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

Five of 80 (6.2%) nulliparous women sustained uterine trauma in association with midtrimester abortion induced by intra-amniotic prostaglandin F2alpha and intravenous oxytocin. All five women suffered cervical lacerations, one extending to the lower uterine segment of the corpus and another associated with myometrial necrosis caused by cornual sacculation and ischemia. No uterine trauma was observed among 95 parous women aborted in the same fashion during this study. The different mechanisms of cervical dilation in the parous woman and the nullipara are offered as an explanation for this difference. Thirty-nine other cases of uterine injury associated with the use of intraamniotic prostaglandin F2alpha from the literature were reviewed, and found to indicate that midtrimester abortion induced by intra-amniotic prostaglandin F2alpha is associated with a significant risk of uterine trauma in the nullipara. The risk seems to increase with the use of oxytocin and with increasing gestational age.
 ...
PMID:Uterine trauma associated with midtrimester abortion induced by intra-amniotic prostaglandin F2alpha with and without concomitant use of oxytocin. 88 3

The effects of oxytocin and prostaglandin E2 (PGE2) infusions on regional blood flow (measured by radioactive microspheres) and myometrial contractility were studied in 18 pregnant rhesus monkeys near term. We observed no significant differences between PGE2 and oxytocin in cardiac output, hemodynamics, or uterine activity. Their effects on the regional distribution of systemic blood flow were similar although the gastrointestinal tract received an increased percentage of cardiac output after PGE2. A relative placental ischemia, together with a myometrial hyperemia, was observed during labor. Uterine contraction produced a large reduction (average 73 per cent) in placental blood flow whereas myometrial blood flow was maintained or sometimes increased. A significant negative correlation was observed between intra-amniotic pressure and placental blood flow. During uterine relaxation, placental flow partially recovered whereas myometrial flow nearly doubled the prelabor values. We conclude that (1) in the dose ranges studied, oxytocin and PGE2 produce similar effects on myometrial contractility and uteroplacental blood flow, and (2) the vascular beds of the placenta and myometrium respond differently to labor of moderate intensity.
 ...
PMID:Uterine contractility and regional blood flow responses to oxytocin and prostaglandin E2 in pregnant rhesus monkeys. 109 12

In order to estimate the human placental lactogen (HPL) level and its value as an indicator of fetoplacental function during labor, we determined HPL levels (N equals 225) before, during, and after labor in normal (N equals 16) and preeclamptic (N equals 14) subjects or in patients with benign intrahepatic cholestasis of pregnancy (N equals 5). During labor, greater decreases in this value were found in preeclamptic than in normal subjects and similarly in mothers with fetoplacental dysfunction than with normal fetoplacental function. The rupture of the membranes had no effect on the level of HPL, which was not related to parity, oxytocin infusion, time interval from rupture of the membranes to delivery, nor to relative placental weight. The half-life of HPL varied in the range of 20-23 minutes immediately after delivery and in the range of 30-39 minutes some time later. During labor, greater decreases in HPL level in cases of preeclampsia or fetoplacental dysfunction may be caused by relative uteroplacental ischemia during uterine contractions, but from this finding it is hard to expect any advantage of HPL as a monitor of fetoplacental function during labor.
 ...
PMID:Human placental lactogen levels during and after labor. 115 51

The urinary output of prostaglandin E2 (PGE2) during and following Cesarean section (CS) was investigated in 21 patients. Urinary PGE2, probably reflecting renal production of PGE2, increased about two-fold during anesthesia and surgery and persisted for at least one additional hour. PGE2 output also correlated with the dose of oxytocin administered. The possibility that renal perfusion may be compromised during CS and that increased synthesis of prostaglandins (PGs) may serve to protect the kidney against ischemia is suggested.
 ...
PMID:Urinary prostaglandin E2 output increases in cesarean section. 386 93

The anatomy of the human uterine vascular tree changes repeatedly with the variations in hormonal state during each menstrual cycle, with progressive differentiation of arterioles up to the premenstrual state. Hormonal factors also influence the innervation of uterine arteries, both cholinergic, adrenergic and peptidergic, and regulate the spontaneous contractile activity of the smooth muscle of vessel walls as well as the motor responses of these tissues to different vasoactive substances. The smaller branches of uterine arteries, i.e., the resistance arteries appear to be of particular importance in the regulation of uterine blood flow, since they are most densely innervated. Furthermore, the most effective uterine vasoconstrictors in vitro, vasopressin, endothelin, oxytocin and noradrenaline have a more pronounced effect on these vessels than on the main branches of the uterine artery. Vascular compression may also result from changes in the myometrial activity. A hormonal disturbance may cause dysfunctional bleeding by changing vessel growth as well as the uterine smooth muscle activity of both vessels and myometrium. An example of the latter phenomenon is primary dysmenorrhoea, women with this condition having an increased secretion of vasopressin. By an action on type V1 vasopressin receptors of the uterus, this peptide causes myometrial hyperactivity and vasoconstriction, with resultant uterine ischemia and pain. Further support for a pathophysiological role of vasopressin and also of oxytocin in dysmenorrhoea is the therapeutic effect of a competitive type V1 vasopressin and oxytocin receptor antagonist in the condition.
 ...
PMID:Vascularization of human endometrium. Uterine blood flow in healthy condition and in primary dysmenorrhoea. 797 51

We examined the effects of hypoxic/ischemic stress on cerebral arteriolar responses to oxytocin in anesthetized piglets. Pial arteriolar diameters were measured using a cranial window and intravital microscopy. First, we evaluated arteriolar responses to topical application of oxytocin during normoxic conditions. We then determined whether 5-10 min of arterial hypoxia, ischemia, or asphyxia alters oxytocin-induced responses. Arterial hypoxia was produced by inhalation of 7.5% O2-92.5% N2 for 10 min. Ischemia was achieved by increasing intracranial pressure for 10 min. Asphyxia was achieved by turning off the ventilator for 5 min. During normoxic conditions, oxytocin dilated pial arterioles by 9 +/- 1% at 10(-8) and by 16 +/- 1% at 10(-6) mol/l (n = 47, p < 0.05). Arteriolar responses to oxytocin did not change with repeated applications (n = 10). Following hypoxia, dilator effect of oxytocin was not changed at 10(-8) (8 +/- 2%) but it was reduced at 10(-6) mol/l (7 +/- 2%; p < 0.05, n = 8). After asphyxia or ischemia, oxytocin did not dilate arterioles at 10(-8) mol/l, whereas 10(-6) mol/l resulted in a mild vasoconstriction (-4 +/- 3 to -6 +/- 4%, n = 6 and 8). Topically applied superoxide dismutase did not preserve arteriolar responses to oxytocin after asphyxia although the arterioles did not constrict to 10(-6) mol/l oxytocin (n = 5). Dilatation of cerebral arterioles in response to oxytocin was reversed to constriction by N(omega)-nitro-L-arginine methyl ester (L-NAME) (15 mg/kg, i.v.; n = 5) and by endothelial impairment by intra-arterial infusion of phorbol ester (10[-5] mol/l; n = 5). We conclude that the absence of pial arteriolar dilation to oxytocin after ischemia and asphyxia indicates endothelial dysfunction which may be involved in the pathology of perinatal brain injury.
 ...
PMID:Influence of hypoxia/ischemia on cerebrovascular responses to oxytocin in piglets. 925 92

In the present study we investigated the effects of brain ischemia on endothelin expression in the hypothalamo-neurohypophysial system of the rat using the post-embedding immunogold technique for electron microscopy. From 24 hours to six months after ischemia, a relatively high endothelin immunoreactivity was observed in some neurosecretory cells of the supraoptic and paraventricular nuclei as well as in endothelial cells of some microvessels of the hypothalamus and neurohypophysis. The results indicate that ischemia is a potent stimulus for increased production of endothelin. The distribution of endothelin-immunoreactive neurons in the hypothalamus was similar to that of vasopressin and oxytocin, so it seems possible that endothelin participates directly in controlling hormonal synthesis and release from vasopressinergic and oxytocinergic neurons in the hypothalamo-neurohypophysial system.
 ...
PMID:Protracted elevation of endothelin immunoreactivity in hypothalamo-neurohypophysial system after ischemia. 937 75

Both oxytocin and vasopressin cause potent and long-lasting vasoconstriction of uterine arteries from several species, including humans, and the resulting tissue ischemia is thought to be involved in the pathogenesis of primary dysmenorrhea. We have studied the effects of oxytocin and vasopressin in isolated resistance arteries (diameter, 90-120 microm) from non-pregnant rat uteri using two potent and selective receptor antagonists, SR 49059, a selective vasopressin V1A antagonist, and atosiban, a selective oxytocin antagonist. Uterine arteries with intact endothelium were mounted in a microvessel chamber, and pressurized to 75 mm Hg to allow the development of myogenic tone. Both vasopressin and oxytocin elicited a concentration-dependent vasoconstriction with a similar maximum effect (i.e., total vessel occlusion). The EC50 was 0.44 +/- 0.02 and 25 +/- 3.1 nM for vasopressin and oxytocin, respectively. Thus, vasopressin was 57-fold more potent than oxytocin. Schild analysis indicated that SR 49059 yielded a similar pA2 value against vasopressin-induced (pA2 = 8.96 +/- 0.60) or oxytocin-induced (pA2 = 9.06 +/- 0.23) contractions, suggesting that both agonists activated the vasopressin V1A receptor. In addition, atosiban (10(-7) M), a selective antagonist of the oxytocin receptor in the rat, did not antagonize the effect of vasopressin and oxytocin, showing that the oxytocin receptor is not involved in the response. In conclusion, these results suggest that V1A receptor stimulation is responsible for the vasoconstricting effects of both vasopressin and oxytocin in small diameter resistance arteries from the rat uterus.
 ...
PMID:Oxytocin and vasopressin constrict rat isolated uterine resistance arteries by activating vasopressin V1A receptors. 1044 88

The objective of this study was to establish an experimental model for extracorporeal perfusion of swine uterus. In order to validate this model, we examined some biochemical parameters and determined the effect of oxytocic drugs (Oxytoxin, Prostaglandin E (2)) on extracorporeal perfused swine uteri. Thirty swine uteri were perfused with Krebs-Ringer bicarbonate-glucose buffer for a period up to eleven hours with the aim to preserve a viable organ, which should be responsive to hormones. The intrauterine pressure was recorded after administration of various concentrations of oxytocin and prostaglandin E (2). Perfusate pH, perfusate lactate, partial oxygen and carbon dioxide tensions, oxygen saturation, and hydrogencarbonate levels in the perfusate, all indicators of tissue ischemia or cell necrosis, showed good preservation of the organ for up to seven hours. We examined the relation of intrauterine pressure to oxytocin and prostaglandin E (2). Both were able to induce contractions of the uterus, whereas prostaglandin E (2) produced rhythmical contractions of smaller amplitude and a higher frequency. We could demonstrate that our perfusion system was able to preserve the swine uterus in a functional condition appropriate for the study of physiological questions.
 ...
PMID:The extracorporeal perfusion of swine uterus as an experimental model: the effect of oxytocic drugs. 1451 66

1. Cell swelling induces exocytosis of material stored in secretory vesicles resulting in a secretory burst of peptidic hormones or enzymes from various types of cells including endocrine cells and neurons. We have previously shown that swelling-induced exocytosis possesses limited selectivity; hypotonic medium evokes TRH but not oxytocin release from hypothalamic paraventricular nucleus (PVN) and neurohypophysis (NH). 2. It is the aim of this study to ascertain whether the swelling-induced oxytocin secretion could be unmasked by the inhibition of specific osmotic response using Ca(2+)-free medium and GdCl(3), an inhibitor of stretch activated channels. 3. Oxytocin release from the PVN was stimulated by the hypotonic medium only in the presence of 50 or 100 microM GdCl(3.) Oxytocin release from supraoptic nucleus (SON) was also stimulated by the Ca(2+)-free hypotonic medium in the presence of GdCl(3). Oxytocin secretion from the NH was not stimulated even in the presence of GdCl(3), both in Ca(2+) containing and Ca(2+)-free medium. TRH response to swelling-inducing stimulus was not affected by the presence of GdCl(3). 4. An intranuclear oxytocin secretion to hyposmotic stimulation within the PVN and the SON could be unmasked by the inhibiting specific response by GdCl(3). At these conditions general secretory response to swelling-inducing stimuli emerged. Secretion of oxytocin from the NH was not affected by any of these treatments. 5. Peptides and proteins released after cell swelling can play an important role in the pathophysiology of ischemia and could be mediators of local or remote preconditioning. Disruption of mechanosensitive gating in magnocellular neurosecretory cells could result in an inadequate secretory response (e.g. stimulation instead of inhibition and vice versa) of hormones engaged in water and salt metabolism regulation.
 ...
PMID:The effect of swelling on TRH and oxytocin secretion from hypothalamic structures. 1662 32


1 2 3 4 5 6 Next >>