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Biomedical subjects

L M Gartner

Publications and source records attributed to L M Gartner.

At least 55 records · Page 3Linked to original sources
PubMed1978

Measurement of bilirubin-albumin binding. I. Comparative analysis of four methods and four human serum albumin preparations.

Four methods for the measurement of bilirubin-albumin binding have been compared. Three of these, the fluorescent dye binding (Direct Yellow 7), Sephadex G-25 column chromatography, and the 2-(4-hydroxyazobenzene)benzoic acid (HBABA) dye binding methods demonstrate significant correlations of measured binding capacities for bilirubin over a range of bilirubin/albumin molar ratios. All three methods concurred in the demonstration that fresh adult human sera had a higher molar albumin binding capacity for bilirubin than the purified human serum albumin preparations. The fluorescent dye binding and Sephadex column methods agreed most closely in defining presumed deficiency in binding capacity. The HBABA dye binding method was less consistent and appeared to measure non-bilirubin binding sites on albumin in addition to bilirubin binding sites. The fourth method, the saturation index, yielded highly variable results as compared with the other methods because of an inherent excessive risk of laboratory error.

Adult↗
PubMed1977

The narcotic-dependent mother: fetal and neonatal consequences.

During the years 1971--1974, 230 infants born to drug-dependent women and 33 infants born to ex-addicts were studied. Heroin abuse declined while methadone usage increased during those years. Compared to heroin abuse, methadone maintenance treatment during pregnancy was associated with more consistent prenatal care, more normal fetal growth and reduced fetal mortality. Meconium staining of amniotic fluid was increased in the heroin and heroin-methadone groups; this was not associated, however, with an increase in meconium aspiration or a reduction in Apgar scores. Of special note was the equally severe intrauterine growth retardation of infants of former heroin addicts who were free of narcotic use during pregnancy. Neonatal withdrawal from methadone appeared to be more severe than from heroin, as judged by amount of medication required to control symptoms and duration of treatment. In all groups, central nervous system signs were the most common manifestations of withdrawal. Severity of withdrawal did not correlate with late pregnancy maternal methadone dosage. Neonatal seizures occurred in 1.5% of the heroin group and 10% of the methadone group. Discharge of an infant to a parent rather than to an alternate care-taker was more likely if the mother was enrolled in a methadone treatment program. Methadone maintenance programs appear to offer significant therapeutic benefits, balancing the untoward effects of the drug on the newborn infant.

Adult↗
PubMed1977

Development of bilirubin transport and metabolism in the newborn rhesus monkey.

Hepatic transport and metabolism of bilirubin have been examined in term, premature, and postmature newborn Macaca mulatta (rhesus) monkeys with and without prior phenobarbital treatment of pregnant mother and neonate. In untreated neonates a biphasic pattern of physiologic unconjugated hyperbilirubinemia has been observed. Phase I was characterized by a rapid increase in serum bilirubin concentration to 4.5 mg/dl by 19 hours and an equally rapid decline to 1.0 mg/dl by 48 hours of age. Phase II was characterized by a stable elevation at 1.0 mg/dl (four times greater than in the adult) from 48 to 96 hourse of age, followed by a decline to normal adult concentrations thereafter. An identical pattern was observed in 29 normal, term human neonates, but the duration of each phase was approximately three times as long as that in the monkey. Phase I hyperbilirubinemia appears to result from a sixfold increase in bilirubin load presented to the liver in the neonatal period, combined with marked deficieny in hepatic bilirubin conjugation, the rate-limiting step during Phase I. Hepatic uptake of bilirubin is not rate limiting during Phase I but may contribute to Phase II hyperbilirubinemia. An increased bilirubin load persists throughout the first 19 days of life in the monkey. Phase I physiologic jaundice in the monkey neonate was completely eliminated by prenatal maternal and neonatal administration of phenobarbital. A threefold enhancement of hepatic conjugation of bilirubin (glucuronyl transferase activity) during Phase I entirely accounted for the prevention of hyperbilirubinemia. The bilirubin load was unaffected by administration of phenobarbital. Whereas in control neonates the bilirubin load slightly exceeded hepatic bilirubin conjugating capacity and resulted in retention of bilirubin, in phenobarbital-treated neonates, hepatic conjugating capacity slightly exceeded that required for the bilirubin load. Administration of phenobarbital failed to alter Phase II hyperbilirubinemia and did not enhance either maximal hepatic uptake or excretion of bilirubin. Hepatic glucuronly transferase activity was increased threefold during Phase II and during the remainder of the neonatal period. Premature birth retarded maturation of hepatic glucuronyl transferase activity. In one phenobarbital-treated premature monkey neonate, there was no apparent response to treatment. Accelerated maturation of bilirubin uptake, conjugation, and excretion of bilirubin was observed in one postmature monkey neonate.

Animals↗
PubMed1977

Unconjugated hyperbilirubinemia in very low birth weight infants.

In very low birth weight infants, the occurrence of bilirubin-related brain damage has been repeatedly observed at low serum bilirubin concentrations in close association with altered pathophysiologic status (hypoxia, acidosis, hypothermia, and so on). This increased susceptibility is accompanied by increased severity and duration of unconjugated hyperbilirubinemia as compared with more mature infants. Clinical manifestations of kernicterus in very low birth weight infants are almost always nonspecific. No single biochemical or physiologic measurement is sufficient to predict the risk for development of the bilirubin-related brain damage in this group. Prevention of bilirubin-related brain damage in very low birth weight infants requires not only the maintenance of physiologic and biochemical milieu within normal limits, but also specific therapy to alleviate unconjugated hyperbilirubinemia. Although exchange transfusion has been the mainstay of therapy for unconjugated hyperbilirubinemia, the increased morbidity and mortality associated with exchange transfusion in these immature infants and the need to maintain very low serum bilirubin concentrations suggest that prophylactic phototherapy may be more beneficial for this group.

Bilirubin↗
PubMed1977

Development of bilirubin metabolism and transport in the neonate.

Comprehensive physiologic study of the developmental processes of bilirubin metabolism and transport reveal a complex interaction of various steps. Phase I Physiologic Jaundice results from the simultaneous increase in bilirubin load presented to the liver and decrease in bilirubin conjugating capacity. Phase II appears to result from a mild decrease in hepatic uptake capacity, coupled with the continuing increase in bilirubin load. Since these results are based upon studies of newborn rhesus monkeys, confirmatory studies in human neonates are required. Perhaps the most challenging aspect of these observations relates to the concept of a developmentally determined delicate imbalance between two functions. It is unlikely that pharmacologic agents could radically alter a single function. Therefore, it is perhaps more realistic to think that drug treatments which only slightly alter two functions simultaneously but in the appropriate directions could more effectively reduce the risk of toxicity. Thus, a mild increase in bilirubin conjugation coupled with a small but significant decrease in bilirubin load could markedly alleviate the severity of physiologic jaundice.

Bilirubin↗
PubMed1976

Determinants of the neonatal mortality.

A recent sharp decline in the neonatal mortality in our medical center prompted a critical analysis of viral statistics of the newborn service during the years 1966 through 1973. The mean neonatal mortality for the entire period was 15.4 per 1,000 live births, and 11.0 in the period 1972 through 1973. The annual neonatal mortalities bore a direct relationship to the annual incidences of infants with birth weights of 1,500 gm or less. The reduction in the proportion of infants in the latter weight group during 1972 through 1973 accounted for three quarters of the improvement in the neonatal mortality as compared to that of the previous years. One quarter of the improvement could be attributable to a decrease in mortality that occurred only in infants in the latter weight group during the same period.

Birth Weight↗
PubMed1976

Possible effect of maternal promethazine therapy on neonatal immunologic functions.

The effect of the administration of promethazine in the treatment of erythroblastosis fetalis was studied in four maternal-fetal pairs. The three infants exposed for a prolonged period of time had decreased neonatal number and function of T cells, and abnormal specific humoral immune responses. The possible role of promethazine in the induction of fetal immunoincompetence is discussed.

Antibodies↗
PubMed1976

Various bilirubin conjugates in pregnant and nonpregnant rats with and without phenobarbital treatment.

The relative participation of bilirubin conjugating systems other than uridine diphosphate glucuronic acid-dependent bilirubin glucuronyl transferase in 21-day pregnant (P) and nonpregnant (NP) rats with and without prior phenobarbital (PB) administration was studied. Relative enzyme activities of 74.5%, 17.6%, and 7.9% were observed for glucuronic acid, xylose, and glucose conjugates, respectively, in untreated NP rats. Pregnancy itself did not alter the relative activities. In response to PB administration, P rats increased activity less than NP animals for all three enzymes. The ratios of the three conjugates remained unchanged in both P and NP groups after PB stimulation.

Animals↗
PubMed1976

Spectrophotometric characteristics of bilirubin.

Spectrophotometric characteristics of bilirubin at low concentrations (0.005-2.500 mg/100 ml) have been studied under various physical conditions in order to gain a better understanding of the state of bilirubin when preparing "solutions" for laboratory use. Standing, minimal shaking, or stirring of the bilirubin preparations at pH 7.4 progressively reduced and altered the maximal spectral absorption of bilirubin (440 nm) in aqueous buffered media. The shift to 415-420 nm is attributed to oxidation of the pigment whereas shoulder formation is attributed to the formation of large size particles (flocculants). In the presence of antixidants (L-ascorbic acid and nitrogen gas) and EDTA the maximal absorption peak remained at 440 nm but decreased in magnitude concomitant with development of progressively increasing shoulder at 480-560 nm. In the absence of antioxidants and EDTA maximal absorption shifted to 415-420 nm and the magnitude of 480-560 nm shoulder formation was less. At the higher concentrations of bilirubin and with reduction in pH of the buffer in the absence of antioxidants, the shift to lower wave lengths was reduced and 450-560 nm shoulder formation was increased. In the absence of antioxidants and EDTA at the lower concentrations of bilirubin and in more alkaline media, the reduction at 440 nm and the shift of maximal absorption to the shorter wave lengths was enhanced. At pH 12, stirring of antioxidant-EDTA-containing solutions of bilirubin resulted in neither a shift of maximal absorption to the shorter wave lengths nor the formation of 480-560 nm shoulder. The formation of 480-560 nm shoulder was accompanied by the visual appearance of turbidity. The formation of flocculants when a "solution" is agitated indicates that significant portions of the pigment were in fact, not in solution and must have existed previously as a finely dispersed colloidal sol or supersaturated solution which progressed to a colloidal sol. Spectral curves of bilirubin, therefore, may represent a composite resulting from four physical states of bilirubin: (1) bilirubin truly in solution with the spectral peak at 440 nm; (2) bilirubin in the fine colloidal dispersion with spectral characteristics similar to those of bilirubin in solution; (3) bilirubin flocculant giving 480-560 nm shoulder; and (4) oxidation products of bilirubin with the spectral peaks lower than 440 nm. Increasing the pH of the aqueous media containing bilirubin (0.05 mg/100 ml) from 7.4 to 12.0 increased the molar extinction coefficient of bilirubin, E1M/440 1cm, progressively to a maximum at pH 12 of 6.35 X 10(4). Very dilute bilirubin preparations (0.005-0.050 mg/100 ml) in aqueous media, pH 7.4, exhibited spectral evidence of rapid oxidation (more so at higher pH), but spectral shoulder formation was still observed after mechanical agitation. Thus, the solubility of bilirubin in 0.1 M phosphate buffer at pH 7.4 appears to be less than 0.005 mg/100 ml.

Ascorbic Acid↗
PubMed1976

The effect of promethazine hydrochloride on bilirubin metabolism in the rat.

The effect of 21 days of promethazine-HC1 administration on hepatic bilirubin metabolism and transport was studied in adult rats. A significant increase in mean cumulative hepatic bilirubin uptake (84.5 +/- 7.6 (SE) mug/100 g/min in controls vs. 110.0 +/- 4.3 in treated rats), mean hepatic glucuronide conjugation (1,330 +/- 86 (SE) mug bilirubin conjugated/g liver/40 min in controls vs. 1.713 +/- 61 in treated rats), and mean maximal hepatic excretion (47.2 +/- 4.9 (SE) mug/100 g/min vs. 63.5 +/- 2.7) was observed in treated animals. Mean total liver weight and total hepatic protein also increased significantly. These observations suggest that promethazine is an inducer of protein and enzyme synthesis in rat liver and is capable of significantly stimulating the three major steps in hepatic disposal of bilirubin.

Animals↗
PubMed1976

Xylose, glucose, and glucuronic acid conjugation of bilirubin in the newborn rat.

The development and relative contribution of hepatic bilirubin conjugation with glucuronic acid, xylose, and glucose was studied in vitro in newborn rats 1-20 days old. In adult control rats, 75% of the conjugates formed were with glucuronic acid, whereas in 1-day-old newborns, only 50% of the conjugates were with glucuronic acid (P less than 0.02) while xylose and glucose conjugates of bilirubin together were equal to that of glucuronic acid. By day 4, total conjugating capacity increased to adult levels and a mature pattern of distribution. In response to phenobarbital treatment, xylose and glucose conjugation increased 4 days earlier than glucuronide conjugation and maximal induction occurred 8 days sooner for nonglucuronide conjugation than for glucuronide.

Age Factors↗