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Biomedical subjects

A Langslet

Publications and source records attributed to A Langslet.

At least 19 recordsLinked to original sources
PubMed1994

Functional characterization of an ex vivo preparation of atrial myocardium from children with congenital heart defects: sensitivity to tyramine and adrenoceptor antagonists.

Small pieces of atrial tissue removed from the cannulation site before cardioplegia were used to develop a method for studying adrenergic regulation of the myocardial contractile force in children operated on for congenital heart defects (CHD). We measured the development of the isometric force of contraction dT/dtmax (T'max). Reduction in basal contractility induced by the beta-adrenoceptor antagonist timolol indicated that the myocardium was about half-maximally stimulated by endogenous norepinephrine (NE), probably released from nerve endings by the electrical stimulation. The inotropic effect of endogenous NE could be further increased by tyramine (EC50 approximately 5 microM). A maximal concentration of tyramine increased T'max by a median of 62.5% above the basal level. Sequential blockade of the beta- and alpha 1-adrenoceptors after tyramine stimulation by timolol and prazosin, respectively, indicated that a near-maximal response to combined adrenoceptor stimulation by endogenous NE was mediated by both beta-adrenoceptors (median 77%) and alpha 1-adrenoceptors (median 23%). The basal level of endogenous NE may conceal inotropic effects by exogenous alpha-agonists added to this type of preparation. This preparation is suitable for studying adrenergic regulation by reversing the effects of endogenous NE.

Adolescent↗
PubMed1985

A new syndrome: thrombocytopathia, muscle fatigue, asplenia, miosis, migraine, dyslexia and ichthyosis.

A new multifacetted syndrome inherited as an autosomal, dominant trait is described encompassing not only two hitherto undescribed hereditary defects--thrombocytopathia and asplenia--but also muscle contractile defect, migraine-like headache, miosis, dyslexia and ichthyosis. None of these defects has so far been assigned to a specific chromosome or linkage group. Further studies on the various aspects of the syndrome are in progress.

Child↗
PubMed1985

Demonstration of an alpha adrenoceptor-mediated inotropic effect of norepinephrine in human atria.

It has been claimed by other investigators that norepinephrine does not evoke a significant alpha adrenergic inotropic effect in human atria in contrast to epinephrine and phenylephrine, indicating a limitation of a possible functional role of the cardiac alpha adrenoceptors. We therefore characterized the inotropic effects of norepinephrine in isometrically contracting muscle strips from human atria obtained during open heart surgery. Both contraction and relaxation were studied by measuring developed tension and its first and second derivatives. Both the influence of propranolol and prazosin upon the inotropic responses to norepinephrine and the qualitative characteristics of the responses revealed that norepinephrine evoked both alpha and beta adrenergic inotropic effects. The alpha adrenergic response to norepinephrine was qualitatively different from the beta adrenergic effect and qualitatively similar to the alpha adrenergic effect of norepinephrine observed in other mammalian species. Although the alpha adrenergic effect was marked, the beta adrenergic effect was the dominating one as has also been found in other species. It is concluded that also in human atria norepinephrine evokes inotropic effects through both alpha and beta adrenoceptors.

Heart Atria↗
PubMed1982

Auditory brainstem responses (ABR) in high-risk neonates.

In the present study, auditory brainstem responses (ABR) were recorded in 60 high-risk neonates in the intensive care unit selected by the following criteria: Birth-weight less than 2000 g, hyperbilirubinemia requiring phototherapy or exchange transfusion, idiopathic respiratory distress syndrome, artificial ventilation, asphyxia, sepsis or meningitis, intracranial haemorrhage, neurological symptoms and potential ototoxic medication (aminoglycoides, furosemide). The infants tested ranged in gestational age from 27-44 weeks. The ABR testing was performed in a sound-proof room using the Madsen (ERA-74) equipment. Four infants did not reveal responses to 70 dB HL ("nonresponders"), and the total of 10 neonates (16.6%) had abnormal ABR-tests, when the physiological changes related to gestational age and conceptional age (gestational age plus the age after birth) were taken into account. The 10 neonates with abnormal tests were reexamined after discharge, and in six there were no improvement of threshold sensitivity. three of the "nonresponders" were retested several times within the two years after birth (one died at age 18 months of pertussis), and none of them revealed ABR at stimulus intensity of 70 dB HL. They all attend an audiological training program started at age of six months as a consequence of the early diagnosis of impaired auditory function. It is our opinion that a routine ABR-evaluation should be performed on high risk neonates (criteria mentioned above) in the newborn intensive care unit. Retesting of infants with abnormal responses within three months, and several times within the next two years if abnormal responses persist, is important. Transient impairment of auditory functions is not uncommon in these infants. However, the children with persisting hearing impairment should be discovered early to attend an early audiological training program.

Age Factors↗
PubMed1982

Activation of the kallikrein-kinin system in premature infants with respiratory distress syndrome (RDS).

Plasma prekallikrein levels, kallikrein activity and antikallikrein levels were investigated in nine premature infants with respiratory distress syndrome (RDS) and six premature infants without. Plasma prekallikrein and kallikrein were determined with a chromogenic substrate measuring amidolytic activity. Antikallikrein was measured with a functional assay. In infants with severe RDS, prekallikrein levels were significantly reduced (median 58% of initial values (p less than 0.01) about 48 hours after onset of symptoms. In infants with moderate RDS prekallikrein level was reduced less, while in babies without RDS there were no significant changes in prekallikrein levels the first 5-7 days of life. Antikallikrein levels did not change significantly in any babies. The results suggest that the kallikrein-kinin system might be involved in RDS. This could explain several features of this syndrome such as hypotension and edema. Furthermore the findings show that homeostatic functions are altered in this disease, and they suggest that other cascade systems as the coagulation, fibrinolytic and complement system may be involved as well. The findings emphasize that trauma might be a significant pathogenetical factor for development of this syndrome and indicate that RDS is not simply a biochemical disease with lack of surfactant as the only pathogenetic factor.

Blood Gas Analysis↗
PubMed1979

Surgical repair of isolated ventricular septal defects in the first year of life.

Since October 1975, 6 infants ranging in age from 5 to 9 months and weighing from 5.2 to 7.8 kg have been treated with primary closure of ventricular septal defect (VSD) at Ullevål Hospital. The indications for operation were large left-to-right shunts combined with persistence of heart failure in 4 patients, a large left-to-right shunt only in one and elevated pulmonary arterial resistance in one patient. Conventional cardiopulmonary bypass was used in all cases. There were no early or late deaths during the mean observation period of 17.3 months (range 3--25 months). One patient developed a recurrent VSD and was successfully re-operated on 8 months after the first operation; otherwise no signs of recurrence were found. The growth and weight gains have been satisfactory and the psychosomatic development of all the infants has been normal. All are in sinus rhythm with right bundle branch block in 4. Cardiac arrhythmias have not been in evidence.

Cardiopulmonary Bypass↗
PubMed1978

Plasma concentration of diazepam and N-desmethyldiazepam in children after a single rectal or intramuscular dose of diazepam.

The absorption of diazepam and N-desmethyldiazepam after administration of diazepam solution for parenteral injection per rectum and intramuscularly was studied in 9 children (ages 3--12 years). Rectal administration of diazepam 1 mg/kg led to rapid absorption with plasma levels of 270--320 ng/ml within 5 min, and peak levels of 600--1300 ng/ml 10--60 min after administration. The absorption was comparable to that after intramuscular administration. A second peak in plasma diazepam concentration 6--12 h after dosing was observed in 6 children, which may have been due to mobilization of diazepam from the gastrointestinal mucosa produced by feeding 4 h after administration of the drug. A slowly increasing plasma level of N-desmethyldiazepam was observed during the first 24 h after administration of diazepam.

Child↗
PubMed1978

Plasma concentrations of diazepam and N-desmethyldiazepam in newborn infants after intravenous, intramuscular, rectal and oral administration.

Five newborn infants (birth weight 2900--3600 g) were given diazepam (Valium, LaRoche) for convulsive disorders in 4 equal doses intravenously, intramuscularly, rectally and orally with at least 24 hours intervals. Three infants were given doses of 1 mg diazepam/kg body weight, and 2 0.5 mg/kg. The parenteral solution of the drug was given intravenously, intramuscularly and rectally. Powder of tablets was given orally. After intravenous administration very high peak values of plasma-diazepam concentration were obtained (5775--10800 ng/ml after 1 mg/kg, 2750 and 6450 ng/ml after 0.5 mg/kg). Next to intravenous administration rectal administration caused the most rapid increase in plasma-diazepam concentration. Presumed anticonsulsive concentrations (150--300 ng/ml) were obtained within 5 min with 1 mg/kg as well as 0.5 mg/kg rectally. Rectal administration therefore could be a suitable treatment for seizures in the newborn infant. Accumulation of the main depressive metabolite N-desmethyldiazepam occurred in all infants. This phenomenon must be taken into account when repeated doses of diazepam are administered.

Administration, Oral↗