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Biomedical subjects

C Leffler

Publications and source records attributed to C Leffler.

15 recordsLinked to original sources
PubMed1992

Heart rate variability in normal sleeping full-term and preterm neonates.

To assess maturation of the Autonomic Nervous System (ANS) and sleep states, Heart Rate Variability (HRV) was studied in 24 healthy sleeping newborns, aged from 31 to 41 weeks, conceptional age (CA). Spectral analysis of the interbeat interval (RR) signal, was performed by Short-Time Fourier Transform, in three frequency bands: high (HF), of purely vagal origin, mid (MF), and low (LF), vagal and sympathetic, thus allowing evaluation of both branches of the ANS, observed in Active Sleep (AS = REM Sleep) and in Quiet Sleep (QS = nREM Sleep). Principal Component Analysis, Discriminant Analysis, and hypothesis tests were used to investigate the evolution of spectral variables and their relation with sleep states. HF, MF, LF, and mean RR all increased with age; the differences from the premature to the full-term group, were more marked, as a whole, in AS than in QS. HF showed the highest increase from the premature (31-36 weeks CA) to the intermediate (37-38) group, whereas LF showed equal differences from the premature to the intermediate, and from the intermediate to the full-term (39-41) groups. These results suggest a steep increase in vagal tone at 37-38 weeks CA, with stability afterwards, and a more regular increase in sympathetic tone from 31 to 41 weeks CA.

Analysis of Variance↗
PubMed1992

Sigh-related heart rate changes during sleep in premature and full-term newborns.

The functional linkage in the cardio-respiratory system demands precise coordination of their activity. Sighs provide an opportunity to study the interaction and the maturation of the autonomic nervous system. In 4 groups of normal, sleeping newborns (31 to 41 weeks conceptional age [wCA], 2 to 10 days postnatal age) we investigated heart rate changes caused by sighs by means of polygraphy. In full-term (39-41 wCA) and near-term newborns (37-38 wCA) sighs during quiet sleep (QS) were accompanied by heart rate acceleration (p < 0.01) and thereafter by heart rate deceleration (p < 0.01). During active sleep (AS) only heart rate acceleration (p < 0.01) was observable. In prematures (35-36 wCA) acceleration could be observed in QS (p < 0.01) and AS (p < 0.01) but no deceleration in QS. In prematures of 31-34 wCA no changes during AS and QS could be detected. Body movements caused heart rate acceleration but no heart rate deceleration. In conclusion, it can be hypothesized that heart rate acceleration may be caused by reduced vagotonus initiated by augmented lung volume and movements. Sigh-related changes responsible for heart rate deceleration occur solely during quiet sleep. In prematures of 31-34 wCA these reflexes are not developed.

Electroencephalography↗
PubMed1990

Increased airway leukotriene levels in infants with severe bronchopulmonary dysplasia.

The sulphidopeptide leukotrienes (C4, D4, and E4) are potent airway constrictors that have been detected in the airways of infants with pulmonary hypertension and viral infections. The present study was undertaken to test the hypothesis that leukotrienes in tracheal lavage fluid are elevated in bronchopulmonary dysplasia. Twenty-six intubated infants (10 with bronchopulmonary dysplasia, 9 with hyaline membrane disease, and 7 normal controls) had tracheal lavage leukotriene levels determined by radioimmunoassay. Lavage fluid cell counts (alveolar macrophages) and leukotriene levels were significantly increased in infants with severe bronchopulmonary dysplasia. The increased concentration of leukotrienes seen in the infants with bronchopulmonary dysplasia would suggest a possible role for these compounds in the pathophysiology of this disease.

Bronchopulmonary Dysplasia↗
PubMed1990

Role of prostanoids in cerebrovascular responses to asphyxia and reventilation in newborn pigs.

Cerebral hemodynamics during asphyxia and reventilation were investigated in normothermic, hypothermic (35 degrees C), and indomethacin-pretreated (5 mg/kg iv) anesthetized, newborn pigs. In the normothermic group, total cerebral blood flow (CBF) measured with radioactive microspheres was 57 +/- 12 ml.min-1 x 100 g-1 during baseline, 104 +/- 19 at 1 min of asphyxia, 39 +/- 5 at 5 min of asphyxia, 186 +/- 16 at 8 min of reventilation, and 95 +/- 20 at 16 min of reventilation. During asphyxia and reventilation blood flow to brain stem was better regulated than to cerebrum or cerebellum. Baseline CBF was similar in the indomethacin and hypothermic groups (32 +/- 2 and 41 +/- 5 ml.min-1 x 100 g-1, respectively; n = 5 for each group). However, during asphyxia, blood flow was never less in either one of these groups than in the normothermic group in spite of a lack of arterial hypercapnia at 1 min in the hypothermia group. During reventilation, blood flow was sometimes lower in the hypothermic and indomethacin groups than the normothermic group but never lower when considered on a percentage change from baseline basis. We conclude that inhibition of prostanoid production with indomethacin did not limit vasodilation during these conditions.

Animals↗
PubMed1989

Low-dose aspirin in pregnancy.

In a prospective study, we evaluated the effects of low-dose aspirin on maternal and neonatal plasma 6-keto-prostaglandin (PG) F1 alpha concentration, platelet aggregation, platelet thromboxane production, and neonatal transitional circulation. Forty women, at a mean (+/- SD) of 37 +/- 2 weeks' gestation, were randomized to receive (N = 10 each) placebo or 20, 60, or 80 mg of aspirin per day until delivery. Maternal serum 6-keto-PGF1 alpha levels were not affected by these doses of aspirin, whereas thromboxane B2 generated during clotting of maternal blood was decreased significantly by 60 and 80 mg of aspirin by 1 week of therapy. Maternal platelet thromboxane B2 production in response to adenosine diphosphate or collagen was reduced 98% by the 80-mg dose after 1 week of aspirin therapy. The 60-mg dose reduced maternal platelet thromboxane B2 production in response to adenosine diphosphate (50% decrease) or collagen (60% decrease) after 1 week of treatment, a nonsignificant difference. After 2 weeks of treatment with 60 mg of aspirin, platelet thromboxane B2 production induced by both collagen and adenosine diphosphate was inhibited significantly (P less than .01). Neonatal serum levels of 6-keto-PGF1 alpha and thromboxane B2 were not affected by any doses of aspirin. Further, neonatal platelet aggregation in response to platelet stimulation by collagen and adenosine diphosphate was not inhibited. All neonates had echocardiographic evidence of a patent ductus arteriosus, and noninvasive estimates of pulmonary arterial pressure were similar among the groups of infants.(ABSTRACT TRUNCATED AT 250 WORDS)

Alprostadil↗
PubMed1988

Postasphyxial increases in prostanoids in cerebrospinal fluid of piglets.

The dilator stimuli that contribute to postasphyxial increases in cerebral blood flow in the neonate are unclear. To assess the possible role of cyclooxygenase products in these responses, we measured pial arteriolar diameter in six piglets and determined levels of prostaglandin (PG) E2 and 6-keto-PG F1 alpha (hydrolysis product of PGI2) in cerebrospinal fluid (CSF) bathing the parietal cortex during control conditions, after 4-10 min of complete respiratory arrest (asphyxia), and after 5-12 min of reventilation. Pial arterioles are important resistance vessels in the cerebral circulation. Baseline pial arteriolar diameter was 220 +/- 40 micron (mean +/- SEM) and increased to a maximum of 252 +/- 49 and 267 +/- 56 micron after asphyxia and reventilation, respectively. During control conditions, CSF PGE2 (n = 6) and 6-keto-PGF1 alpha (n = 4) levels were 1947 +/- 310 and 794 +/- 147 pg/ml, respectively. During asphyxia, CSF levels of PGE2 did not increase, whereas 6-keto-PGF1 alpha increased modestly. During reventilation, CSF PGE2 increased to 3576 +/- 499 pg/ml, and 6-keto-PGF1 alpha increased to 2846 +/- 123 pg/ml. In other experiments, we determined that these CSF levels of PGE2 and PGI2 (as 6-keto-PGF1 alpha) were within the vasodilator range for pial arterioles. We conclude that postasphyxial increases in pial arteriolar diameter are associated with a rise in CSF levels of dilator prostanoids.

Animals↗
PubMed1987

Relationship between mean airway pressure, cardiac output, and organ blood flow with normal and decreased respiratory compliance.

We investigated the relation between blood flow and mean airway pressure in two groups of anesthetized newborn piglets. The first group had normal respiratory compliance; the second group had pulmonary surfactant depleted by repeated saline lavage, which decreased static respiratory compliance by 42%. In the normal group, cardiac output decreased linearly from 292 +/- 43 mL/min/kg at 5 cm H2O airway pressure to 134 +/- 37 ml/min/kg at 20 cm H2O airway pressure, a drop of 43% (r2 = 0.79). Blood flow to the heart, kidney, and intestines had a similar decline, but brain, hepatic artery, and adrenal flow were constant. Mean arterial blood pressure did not decrease significantly until the highest airway pressure was reached, whereas sagittal sinus pressure increased as mean airway pressure increased. In contrast, the surfactant-depleted group maintained cardiac output up to a mean airway pressure of 15 cm H2O. At 20 cm H2O, cardiac output fell to 40% of the original value. Blood flow to the heart and kidneys fell at a mean airway pressure of 20 cm H2O; intestinal blood flow decreased beginning at 10 cm H2O. As in the normal piglets, brain, hepatic arterial, and adrenal blood flow were not affected by increasing ventilation pressure. Our data show that positive pressure ventilation in the neonate has important cardiovascular effects that are blunted when respiratory compliance is decreased. More important, because cardiac output decreased prior to a significant decline in arterial blood pressure, these data suggest that in a clinical setting considerable cardiovascular alterations can occur before a decline in arterial blood pressure is detected.

Airway Resistance↗
PubMed1987

Increasing ventilation pressure increases cortical subarachnoid cerebrospinal fluid prostanoids in newborn pigs.

This study examines the responses of pial arterioles and venules to increased mean airway pressure (P aw-) in newborn pigs. We further characterized the changes in cortical subarachnoid cerebrospinal fluid prostanoids with increased P aw-, both before and after cyclooxygenase inhibition with indomethacin. Eight chloralose anesthetized newborn pigs were equipped with closed cranial windows and ventilated with a conventional infant pressure-cycled respirator. Increasing P aw- from 3.2 +/- 0.3 cm water to 14.3 +/- 0.6 cm water did not change pial arteriole or venule diameters. Cerebrospinal fluid prostanoids (6-keto-PGF1 alpha, TxB2, PGE2, and PGF2 alpha), however, were increased reversibly (3- to 5-fold) by increasing P aw-. After indomethacin (5 mg/kg, intravenous) pial arterioles constricted approximately 15% with increased P aw-. These results suggest that increasing ventilation pressure increases brain prostanoid production. Prostanoids appear to inhibit vasoconstriction and may be important in maintaining cerebral blood flow during the stress of mechanical ventilation.

Animals↗
PubMed1979

Pulmonary and systemic vascular responses of perinatal goats to prostaglandins E1 and E2.

Effects of prostaglandins of the E series and their metabolites on pulmonary and systemic circulations of newborn and exteriorized fetal goats (anesthetized with chloralose) were evaluated in situ using an isolated perfused left lung lobe preparation. Prostaglandin E1 (PGE1) and, to a lesser extent, prostaglandin E2 (PGE2) infusions resulted in decreases of pulmonary vascular resistance (PVR) of fetal and neonatal goats. Infusions of PGE1 or PGE2 (less than 2 microgram.kg-1.min-1 for 1 min) directly into left pulmonary arterial blood did not affect systemic arterial pressure (SAP). Infusions of PGEs (greater than 2 microgram.kg-1.min-1 for 1 min) resulted in decreases in SAP and heart rate. The dose-response characteristics of the pulmonary circulation in response to PGE1 and PGE2 were not different in fetal and newborn goats. Fetal asphyxia did not alter the dose-response characteristics of pulmonary circulation in response to PGE1. Metabolites (15-keto) of PGE1 and PGE2 had no effect upon PVR or SAP of perinatal goats. These results demonstrate in perinatal mammals 1) vasodilator action of PGE1 and PGE2 on the pulmonary and systemic circulations, and 2) catabolism by the lungs of these prostaglandins.

Animals↗
PubMed1976

Use of indomethacin to reverse neonatal hypotension.

Treatment with indomethacin elevated systemic arterial pressure and pulmonary vascular resistance in hypotensive newborn goats. Indomethacin may be of value in restoration of systemic arterial pressure in stress-induced hypotension.

Animals↗
PubMed1975

Effects of prostaglandins of the E-series on pulmonary and systemic circulations of newborn goats during normoxia and hypoxia.

Effects of exogenous prostaglandins of the E-series on pulmonary and systemic circulations of newborn goats were investigated during normoxia and hypoxia. Pulmonary arterial infusion of prostaglandins E1 and E2 decreased pulmonary vascular resistance 20% and 14%, respectively, without systemic effects. Prostaglandin E1 abolished the pulmonary pressor response to hypoxia. Prostaglandin E2 was less effective in counteracting this hypoxic response. The increased pulmonary vascular resistance and augmented response to hypoxia following indomethacin administration was reversed by prostaglandin E1. Infusion of prostaglandin E1 directly into the pulmonary circulation may be of benefit to the distressed newborn with elevated pulmonary vascular resistance.

Animals↗
PubMed1975

The effects of indomethacin on the pulmonary vascular response to hypoxia in the premature and mature newborn goat.

The effects of indomethacin on the pulmonary circulation and the response of the circulation to hypoxia were investigated in premature and mature newborns using an isolated perfusion technique on otherwise intact left lungs in situ. There was an increase in pulmonary vascular resistance and augmentation of the increase in pulmonary vascular resistance during hypoxia following indomethacin. These effects were greater in the premature than in the mature newborn. Indomethacin effectively removes a dilator influence on the pulmonary circulation. The results are consistent with the concept that prostaglandins are important in regulating pulmonary vascular resistance.

Animals↗