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J V Aranda

Publications and source records attributed to J V Aranda.

126 records · Page 7Linked to original sources
PubMed1976

NADPH-dependent lipid peroxidation and its effects on aminopyrine N-demethylation in subcellular fractions of human neonatal liver.

NADPH-dependent lipid peroxidation was determined in humans, using subcellular fractions of livers obtained from newborn infants. As reported for other species, activity was concentrated in the microsomal fraction and was similar to that found in the rat. High activity of lipid peroxidation induced by iron decreased aminopyrine N-demethylation and slightly reduced linearity time for the reaction. Compared with the rat, however, human microsomes were more resistant to the effects of lipid peroxidation. If liped peroxidation occurs in vivo it is unlikely to affect drug oxidation to any great degree in human infants.

Aminopyrine N-Demethylase↗
PubMed1975

Alterations of hepatic microsomal drug metabolism by glucagon.

The effect of glucagon on the components of the hepatic microsomal electron transport chain (NADPH oxidase, NADPH cytochrome c reductase (EC 1.6.2.4), cytochrome P-450, and NADPH cytochrome P-450 reductase), and on two representative oxidative pathways (aminopyrine N-demethylation, a type I substrate oxidation; and aniline p-hydroxylation, a type II substrate oxidation) was determined. Microsomes from rats pretreated with glucagon (300 mug/kg per day for 3 days) showed a significant decrease in NADPH oxidation and in aminopyrine N-demethylation with a prolonged hexobarbital sleeping time, and a significant increase in aniline p-hydroxylation. Microsomes from rats pretreated with a lower dose of glucagon (30 mug/kg per day for 3 days) showed a significant decrease in the microsomal N-demethylation of aminopyrine. Glucagon had no effect when added in vitro to microsomes, suggesting that the in vivo effects of glucagon are mediated indirectly in the intact animal.

Aminopyrine N-Demethylase↗
PubMed1974

Hepatic microsomal drug oxidation and electron transport in newborn infants.

Many drugs require oxidative metabolism for termination of action and/or for elimination from the body. Many oxidative reactions are catalyzed by hepatic microsomal enzymes. The activities of various drug-metabolizing enzymes, namely, NADPH cytochrome c reductase, NADPH oxidase, aminopyrine-N-demethylase, and analine P-hydroxylase, and the content of cytochrome P-450, were measured in hepatic microsomes obtained from seven newborn infants and four adult patients. The results in the newborn infant show increasing activities of these enzymes (except aminopyrine-N-demethylase) related to advancing age. Good correlation between three components of the hepatic microsomal mixed function oxidase system and aniline p-hydroxylase was established, whereas only NADPH oxidation correlated with aminopyrine N-demethylation. The rate of substrate or drug oxidation and the activities of the components of the microsomal electron transport pathway were lower than comparable values in the adult. The data demonstrate a possible biochemical basis for the transient deficiency in drug metabolism seen in newborn infants.

Adult↗
PubMedDate not supplied

Protein binding and bilirubin displacing properties of bumetanide and furosemide.

We evaluated the protein binding and comparative bilirubin displacing properties of bumetanide and furosemide in pooled adult and cord serum by ultrafiltration (UF), difference spectra (DS), and Sephadex Gel-25 (SG-25) filtration. By UF, bumetanide was found to be highly protein bound (96.7 per cent), similar to published data on furosemide (97.2 per cent). SG-25 filtration and DS showed an equal shift to the left of the free bilirubin curve when bumetanide and furosemide were added to serum, in adult and cord, at equimolar concentrations and both shifted the free bilirubin curve equally. Bilirubin displacement was greater (P less than 0.001) in cord than in adult serum with both drugs. When "presumed therapeutic" plasma concentration of furosemide (1-2 mg/liter) and bumetanide (0.5 mg/liter) were compared, it was noted that bumetanide displaced significantly less (P less than 0.001) bilirubin from albumin in cord blood than furosemide. Hence, bumetanide displaces less bilirubin at "presumed therapeutic" plasma concentrations than furosemide, suggesting that it might be more prudent to use bumetanide in sick neonates with hyperbilirubinemia. Data also provide evidence that bilirubin displacement by both diuretics is greater in neonatal serum albumin than in the adult.

Adult↗
PubMedDate not supplied

The role of prostanoids in neonatal cerebral blood flow autoregulation.

The regulatory role of prostanoids in acute cerebrovascular adaptations in newborns was determined using awake neonatal piglets (ages 0-5 days, n = 60). Cerebral blood flow (CBF) was measured by radiolabelled microspheres before and 45 s after intracarotid injections of PGE1 (0.1-10 micrograms/kg, n = 6), PGE2 (0.01-2 micrograms/kg, n = 6), PGF2 alpha (0.01 microgram/kg, n = 8) and PGI2 (0.1 microgram/kg, n = 6). CBF increased with PGE1 (10 micrograms/kg) by 39.5% and with all doses of PGE2 (p < 0.01) compared to zero dose. PGF2 alpha, a known adult vasoconstrictor increased total CBF from 97 +/- 8 to 130 +/- 14 ml/min per kg. PGI2 also increased CBF by 27% (p < 0.01). When CBF and prostanoid levels were measured with balloon catheters placed at the aortic root and the descending aorta and were inflated to adjust arterial blood pressure (BP) from 17 to 117 mmHg, sagittal sinus concentrations of prostanoids inversely correlated with total CBF (for PGs, tau = -0.52 to -0.66, p < 0.001; for TXB2, tau = -0.91 to 0.99, p < 0.0001). During hypotension (MABP < 50 mmHg) PGE, PGF2(2)alpha, 6-keto-PGF1 alpha and TXB2 increased by 311 +/- 56, 330 +/- 50, 301 +/- 44 and 658 +/- 44%, respectively. Net cerebrovascular production [total CBF x (sagittal sinus-arterial plasma prostanoid concentration)] of PGE, PGF2 alpha, and 6-keto-PGF1 alpha and TXB2 increased during hypotension compared to normotension (BP = 50-90 mmHg). At MABP = 91-117 mmHg, net production of prostanoids increased by 142-31%.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Comparative efficacy of exosurf and survanta surfactants on early clinical course of respiratory distress syndrome and complications of prematurity.

OBJECTIVES: To determine the comparative efficacy of Exosurf Neonatal and Survanta surfactants on the early course of respiratory distress syndrome (RDS), arterial blood gases, ventilatory support, outcome morbidity rate, and complications of prematurity and RDS. STUDY DESIGN: Medical records from 203 premature newborn infants undergoing mechanical ventilation for respiratory distress syndrome, and who received up to four rescue doses of either Exosurf or Survanta, were retrospectively reviewed. RESULTS: All groups were comparable for birth weight and gestational age. Although the two randomized groups were similar in severity of RDS based on fraction of inspired oxygen (FIO2) and ventilatory support, a significantly greater improvement in respiratory function as evidenced by FIO2, mean airway pressure, alveolar-arterial partial pressure of oxygen difference, and oxygen index, was observed in the Survanta group from 12 hours (p < 0.05) through 48 hours (p < 0.01). Comparison of outcome morbidity rate by gestational age showed a higher occurrence of retinopathy of prematurity (p < 0.02) among the older infants (28 to 32 weeks) who were treated with Exosurf. CONCLUSION: Survanta exerted a significantly faster response in the early clinical course of RDS compared with Exosurf. However, no difference in the impact on eventual respiratory outcome was observed. We therefore conclude that both surfactants are effective for the treatment of RDS.

Biological Products↗