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A Megevand

Publications and source records attributed to A Megevand.

4 recordsLinked to original sources
PubMed1999

Platelet-activating factor may act as an endogenous pulse generator for sheep of luteolytic PGF2alpha release.

Pulsatile release of uterine prostaglandin F2alpha (PGF2alpha) induces luteolysis in ruminants. However, the mechanism(s) that initiates and maintains luteolysis has not been defined. The present study tested the hypothesis that the endogenous PGF2alpha pulse generator is uterine-derived platelet-activating factor (PAF). Ovariectomized ewes were given exogenous progesterone (P), estradiol (E), or both (P+E, mimicking the normal luteal phase). Only ewes treated with steroids released PAF into the uterine lumen and had increased PAF:acetylhydrolase activity in the uterine lumen. Steroid treatment also influenced the capacity of the uterus to release PGF2alpha in response to exogenous PAF. PAF infusion did not affect plasma PGF2alpha metabolite (PGFM) levels in control (no steroid treatment) ewes but increased plasma PGFM levels in P+E ewes (P < 0.001) and ewes treated with P or E alone (P < 0.05). Infusion of PAF followed by or coincident with oxytocin (OT) acted in a synergistic manner to increase plasma PGFM levels. Repeated infusion of PAF into the uterus at 1-h intervals induced tachyphylaxis of the PGFM response to PAF; however, sensitivity of the uterus to PAF returned spontaneously by the 6th h. Interferon-tau (IFN-tau) inhibits pulsatile release of PGF2alpha during pregnancy to prevent luteolysis. Exogenous recombinant ovine IFN-tau (50 microgram) inhibited the uterine response to PAF alone or the combined effects of PAF and OT. These results indicate that uterine PAF fulfills many of the criteria for an endogenous PGF2alpha pulse-generator: steroid induction of PAF production and uterine responsiveness to PAF-induced release of PGF; synergistic stimulation of PAF-induced PGF release by OT; inhibition of PAF effects by IFN-tau; and PAF's ability to induce pulses of PGF with a periodicity during a period of chronic exposure of the uterus to PAF.

1-Alkyl-2-acetylglycerophosphocholine Esterase↗
PubMed1999

Why the prone position is a risk factor for sudden infant death syndrome.

INTRODUCTION: The laryngeal chemoreflex may explain why prone sleeping increases the risk of sudden infant death syndrome (SIDS). Swallowing and arousal are crucial to prevent laryngeal chemoreflex stimulation. Our aim was to examine these reflexes and breathing responses in healthy neonates after pharyngeal infusion of water in the supine versus the prone position, controlling for sleep state. METHODS: A total of 10 term infants were recruited after parental consent and ethics approval. Polygraphic recordings included sleep state (active and quiet sleep by electroencephalogram, eye movements, breathing, and behavior), cardiorespiratory measurements (nasal airflow, chest wall movements, heart rate, and oxygen saturation), swallowing, and esophageal activity (solid state pressure catheter). Initial sleeping position was assigned randomly. Measurements were made for 1 minute before and after 0.4 mL of water was instilled into the oropharynx. To detect a 30% decrease in swallowing, power analysis indicated that >/=10 babies were required. Analysis, blinded to position, was made using nonparametric statistics. RESULTS: Of the 164 infusions, the most commonly evoked airway protective responses to pharyngeal infusion were swallowing (95%) and arousal (54%). After infusion in active sleep, there was a significant reduction in swallowing and breathing when the prone position was compared with the supine position (prone: 21.3 [1.0] swallows/min and -9.6 [2.1] breaths/min; and supine: 32 (2.2) and -2. 9 (1.5), respectively). However, there was no difference in the occurrence of arousal after water infusion. CONCLUSION: These data suggest that airway protection is compromised in the prone sleeping position during active sleep, even in healthy infants exposed to minute pharyngeal fluid volumes of 0.4 mL. This is because swallowing rate is reduced significantly, and there is no compensatory increase in arousal. The reduction in airway protective reflexes when in the prone position and in active sleep may be the mechanism for the increased risk of SIDS in the prone position.

Arousal↗