change in the status of the ductus arteriosus. Pre- and postductal pulmonary artery PO2 were not altered during ATP-MgCl2 infusion, thus corroborating the transit time determinations. From these results, we conclude that an infusion of ATP-MgCl2 does not alter the functional status of the ductus arteriosus.
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Base de dados:
MEDLINE
Assunto principal:
Trifosfato de Adenosina
/
Canal Arterial
/
Hipertensão Pulmonar
/
Magnésio
Limite:
Animals
Idioma:
En
Ano de publicação:
1989
Tipo de documento:
Article