Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We conducted a prospective evaluation of the comparative effects of lumbar epidural and general anesthesia on the hemodynamic and neuroendocrine stress response to cesarean delivery in 21 women with severe preeclampsia. In the epidural group (n = 11), anesthesia extending to the T-4 dermatome level was obtained using 2% plain lidocaine in divided doses. In the general anesthesia group (n = 10), anesthesia was induced after pretreatment with labetalol or nitroglycerin. In the epidural group, mean arterial pressure (MAP) gradually decreased from 133.3 +/- 5.6 mm Hg to 119 +/- 4.4 mm Hg (P less than 0.002). After pretreatment with labetalol or nitroglycerin, MAP in the general group decreased from 131.5 +/- 4.9 mm Hg to 112.2 +/- 3.5 mm Hg (P less than 0.001). At skin incision (after tracheal intubation), MAP increased from 112.2 +/- 3.5 mm Hg to 143 +/- 5.4 mm Hg (P less than 0.001); however, this was not significantly different from baseline MAP. In the epidural group, there were no further changes in MAP. The difference in MAP at skin incision and postpartum period between the two groups was significant (P less than 0.004 and P less than 0.009, respectively). In the general anesthesia group, both adrenocorticotropic hormone and beta-endorphin-like immunoactivity increased significantly from base levels at skin incision. The catecholamines also increased significantly and remained so throughout the study period. In the epidural group, the concentrations of these hormones decreased or remained unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Anesthetic modification of hemodynamic and neuroendocrine stress responses to cesarean delivery in women with severe preeclampsia. 153 Jul 30

The concentration of corticotropin-releasing hormone (CRH) in maternal plasma increases greatly during the last trimester of normal pregnancy. This CRH has been proposed to originate from the placenta. We studied plasma immunoreactive CRH in 46 uncomplicated pregnancies, in 10 pregnant women with chronic hypertension, in 17 women with pregnancy-induced hypertension (PIH) and in 24 women with pre-eclampsia, and correlated it to the levels of corticotropin (ACTH) and cortisol. CRH levels were greatly increased in women with pre-eclampsia, less significantly in women with PIH, while no change was found in pregnant women with chronic hypertension. ACTH levels also were increased in pregnancies with pre-eclampsia or PIH and there was a positive correlation between CRH and ACTH levels. CRH levels in cord venous plasma were significantly increased in pregnancies with pre-eclampsia but cortisol did not show any significant increase. These findings suggest that placental release of CRH into the maternal and fetal circulation is increased in pre-eclampsia.
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PMID:Corticotropin-releasing hormone in maternal and cord plasma in pre-eclampsia. 185 89

The effects of intrauterine stress and birth asphyxia on the plasma concentration of beta-endorphin (beta-E) in cord blood and in venous blood at the age of 2 h was investigated in newborn infants. Term infants with acute birth asphyxia (n = 11), infants born to mothers with preeclampsia (n = 15), and prematures with respiratory difficulties (n = 4) were entered into the study. Twenty control infants were studied; 12 were born after spontaneous delivery and eight after elective cesarean section. After normal spontaneous delivery, the plasma beta-E level decreased significantly, the median values being 17 pmol/liter at birth and 9.3 pmol/liter at the age of 2 h, whereas after elective cesarean section it remained unchanged (13 and 13 pmol/liter, respectively). In acute asphyxia the plasma beta-E level varied widely at birth, from 9.7 to 108 pmol/liter. At the age of 2 h, the beta-E level was high (26 to 83 pmol/liter) in those asphyctic infants who required prolonged mechanical ventilation, but it fell to the range of 1.6-13 pmol/liter when the infant recovered rapidly. The beta-E level was not increased in the preeclampsia group, not even in small for gestational age infants. In preterm newborn infants with respiratory difficulties, a significant postnatal rise of plasma beta-E level was found, the beta-E value varying from 7.3 to 16 pmol/liter at birth and from 61 to 168 pmol/liter at the age of 2 h. These results indicate that increased beta-E secretion is associated with respiratory difficulties in the newborn infant.
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PMID:Plasma beta-endorphin in perinatal asphyxia and respiratory difficulties in newborn infants. 294 May 6

Corticotropin-releasing hormone was discovered in the placenta, and its concentration in the maternal plasma was found to increase greatly during the latter half of pregnancy. We studied the concentration of immunoreactive corticotropin-releasing hormone in amniotic fluid in 59 uncomplicated and in 73 complicated pregnancies. The mean (+/- SE) value of corticotropin-releasing hormone in amniotic fluid in uncomplicated pregnancies was significantly higher in the third (24.1 +/- 3.3 pmol/L) than in the second (9.1 +/- 0.7 pmol/L) trimester, but no change was found during labor. In groups matched by gestational age, larger mean values of corticotropin-releasing hormone and cortisol were observed in the group in which the lecithin/sphingomyelin ratio was greater than 2 or the phosphatidylglycerol test was positive than in the group with a lecithin/sphingomyelin ratio less than 2 or a negative phosphatidylglycerol test result. In samples taken at an interval of 1 to 3 weeks, concomitant increases in corticotropin-releasing hormone and cortisol levels were found with the appearance of phosphatidylglycerol. Concentrations of corticotropin-releasing hormone in amniotic fluid were elevated in patients with diabetes and in women with preeclampsia and intrauterine growth retardation. We conclude that the intrauterine release of corticotropin-releasing hormone increases during the last trimester. This may stimulate the fetal pituitary-adrenal axis and promote fetal maturation.
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PMID:Corticotropin-releasing hormone in amniotic fluid during gestation and labor and in relation to fetal lung maturation. 326 45

Concentration of corticotropin-releasing hormone (CRH) has earlier been found to increase greatly in maternal plasma during the last trimester of normal pregnancy and even more in preeclampsia. This CRH is thought to be of placental origin, and it may stimulate maternal or fetal pituitary adrenal axis. We studied CRH in umbilical cord venous plasma in relation to gestation, labor, and fetal distress. There was a great maternal-to-fetal concentration difference in plasma CRH levels, a hundredfold at term pregnancy, suggesting that the placenta releases CRH mainly into the maternal rather than into the fetal circulation. Length of gestation or the mode of delivery did not affect CRH levels in cord plasma. Cord CRH levels were higher (median, 24.1, range, 14.2 to 67 pmol/liter) in six preterm infants with chronic fetal distress, born to mothers with severe preeclampsia and in nine infants born after premature rupture of membranes (median, 17.0, range, 7.65 to 53 pmol/liter), than in 12 preterm control infants born after uncomplicated pregnancy (median, 6.3 range, 1.0 to 27.5 pmol/liter). No significant correlation was found between CRH and cortisol levels in cord plasma. Increased cortisol levels in cord plasma were associated with spontaneous vaginal delivery but not with chronic fetal distress. These findings demonstrated that placental release of CRH into the fetal circulation may be increased in pregnancy complications with chronic fetal distress but failed to prove any relationship between placental CRH and fetal adrenal function.
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PMID:Corticotropin-releasing hormone and cortisol in cord plasma in relation to gestational age, labor, and fetal distress. 847 73

The role of corticotropin-releasing hormone (CRH) in the regulation of pituitary adrenocorticotropin secretion and the stress response is well established. However, in recent years this peptide has been found to serve a number of functions outside the classic neuroendocrine domain. During pregnancy, CRH derived from the placenta is thought to play a crucial role in the regulation of foetal maturation and the timing of delivery, and CRH has also been implicated in the control of foetal-placental bloodflow. Abnormalities of the placental CRH system might be involved in the pathogenesis of preterm labour, foetal growth retardation and pre-eclampsia, which are the three leading causes of perinatal morbidity and mortality in developed countries.
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PMID:Corticotropin-releasing Hormone in Human Pregnancy and Parturition. 1037 Feb 25

The understanding of epilepsy has advanced substantially in the past decade, and new anticonvulsant drugs with novel mechanisms of action are continually being developed. Some of these newer (and older) medications have been discussed in this article. A wide variety of other drugs is occasionally used in the management of epilepsy. Although parenteral magnesium sulfate is used mainly for the prevention and control of seizures in severe preeclampsia or eclampsia, parenteral magnesium sulfate may also be useful in controlling epileptic seizures associated with low plasma magnesium concentrations. Although considered obsolete, bromides have been useful in the management of tonic-clonic or myoclonic seizures in some infants and preadolescent children when other drugs were unsuitable. Acetazolamide may be useful in the management of refractory partial, myoclonic, absence or primary generalized tonic-clonic seizures; however, tolerance develops to the effect of the drug. Corticotropin and corticosteroids are sometimes used in the management of myoclonic seizures in infants. Steroids may be used in seizures due to intracerebral malignancies and metastasis but are more effective in blunting the intracranial swelling associated with these diseases. Recognition of these new drugs may allow the paramedic or EMT to identify seizure patients in the field. Knowledge of the side effects of these medications may be used to guide patients into appropriate treatment pathways.
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PMID:Anticonvulsant medications. 1145 38

During pregnancy, major changes of the corticotroph axis activity are observed. The placenta synthetizes Corticotropin-Releasing Hormone (CRH) and pro-opio-melanocortin (POMC), and the plasma levels of both peptides are highly increased during pregnancy. The cortisol plasma levels are two-fold elevated compared to the levels observed in non pregnant women. This increase in cortisol level is mainly due to the doubling of the Cortisol Binding Globulin (CBG). Untreated Cushing's syndrome during pregnancy is associated with a high maternal as well as fetal morbidity (hypertension, preeclampsia, diabetes mellitus, premature birth.). Adrenocortical tumors are the major cause of Cushing's syndrome diagnosed in pregnancy. The treatment of hypercortisolism during pregnancy required a multidisciplinary approach by highly specialized teams. Adrenal insufficiency is rarely diagnosed during pregnancy. Untreated adrenal failure is associated with a high maternal and fetal morbidity and mortality. On the other hand, steroid replacement therapy appropriately monitored during pregnancy is associated with a very favorable outcome in pregnant women with adrenal insufficiency. During labor steroid replacement therapy should be adapted as for any surgical procedure.
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PMID:[Cushing's syndrome and adrenal insufficiency in pregnancy]. 1244 88

This prospective study was undertaken to determine the maternal plasma beta-endorphin levels in pre-eclamptic women during labour and to explore any correlation between the levels and the severity of pre-eclampsia. A total of 50 primiparous women at term were recruited over a period of 5 years. Twenty-five with pre-eclampsia and 25 healthy women considered as a control group. The mean concentration of maternal plasma beta-endorphin in pre-eclamptic group (22.73+/-8.02 pmol/l) was significantly lower (p<0.001) than that of the control group (48.38+/-5.94 pmol/l). A highly significant (p<0.001) negative correlation was found between maternal plasma beta-endorphin levels and both systolic and diastolic blood pressures in pre-eclamptic group.
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PMID:A study of maternal plasma beta-endorphin in pre-eclamptic women during labour. 1609 10

Abnormalities in the process of trophoblast invasion may result in abnormal placentation. Both the embryonic trophoblast and maternal decidua produce corticotropin-releasing hormone (CRH), which promotes implantation. Carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1), which is expressed in extravillous trophoblasts (EVTs) of normal human placenta, may also function in tro-phoblast/endometrial interactions. We investigated whether locally produced CRH plays a role in trophoblast invasion, primarily by regulating CEACAM1 expression. We examined cultures of freshly isolated human EVTs, which express CEACAM1, and an EVT-based hybridoma cell line, which is devoid of endogenous CEACAM1. CRH inhibited EVT invasion in Matrigel invasion assays, and this effect was blocked by the CRH receptor type 1 (CRHR1)-specific antagonist antalarmin. Additionally, CRH decreased CEACAM1 expression in EVTs in a dose-dependent manner. After transfection of the hybridoma cell line with a CEACAM1 expression vector, the invasiveness of these cells was strongly enhanced. This effect was inhibited by addition of blocking monoclonal antibody against CEACAM1. Furthermore, blocking of endogenous CEACAM1 in EVTs inhibited the invasive potential of these cells. Taken together these findings suggest that CRH inhibits trophoblast invasion by decreasing the expression of CEACAM1 through CRHR1, an effect that might be involved in the pathophysiology of clinical conditions, such as preeclampsia and placenta accreta.
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PMID:Corticotropin-releasing hormone modulates human trophoblast invasion through carcinoembryonic antigen-related cell adhesion molecule-1 regulation. 1640 17


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