Adenosine is a pulmonary vasodilator in newborn lambs.

We investigated the systemic and pulmonary vascular effects of adenosine and determined plasma adenosine levels in pulmonary circulation in 12 newborn lambs during normoxia and during alveolar hypoxia (10% O2, 5% CO2, and 85% N2). Lambs were instrumented at 7 days of age with catheters in the descending aorta, main pulmonary artery, and right and left atria, and a flow transducer around the main pulmonary artery, and were studied following a 3-day recovery. Adenosine or an equal volume of normal saline (control) was infused into the right atrial line in doses ranging from 0.01 to 2.5 mumol/kg/min. In normoxic lambs, adenosine caused a significant decrease in pulmonary vascular resistance and increase in heart rate in doses of 0.15 to 2.5 mumol/kg/min and a decrease in systemic vascular resistance, with increase in cardiac output in doses of 0.3 to 2.5 mumol/kg/min. Baseline plasma adenosine levels in pulmonary artery and left atrium decreased significantly during alveolar hypoxia. Adenosine infusion in hypoxic lambs caused decreases in pulmonary artery pressure and pulmonary vascular resistance at all the doses tested. Aortic pressure and systemic vascular resistance decreased, and heart rate and cardiac output increased at doses greater than or equal to 0.3 mumol/kg/min in hypoxic lambs during adenosine infusion. The pulmonary vascular effects of adenosine in hypoxic lambs were attenuated by prior treatment of animals with aminophylline. Thus, adenosine appears to be an important regulator of pulmonary vascular response to hypoxia in newborn lambs. Its vasodilator effects were specific for pulmonary circulation when it was infused in doses less than or equal to 0.15 mumol/kg/min into the right atrium and appear to be mediated by P1 purinergic receptors.

Selective pulmonary vasodilation by low-dose infusion of adenosine triphosphate in newborn lambs.

The systemic and pulmonary vascular effects of adenosine 5'-triphosphate (ATP) were investigated in 12 newborn lambs during normoxia and during alveolar hypoxia (10% oxygen, 5% carbon dioxide, and 85% nitrogen). Lambs had catheters in the descending aorta, main pulmonary artery, and were studied after a 3-day recovery. We infused ATP or an equal volume of saline solution (control) into the right atrial line in doses ranging from 0.01 to 2.5 mumol/kg per minute. In normoxic lambs, ATP caused a significant decrease in pulmonary vascular resistance in doses of 0.08 to 2.5 mumol/kg per minute, and in systemic vascular resistance in doses of 0.3 to 2.5 mumol/kg per minute. Infusion of ATP in hypoxic lambs caused decreases in pulmonary artery pressure and pulmonary vascular resistance in all the doses tested. Systemic vascular resistance decreased, and cardiac output and heart rate increased in doses greater than 0.3 mumol/kg per minute in hypoxic lambs during ATP infusion. The effects of ATP in hypoxic lambs were not blocked by propranolol, indomethacin, or theophylline. Plasma ATP levels in left atrial blood samples did not change significantly during the infusion of ATP. We conclude that ATP is a vasodilator in lambs, and its effects are specific for pulmonary circulation at doses of less than or equal to 0.15 mumol/kg per minute. The vasodilator effects of ATP appear to be independent of P1 purinergic and beta-adrenergic mechanisms, and of prostacyclin synthesis.

Uniform chromatographic conditions for quantifying urinary catecholamines, metanephrines, vanillylmandelic acid, 5-hydroxyindoleacetic acid, by liquid chromatography, with electrochemical detection.

Uniform liquid-chromatographic conditions were developed such that we could quantify norepinephrine, epinephrine, normetanephrine, metanephrine, vanillylmandelic acid, and 5-hydroxyindoleacetic acid in urine by using a single mobile phase of monochloroacetic acid and citric acid, 0.1 mol/L each. All compounds were separated on a C18 column and detected electrochemically at a potential of +0.800 V. Optimization of these uniform chromatographic conditions significantly shortens the changeover time required from one assay to another, resulting in a substantial savings of time and cost to the laboratory.

Automated immunochemical method for determination of urinary protein of plasma origin.

An automated continuous-flow procedure has been developed for the rapid determination of urinary proteins of plasma origin. Antiserum to whole human plasma was used as the reagent, and the antigen-antibody reactions were quantitated by nephelometry. By adding polyethylene glycol (mol wt 6000-7500) to the reaction medium, reaction time was decreased to less than 3 min; no sample blanks were required; and samples were analyzed at a rate of 70 per hour. Recovery studies yielded an average of 98.5% of the added protein. In-run replicate precision (CV) of the method was 1.45%; day-to-day precision was 2.58%.