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  • 1
    ISSN: 1432-1076
    Keywords: Term newborns ; Dyspnoea ; Volume expansion ; Bicarbonate
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Abstract In a prospective, randomised, open trial 103 term newborns with persisting dyspnoea, tachypnoea and/or cyanosis were treated with oxygen for 5–10 min and then with oxygen plus mask continuous positive airway pressure (CPAP) for another 5–15 min. Cases with overt prenatal or intrapartum obstetric pathology had been excluded from the study. Forty-one infants (40%) responded to this procedure within 10–25 min. The remaining 62 infants (60%) were randomly allocated to one of three forms of further treatment: continuation of mask CPAP for 20 min (group A,n=24), volume expansion with 9 ml of 3 ml albumin, 3 ml glucose, and 3 mEq of sodium bicarbonate (group B,n=24), or volume expansion with 4.5 ml albumin and 4.5 ml glucose (group C,n=14). There was no statistical difference in birth weight, gestational age or Apgar scores at 1 and 5 min between the infants of the groups. Time to normalisation of symptoms was significantly shorter in the volume expansion groups (B: 45±41 min, range 20–180, and C: 80±72 min, range 20–210) than in the mask CPAP group (A: 224±256 min, range 30–1200,P=0.02). There were statistical differences in umbilical cord and capillary pH values among the infants of the three groups, but the response to therapy was not related to the degree of acidaemia. Thirty-four infants (33%) who did not respond were admitted to a special care unit for further examination (group A: 21/24, group B: 7/24; group C: 6/14). Of these, 23 had no abnormal findings, 8 infants had radiological signs of transitory respiratory distress, and 1 had a nontension pneumothorax. Septicaemia was found in two infants. No infant was intubated. At discharge all 103 infants did well. Conclusion Incremental application of simple primary care procedures including volume expansion (with or without alkali) in term newborns with persisting postnatal tachypnoea and dyspnoea helps avoid overtreatment and unnecessary separation from the mothers in most cases and reliably selects infants who need close monitoring or special treatment.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-1076
    Keywords: Key words Term newborns ; Dyspnoea ; Volume expansion ; Bicarbonate
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In a prospective, randomised, open trial 103 term newborns with persisting dyspnoea, tachypnoea and/or cyanosis were treated with oxygen for 5–10 min and then with oxygen plus mask continuous positive airway pressure (CPAP) for another 5–15 min. Cases with overt prenatal or intrapartum obstetric pathology had been excluded from the study. Forty-one infants (40%) responded to this procedure within 10–25 min. The remaining 62 infants (60%) were randomly allocated to one of three forms of further treatment: continuation of mask CPAP for 20 min (group A, n = 24), volume expansion with 9 ml of 3 ml albumin, 3 ml glucose, and 3 mEq of sodium bicarbonate (group B, n = 24), or volume expansion with 4.5 ml albumin and 4.5 ml glucose (group C, n = 14). There was no statistical difference in birth weight, gestational age or Apgar scores at 1 and 5 min between the infants of the groups. Time to normalisation of symptoms was significantly shorter in the volume expansion groups (B: 45 ± 41 min, range 20–180, and C: 80 ± 72 min, range 20–210) than in the mask CPAP group (A: 224 ± 256 min, range 30–1200, P = 0.02). There were statistical differences in umbilical cord and capillary pH values among the infants of the three groups, but the response to therapy was not related to the degree of acidaemia. Thirty-four infants (33%) who did not respond were admitted to a special care unit for further examination (group A: 21/24, group B: 7/24; group C: 6/14). Of these, 23 had no abnormal findings, 8 infants had radiological signs of transitory respiratory distress, and 1 had a non-tension pneumothorax. Septicaemia was found in two infants. No infant was intubated. At discharge all 103 infants did well. Conclusion Incremental application of simple primary care procedures including volume expansion (with or without alkali) in term newborns with persisting postnatal tachypnoea and dyspnoea helps avoid overtreatment and unnecessary separation from the mothers in most cases and reliably selects infants who need close monitoring or special treatment.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 351 (1995), S. 229-236 
    ISSN: 1432-1912
    Keywords: Key words BIMU 8 ; BIMU 1 ; Renzapride ; 5-HT4 receptors ; Acetylcholine release ; Myenteric plexus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  The effects of the 5-HT4 receptor agonists BIMU 8, BIMU 1, renzapride and of the 5-HT1p receptor agonist 5-hydroxyindalpine on basal and electrically evoked outflow of tritium were studied in guinea-pig longitudinal muscle myenteric plexus preparations preincubated with [3H]choline. Muscle contractions were recorded simultaneously. BIMU 8 caused a calcium dependent and tetrodotoxin sensitive increase in basal [3H]outflow that was assumed to represent release of [3H]acetylcholine. In addition, BIMU 8 enhanced the release of [3H]acetylcholine and twitch contractions evoked by submaximal electrical stimulation. Ondansetron (1 μmol/l) did not change the effects of BIMU 8, but DAU 6285 and tropisetron (each 1 μmol/l) competitively antagonized the various facilitatory effects of BIMU 8 with pA2 values of 7.0–7.2 (DAU 6285) and 7.0–7.3 (tropisetron). The phosphodiesterase inhibitors IBMX and rolipram did not increase the effects of BIMU 8. BIMU 1 and renzapride also concentration-dependently increased basal release of acetylcholine, and release and contractions caused by submaximal stimulation. The effects of BIMU 1 and renzapride were competitively antagonized by 1 μmol/l tropisetron (pA2 6.6–7.1). The EC50 values for the increase in the evoked [3H]acetylcholine release and contractions were closely similar. 5-Hydroxyindalpine did not change basal release and slightly inhibited the evoked release of [3H]acetylcholine. Release of acetylcholine and contractions elicited by submaximal stimulation were strongly inhibited by (+)-tubocurarine which indicates that nicotinic ganglionic transmission is involved in this kind of release. The results suggest that BIMU 8, BIMU 1 and renzapride stimulate 5-HT4 receptors at cholinergic interneurones and thereby facilitate nicotinic ganglionic transmission in the myenteric plexus. Cyclic AMP is probably not involved in the 5-HT4 receptor mediated facilitation of acetylcholine release.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 351 (1995), S. 229-236 
    ISSN: 1432-1912
    Keywords: BIMU 8 ; BIMU 1 ; Renzapride ; 5-HT4 receptors ; Acetylcholine release ; Myenteric plexus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effects of the 5-HT4 receptor agonists BIMU 8, BIMU 1, renzapride and of the 5-HT1p receptor agonist 5-hydroxyindalpine on basal and electrically evoked outflow of tritium were studied in guinea-pig longitudinal muscle myenteric plexus preparations preincubated with [3H]choline. Muscle contractions were recorded simultaneously. BIMU 8 caused a calcium dependent and tetrodotoxin sensitive increase in basal [3H]outflow that was assumed to represent release of [3H]acetylcholine. In addition, BIMU 8 enhanced the release of [3H]acetylcholine and twitch contractions evoked by submaximal electrical stimulation. Ondansetron (1 μmol/l) did not change the effects of BIMU 8, but DAU 6285 and tropisetron (each 1 μmol/l) competitively antagonized the various facilitatory effects of BIMU 8 with pA2 values of 7.0–7.2 (DAU 6285) and 7.0–7.3 (tropisetron). The phosphodiesterase inhibitors IBMX and rolipram did not increase the effects of BIMU 8. BIMU 1 and renzapride also concentration-dependently increased basal release of acetylcholine, and release and contractions caused by submaximal stimulation. The effects of BIMU 1 and renzapride were competitively antagonized by 1 μmol/l tropisetron (pA2 6.6–7.1). The EC50 values for the increase in the evoked [3H]acetylcholine release and contractions were closely similar. 5-Hydroxyindalpine did not change basal release and slightly inhibited the evoked release of [3H]acetylcholine. Release of acetylcholine and contractions elicited by submaximal stimulation were strongly inhibited by ( + )-tubocurarine which indicates that nicotinic ganglionic transmission is involved in this kind of release. The results suggest that BIMU 8, BIMU 1 and renzapride stimulate 5-HT4 receptors at cholinergic interneurones and thereby facilitate nicotinic ganglionic transmission in the myenteric plexus. Cyclic AMP is probably not involved in the 5-HT4 receptor mediated facilitation of acetylcholine release.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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