ABSTRACT
INTRODUCTION: We report a case of a female neonate who developed respiratory depression following the unintentional administration of methylergonovine. The respiratory depression appeared to improve after the administration of bag mask ventilation, stimulation, and naloxone; and the baby was able to be managed without endotracheal intubation and prolonged positive-pressure ventilation. CASE: A full-term female neonate was delivered vaginally without issue. Approximately 10 min after delivery, the infant was inadvertently administered 0.1 mg of methylergonovine intramuscularly instead of vitamin K. Thirty minutes later the child developed cyanotic extremities and respiratory depression with an oxygen saturation of 75%. Naloxone, 0.4 mg IM, was recommended to mitigate respiratory depression. Within 5 min the patient's respirations improved to 40 breaths per minute, cyanosis improved, and she began resisting ventilations and crying loudly. The child continued to improve and was back to baseline that evening. DISCUSSION: Methylergonovine toxicity in neonates has been commonly associated with respiratory depression necessitating ventilatory support. In consideration of chemical structural similarity between methylergonovine and morphine, as well as signs/symptoms consistent with opioid-induced respiratory depression, naloxone was suggested. CONCLUSION: It appears that naloxone may reverse methylergonovine toxicity in neonates. The identification of a safe and potentially useful antidote to mitigate respiratory depression, potentially avoiding the need for intubation and more invasive interventions in this patient population is important.
Subject(s)
Medication Errors/adverse effects , Methylergonovine/poisoning , Naloxone/therapeutic use , Narcotic Antagonists/therapeutic use , Oxytocics/poisoning , Respiratory Insufficiency/chemically induced , Respiratory Insufficiency/drug therapy , Combined Modality Therapy , Cyanosis/etiology , Female , Humans , Infant, Newborn , Injections, Intramuscular , Methylergonovine/administration & dosage , Methylergonovine/antagonists & inhibitors , Naloxone/administration & dosage , Narcotic Antagonists/administration & dosage , Oxytocics/administration & dosage , Oxytocics/antagonists & inhibitors , Respiratory Insufficiency/physiopathology , Respiratory Insufficiency/therapy , Treatment OutcomeABSTRACT
This study explored the modulatory effects of nitric oxide and thromboxane A2 on contractions to ergonovine and methylergonovine in human coronary arteries. To elucidate the different role of nitric oxide synthase in the response to the ergot alkaloids, the serotonin (5-HT) receptors involved in nitric oxide synthase in the response to the ergot alkaloids, the 5-HT receptors involved in nitric oxide release and the contraction of the vascular smooth muscle were characterized with more selective 5-HT-receptor agonists and antagonists. Rings of human coronary arteries from explanted hearts were suspended in organ chambers for isometric tension recording. After testing for contractile (potassium chloride, 60 mM) and endothelial function (substance P, 10(-8) M), respectively, they were exposed to ergot alkaloids or other agonists in the absence or presence of U 46619 (10(-9) M), or nitro-L-arginine (10(-4) M), or both. Ergonovine and methylergonovine were comparable, weak vasoconstrictors in untreated preparations. Contractions to ergonovine were augmented by U 46619, but not by nitro-L-arginine. Contractions to methylergonovine were augmented only by combining U 46619 and nitro-L-arginine. Serotonin and methylergonovine, but not ergonovine, elicited endothelium-dependent, nitric oxide-mediated relaxations. Nonselective 5-HT(1B/1D)-receptor stimulation caused both contractions and relaxations; selective 5-HT1B stimulation caused relaxations only. In the human coronary artery, contractions to ergonovine are not dependent on NO release but are synergistically augmented by thromboxane. Methylergonovine causes similar effects on the vascular smooth muscle, but contractions are inhibited by the release of NO from the endothelium. The 5-HT receptor on the endothelium appears to be different from the receptor on the vascular smooth muscle, which mediates the contractile response to the ergot alkaloids.
Subject(s)
Ergonovine/pharmacology , Methylergonovine/pharmacology , Muscle, Smooth, Vascular/drug effects , Nitric Oxide/pharmacology , Oxytocics/pharmacology , Thromboxane A2/pharmacology , Vasoconstriction/drug effects , Adult , Child , Coronary Vessels/drug effects , Drug Interactions , Ergonovine/antagonists & inhibitors , Female , Humans , Male , Methylergonovine/antagonists & inhibitors , Middle Aged , Serotonin Antagonists/pharmacology , Serotonin Receptor Agonists/pharmacologyABSTRACT
Intrauterine pressure changes were recorded by microtransducer catheter in 17 women immediately post partum. In all patients, spontaneous contractile activity was recorded, characterized by high contraction amplitudes (110 to 350 mm Hg). The calcium entry blocker nifedipine effectively inhibited these contractions. Both in vitro, in strips of pregnant myometrium, and in vivo, methylergometrine induced a contractile activity that could be blocked by nifedipine. The conclusion is that, for the testing of drugs that affect the contractile activity of pregnant myometrium, the use of intrauterine pressure recording by microtransducer catheters in the early postpartum period provides a suitable model.
