Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01178 (oxytocin)
 15,767 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The distribution of [3H]oxytocin binding sites among various subcellular fractions of rat myometrium paralleled the distribution of 5'-nucleotidase, a plasma membrane marker enzyme, but not of NADPH-cytochrome c reductase or succinate-cytochrome c reductase, which are endoplasmic reticulum and mitochondrial marker enzymes respectively. [3H]Oxytocin binding to the most enriched plasma membrane fraction showed the degree of selectivity with respect to hormone analogues that is expected for the oxytocin receptor. The binding of oxytocin to this fraction showed an apparent Kd of 1.98 X 10(-9) M and a capacity of 1.28 pmol mg-1. It is concluded that the oxytocin receptor is located on the plasma membrane of the smooth muscle cells of the rat uterus.
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PMID:Localization of the oxytocin receptor in the plasma membrane of rat myometrium. 20 28

Sheep corpus luteum homogenates were fractionated by centrifugation on continuous sucrose density gradients, with or without digitonin, and gradient fractions were assayed for progesterone, and for a range of intracellular organelle and plasma-membrane markers. Digitonin had little effect on the density distributions of mitochondrial, rough endoplasmic reticulum (RER) and Golgi-endoplasmic reticulum-lysosomal (GERL) membranes. However, digitonin did disrupt lysosomal membranes, leading to release of acid hydrolases, and induced a decrease in buoyant density of NADH-cytochrome c reductase, a putative smooth endoplasmic reticulum (SER) marker. Oxytocin-containing granules were clearly resolved from other organelles accumulating in a sharp peak (density, 1.20 g/cm3). Luteal cell-surface membrane marker activities equilibrated at similar buoyant densities in control gradients, and pretreatment with digitonin induced a marked increase in their buoyant densities. The majority of the progesterone of the sheep corpus luteum equilibrated at a buoyant density of 1.10 g/cm3 in control gradients, and was highly perturbed by digitonin. These fractions also accumulated [3H]progesterone. The buoyant density profile of progesterone in both control and digitonin-treated gradients most closely resembled that of sheep luteal lactogenic receptor, a putative plasma-membrane marker.
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PMID:Subcellular fractionation of the ovine corpus luteum: association of progesterone with ovine luteal membranes? 319 18

Amniotic Fluid Embolism (AFE) is a rare obstetric catastrophe that occurs in approximately 1/50,000 pregnancies and has a mortality rate in excess of 80%. AFE is a condition that is poorly understood and often difficult to diagnose. We report a case of a healthy 27-yr-old gravid two, 35 wk gestation parturient with a previous Cesarean section two years previously, and presently admitted for emergent Cesarean section due to premature uterine contractions. Induction of general anesthesias was performed with no problem and a male preterm infant with Apgar 8 at 1 min was delivered. Amniotic fluid was bloody and 40% placental abruption existed. Following delivery of the placenta, patient suddenly became plethoric and O2 saturation began to decrease and no pulse could be palpated! Immediate CPR was successful but she was hemodynamically unstable and signs of right heart strain was obvious. Right jugular venous catheterization was performed, vasopressors were administered. After a two hours period of relatively stable vital signs, patient's reflexes returned to normal, however, profound coagulopathy on lab data was reported and she was treated with 10 unit Packed Red Blood Cells (PRBCs), 10 unit FFP and 8 unit platelets, Sodium bicarbonate, oxytocin and Methergine. The patient remained hemodynamically unstable while laparotomy-hysterectomy was performed to stop the bleeding. Unfortunately attempts were unsuccessful and patient died four hours later in ICU. Post-mortem findings showed signs of Disseminated Intravascular Coagulation (DIC), no fetal squamous cells in pulmonary vasculature were found and special staining of Cytokeratin marker shows no positive cells in lumen of vessels. The post-mortem diagnosis of AFE is challenging to forensic investigators and pathologists and can be confirmed by histological confirmation of amniotic fluid contents in the pulmonary vasculature, although they may be difficult to identify. In recent years it has been suggested that AFE is an anaphylactoid reaction to fetal antigens and an elevated serum tryptase level is increasingly being used to support the diagnosis. Sudden onset of cardiovascular collapse and early signs of right heart strain and fulminant DIC supports the diagnosis of AFE in this case, although no fetal debri could be find in pathologic staining.
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PMID:Sudden cardiac arrest during cesarean section -- a possible case of amniotic fluid embolism. 1958 89