ABSTRACT
The synthesis of leukotriene B4 by A23187-stimulated rat peritoneal leukocytes was studied in the presence of 0.1% normal human serum, serum from patients treated with NSAIDs for either an inflammatory (rheumatoid arthritis, RA) or a non-inflammatory condition (lumbar disc protrusion, LDP), and serum from RA patients drawn one week after withdrawal from NSAID treatment. The capacity for LTB4 synthesis was significantly lower in the presence of serum from NSAID treated patients: thirty per cent less than observed in presence of normal serum in the RA group, and fifty per cent in the LDP group. When NSAIDs were withdrawn from RA patients, the LTB4 production in presence of serum increased, but was not completely normalized after one week. These results indicate that NSAID treatment may down-regulate the capacity for leukotriene synthesis by an indirect effect.
Subject(s)
Anti-Inflammatory Agents, Non-Steroidal/therapeutic use , Blood , Leukocytes/metabolism , Leukotriene B4/biosynthesis , Adult , Aged , Animals , Anti-Inflammatory Agents, Non-Steroidal/pharmacology , Arthritis, Rheumatoid/blood , Arthritis, Rheumatoid/drug therapy , Female , Humans , Male , Middle Aged , Rats , Rats, Sprague-Dawley , Spinal Diseases/blood , Spinal Diseases/drug therapyABSTRACT
Pulsed doppler recordings were obtained in the truncus coeliacus in 12 premature born infants (gestational age 30.3 +/- 2.5 weeks) with the clinical signs of patent ductus arteriosus Botalli (PDA) and compared to a control group of 24 healthy infants (gestational age 40.5 +/- 5.3 weeks). In all children the maximal systolic velocity, the endsystolic and the enddiastolic velocity and the pulsatility-index were measured. The 24 healthy newborns showed the following velocities: Maximal systolic velocity: 77 +/- 16 cm X s-1; endsystolic velocity: 31 +/- 10 cm X s-1; enddiastolic velocity; 18 +/- 9 cm X s-1. The pulsatility-index was 0.75 +/- 0.11. In children with PDA the maximal systolic velocity was 72 +/- 21 cm X s-1, the endsystolic velocity 15 +/- 14 cm X s-1 and the enddiastolic velocity -5 +/- 8 cm X s-1. The pulsatility-index was 1.08 +/- 0.12. All infants with large PDA showed a significant decrease of the endsystolic velocity and enddiastolic velocity, whereas the pulsatility-index was significantly increased. The decrease of the endsystolic and enddiastolic velocity in infants with large PDA in comparison to the healthy control group may lead to hypoxemic-ischemic lesions of the intestinal organs. The increased incidence of necrotizing enterocolitis in premature infants with large PDA may be the result of hypoperfusion of the small bowel.
Subject(s)
Ductus Arteriosus, Patent/diagnosis , Infant, Premature, Diseases/diagnosis , Rheology , Blood Flow Velocity , Celiac Artery , Ductus Arteriosus, Patent/surgery , Enterocolitis, Pseudomembranous/diagnosis , Humans , Infant, Newborn , Intestines/blood supply , Ischemia/diagnosisABSTRACT
33 premature infants (age: 32 +/- 3 weeks; birth weight 1,268 +/- 535 gs) with the clinical signs of patent ductus arteriosus Botalli (PDA) and a control group of 96 healthy infants (age: 37 +/- 4 weeks; birth weight 2 348 +/- 944 gs) were investigated. Pulsed doppler recordings were obtained in the anterior cerebral arteries (ACA) and compared with the flow pattern in the truncus coeliacus (TC). In all children the maximal systolic velocity (Vs), the endsystolic (Ves) and the enddiastolic velocity (Ved) and the pulsatility-index (PI) were measured. The 96 healthy premature born infants showed the following velocities: Vs: 41 +/- 12 cm X sec-1; Ves: 19 +/- 7 cm X sec-1; Ved: 10 +/- 4 cm X sec-1. The pulsatility-index was 0.74 +/- 0.08. In children with PDA all velocities were significantly lower than in the healthy control group: Vs: 31 +/- 10 cm X sec-1; Ves: 7 +/- 6 cm X sec-1; Ved: -1 +/- 5 cm X sec-1. Ved was more decreased than Vs resulting in a significant increase in PI (1.04 +/- 0.14). 22 infants with surgically proven large PDA (age: 31 +/- 3 weeks; birth weight: 1,160 +/- 467 gs) showed significant lower velocities (Vs: 34 +/- 8 cm X sec-1; Ves: 4 +/- 4 cm X sec-1; Ved: -4 +/- 4 cm X sec-1) in comparison with the healthy control group and the 11 children with small PDA (age: 33 +/- 4 weeks; birth weight: 1,494 +/- 621 gs).(ABSTRACT TRUNCATED AT 250 WORDS)
Subject(s)
Brain Ischemia/diagnosis , Cerebrovascular Circulation , Ductus Arteriosus, Patent/diagnosis , Infant, Premature, Diseases/diagnosis , Rheology , Birth Weight , Blood Flow Velocity , Cerebral Arteries , Gestational Age , Humans , Infant, NewbornABSTRACT
A cyanotic newborn is described to illustrate and discuss the rare transient tricuspid insufficiency together with functional pulmonary atresia. Etiologically the manifold causes of perinatal asphyxia are to be taken into consideration. The clinical appearance corresponds to type A of transient myocardial dysfunction according to the classification of Rowe together with respiratory distress syndrome and heart failure. Pathogenetically the disease is based on the different histological consequences of myocardial ischaemia of the right ventricle in connection with a delayed fall of the pulmonary arterial resistance. Fetal connections lead to a pronounced right-to-left-shunt. The diagnosis is primarily established by the way of clinical and echocardiographic investigation and pulsed doppler examination. The most important differential diagnosis are in Ebstein-anomaly, obstruction and atresia of the right ventricular outflow tract. Therapy is conservative. Its aim is to improve myocardial performance and to lower right ventricular afterload. Outcome of patients with neonatal tricuspid insufficiency is uncertain and depends on the severity of myocardial ischaemia. In our patient the course has been uneventful after initial difficulties.
Subject(s)
Tricuspid Valve Insufficiency/congenital , Cardiac Catheterization , Diagnosis, Differential , Echoencephalography , Electrocardiography , Humans , Infant, Newborn , Pulmonary Artery/abnormalities , Tricuspid Valve Insufficiency/diagnosisABSTRACT
Forty children with presumed ventricular tachyarrhythmic syncopes in the absence of structural heart disease were studied. Twenty-nine patients, one of whom was deaf, had a prolonged QT-interval in the resting electrocardiogram (Group 1); eleven patients had a normal QT-interval (Group 2). The median QTc-interval vas 0.51 s in Group 1 and 0.40 s in Group 2. Familial occurrence suggesting autosomal dominant inheritance was found in 21 of 28 normally hearing patients in Group 1 and in 2 of 11 patients in Group 2. Syncopes were definitely stress-induced in 22 patients in Group 1 and in all 11 patients in Group 2. Of 23 patients in Group 1 in whom an electrocardiogram was obtained during physical exercise, only one showed severe ventricular dysrhythmia. In contrast, all eleven patients in Group 2 developed severe ventricular dysrhythmia with exercise. Treatment with beta-blocking medication prevented further syncopes in 15 of 19 patients with several previous attacks in Group 1 and in 3 of 5 patients of Group 2. Four of the 29 patients in Group 1 died suddenly and one more remained apallic after an attack. Of the 11 patients in Group 2, four died suddenly and one retains severe cerebral damage after resuscitation from ventricular fibrillation. We conclude that, besides the group of patients with the long QT-syndrome, there may be a distinct group of patients with a consistently normal QT-interval and severe ventricular dysrhythmia with exercise. Patients of both groups are threatened by sudden death and are improved by treatment with beta-blocking medication.
Subject(s)
Syncope/diagnosis , Tachycardia/diagnosis , Adolescent , Adrenergic beta-Antagonists/therapeutic use , Child , Child, Preschool , Electrocardiography , Female , Humans , Infant , Male , Physical Exertion , Syncope/genetics , Syncope/prevention & control , Tachycardia/drug therapy , Tachycardia/geneticsABSTRACT
According to own experiences and after a review of the literature a survey of therapy of cardiac arrhythmias in infancy and childhood is given. In this age group most of the occurring cardiac arrhythmias are harmless and pass without serious circulatory disturbances. Therefore in these cases no specific treatment is necessary, except of course the treatment and management of the disease which is causing the arrythmia. This report is concerned more detailed with the therapy of rhythm disturbances which are life threatening or will become fatal if they continue untreated for a longer period. In spite of the therapeutic recommendations given we are aware of the fact that it is impossible to predict the success of therapy. This turned out to be so especially in the case of tachycardias. The difficulties in long-term management of postoperative heart block are mentioned. Antiarrhythmic drugs, their indications, efficacy, side-effects and contraindications are listed in separate tables ("FdM-Tabellen für die Praxis" Nr. 30/1975, Fortschr. Med. 93, 30: 1447, 1975).
