oxytocin and Hypoxia

A survey is given on the regulation of the formation of corticoliberin and of pro-opiomelanocortin and of ACTH, respectively, and on the significance of these compounds. The formation of pro-opiomelanocortin is furthered by corticoliberin, vasopressin, oxytocin and angiotensin II. Receptors for the binding of corticoliberin appear in numerous parts of the central nervous system. In various diseases the content of corticoliberin in the plasma and in certain tissues is changed. The inhibition of the ACTH secretion by glucocorticosteroids takes place via a decrease of the formation of corticoliberin and by a reduction of the equipment of the corticotrophic cells with receptors for its binding. The secretion of corticoliberin and of ACTH, respectively, is increased by loads, by hypoglycaemia, by blood losses, by hypoxia and by infections. In the glucocorticosteroid receptors there are 2 types with different affinity to cortisol and corticosterone.

Topics: Adrenocorticotropic Hormone; Angiotensin II; Corticotropin-Releasing Hormone; Hemorrhage; Humans; Hypoglycemia; Hypoxia; Infections; Oxytocin; Pro-Opiomelanocortin; Receptors, Cell Surface; Vasopressins

Topics: Adrenocorticotropic Hormone; Animals; Birth Order; Carbachol; Dexamethasone; Dichlorvos; Enterovirus Infections; Female; Fetal Death; Hemoglobins; Hypoxia; Leptospirosis; Obstetric Labor Complications; Oxytocin; Parvoviridae; Pregnancy; Prostaglandins; Rupture; Streptococcal Infections; Stress, Physiological; Swine; Swine Diseases; Umbilical Cord; Virus Diseases

Topics: Amniotic Fluid; Cephalometry; Deglutition; Estrogens; Female; Fetal Death; Fetal Diseases; Fetal Heart; Fetus; Growth; Heart Rate; Humans; Hypoxia; Infant, Newborn; Infant, Premature; Insulin; Leukocytes; Movement; Oxytocin; Phosphatidylcholines; Phospholipids; Placenta; Pregnancy; Sphingomyelins; Transferrin; Ultrasonography; Urea

Topics: Acidosis; Amniotic Fluid; Bicarbonates; Birth Weight; Carbon Dioxide; Estriol; Female; Fetal Diseases; Fetal Heart; Fetus; Growth; Heart Rate; Humans; Hydrogen-Ion Concentration; Hypoxia; Labor, Obstetric; Maternal-Fetal Exchange; Meconium; Muscle Contraction; Oxygen; Oxygen Consumption; Oxygen Inhalation Therapy; Oxytocin; Pregnancy; Pregnancy in Diabetics; Scalp; Ultrasonography; Uterus

Topics: Acetates; Adrenocorticotropic Hormone; Amino Acids; Animals; Butyrates; Carbohydrates; Catecholamines; Cats; Cattle; Cricetinae; Dinitrophenols; Dogs; Ducks; Female; Glucagon; Glucose; Growth Hormone; Hormones; Humans; Hypoglycemic Agents; Hypoxia; In Vitro Techniques; Insulin; Insulin Secretion; Oxytocin; Pancreas; Pregnancy; Propionates; Rabbits; Rats; Sheep; Swine; Sympatholytics; Thyroid Hormones; Vasopressins

During sow parturition, there is need for an alternative uterotonic to oxytocin with less potency so piglets are not at risk of hypoxia and stillbirth. In this study, there was examination of carbetocin, a longer lasting analogue of oxytocin, and whether the lesser contractile force and duration resulting as a consequence of this treatment would improve piglet survivability. Following delivery of the first piglet, sows were serially assigned by parity to receive injections of 10 IU oxytocin (n = 35), 0.07 mg carbetocin (n = 36), or serve as a non-injected control (n = 30). The incidence of dystocia and stillbirths was recorded. To estimate liveborn piglet viability, umbilical cord blood samples were obtained from pigs 1, 2, 3 and 8, 9, 10, and lactate content was quantified to assess hypoxia during delivery. A blood sample collected at 24 h was assayed for total protein in plasma (%) as an indicator of colostrum intake. Treatment with oxytocin and carbetocin reduced farrowing duration (P = 0.023) and sows treated with carbetocin had piglets with the least umbilical cord blood lactate (P  = 0.008) and plasma protein (P = 0.005) concentrations. These data indicate carbetocin has the efficacy to accelerate piglet delivery and reduce piglet hypoxia, although the reason for reduced plasma protein with this treatment remains unexplained.

Topics: Animals; Animals, Newborn; Female; Fetal Blood; Hypoxia; Lactic Acid; Oxytocics; Oxytocin; Parturition; Pregnancy; Swine

Obstructive sleep apnea is a prevalent and poorly treated cardiovascular disease that leads to hypertension and autonomic imbalance. Recent studies that restore cardiac parasympathetic tone using selective activation of hypothalamic oxytocin neurons have shown beneficial cardiovascular outcomes in animal models of cardiovascular disease. This study aimed to determine if chemogenetic activation of hypothalamic oxytocin neurons in animals with existing obstructive sleep apnea-induced hypertension would reverse or blunt the progression of autonomic and cardiovascular dysfunction.. Two groups of rats were exposed to chronic intermittent hypoxia (CIH), a model of obstructive sleep apnea, for 4 weeks to induce hypertension. During an additional 4 weeks of exposure to CIH, 1 group was treated with selective activation of hypothalamic oxytocin neurons while the other group was untreated.. Hypertensive animals exposed to CIH and treated with daily hypothalamic oxytocin neuron activation had lower blood pressure, faster heart rate recovery times after exercise, and improved indices of cardiac function compared with untreated hypertensive animals. Microarray analysis suggested that, compared with treated animals, untreated animals had gene expression profiles associated with cellular stress response activation, hypoxia-inducible factor stabilization, and myocardial extracellular matrix remodeling and fibrosis.. In animals already presenting with CIH-induced hypertension, chronic activation of hypothalamic oxytocin neurons blunted the progression of hypertension and conferred cardioprotection after an additional 4 weeks of CIH exposure. These results have significant clinical translation for the treatment of cardiovascular disease in patients with obstructive sleep apnea.

Topics: Animals; Cardiovascular Diseases; Disease Models, Animal; Heart Diseases; Hypertension; Hypoxia; Neurons; Oxytocin; Rats; Rats, Sprague-Dawley; Sleep Apnea, Obstructive

The present study aimed to explore the role of oxytocin (OT) in myocardial injury induced by ischemia/reperfusion (I/R) and hyperglycemia and its underlying mechanisms. In this study, the isolated rat hearts underwent I/R in Langendorff perfusion model and H9c2 cells were subjected to hypoxia/reoxygenation (H/R) to establish an in vitro model. I/R injury was induced by exposing the rat hearts to 40 min of global ischemia followed by 60 min of reperfusion. H9c2 cells were cultured under the normoglycemic or hyperglycemic condition with or without pretreatment of OT, and then exposed to 4 h of hypoxia and 2 h of reoxygenation. Measurement indicators included myocardial infarct size assessed by triphenyltetrazolium chloride (TTC) staining and hemodynamic parameters in the ex vivo model as well as cell viability detected by cell counting kit 8 (CCK-8), apoptotic rate evaluated by flow cytometry, and the protein expressions by Western blot. The findings demonstrated that OT attenuated myocardial I/R injury. First, OT preconditioning significantly reduced hemodynamic disorders and myocardial infarct sizes. In addition, OT increased cell viability, decreased cell apoptosis and the expressions of IL-18, IL-1β, cleaved-caspase-1, NLRP3, and GSDMD following H/R. NLRP3 activator nigericin eliminated the beneficial effects of OT in H9c2 cells. Furthermore, OT also activated AMPK and decreased the expressions of pyroptosis-related proteins. Administration of AMPK inhibitor compound C blunted OT-induced AMPK phosphorylation and elevated the expressions of pyroptosis-related proteins in H9c2 cells subjected to H/R with hyperglycemia. OT alleviates myocardial I/R injury with hyperglycemia by inhibiting pyroptosis via AMPK/NLRP3 signaling pathway.

Topics: AMP-Activated Protein Kinases; Animals; Glucose; Hyperglycemia; Hypoxia; Myocardial Infarction; Myocardial Reperfusion Injury; Myocytes, Cardiac; NLR Family, Pyrin Domain-Containing 3 Protein; Oxytocin; Pyroptosis; Rats; Reperfusion; Signal Transduction

Previous studies have shown that, oxytocin has anticonvulsant and neuroprotective effects. One of the most important complications of Hypercapnic-hypoxia is drug resistance epilepsy. Effects of chronic intraperitoneal oxytocin treatment on gliosis, neuroinflammation and seizure activity was investigated in a model in which rats were exposed to hypoxia on postnatal day 1 and later challenged to the seizure-inducing pentylenetetrazol Forty pups were included in the study on their first day of birth. 16 pups were exposed to 100% CO

Topics: Animals; Animals, Newborn; Anti-Inflammatory Agents; Brain; Disease Models, Animal; GABAergic Neurons; Gliosis; Hippocampus; Humans; Hypoxia; Inflammation; Neuroprotective Agents; Oxytocin; Rats; Respiratory Distress Syndrome, Newborn; Respiratory Insufficiency

Oxytocin (OT) from the hypothalamus is increased in several cardiorespiratory nuclei and systemically in response to a variety of stimuli and stressors, including hypoxia. Within the nucleus tractus solitarii (nTS), the first integration site for cardiorespiratory reflexes, OT enhances synaptic transmission, action potential (AP) discharge, and cardiac baroreflex gain. The hypoxic stressor obstructive sleep apnea, and its CIH animal model, elevates blood pressure and alters heart rate variability. The nTS receives sensory input from baroafferent neurons that originate in the nodose ganglia. Nodose neurons express the OT receptor (OTR) whose activation elevates intracellular calcium. However, the influence of OT on other ion channels, especially potassium channels important for neuronal activity during CIH, is less known. This study sought to determine the mechanism (s) by which OT modulates sensory afferent-nTS mediated reflexes normally and after CIH. Nodose ganglia neurons from male Sprague-Dawley rats were examined after 10d CIH (6% O

Topics: Animals; Baroreflex; Disease Models, Animal; Electrophysiological Phenomena; Hypoxia; Male; Nodose Ganglion; Oxytocin; Patch-Clamp Techniques; Potassium Channels; Rats; Rats, Sprague-Dawley; Receptors, Oxytocin; Signal Transduction; Sleep Apnea Syndromes; Visceral Afferents

It is widely hypothesized that menstrual pain is triggered by prostaglandin synthesis that evokes high-pressure uterine contractions and ischemia. However, the effects of molecules implicated in menstrual pain on uterine contractility, perfusion, and oxygenation in vivo have been rarely demonstrated. Studies in women that do not respond to nonsteroidal anti-inflammatory drugs (NSAIDs) have reported elevated levels of platelet-activating factor (PAF). To establish in vivo evidence of PAF's capability to impair uterine homeostasis and to elicit visceral pain, we examined the effects of the PAF receptor agonist (carbamyl PAF [CPAF]) in comparison to other molecules hypothesized to play a role in uterine pain in mice. Uterine pressure was increased by oxytocin, prostaglandin F2α (PGF2α), and CPAF. Even in the absence of inflammatory molecules, uterine contractions reduced uterine oxygenation by 38%. CPAF reduced uterine perfusion by 40% ± 8% and elicited further oxygen desaturation approaching hypoxia (9.4 ± 3.4 mm Hg Pao

Topics: Animals; Dinoprost; Female; Hyperalgesia; Hypoxia; Mice; Mice, Knockout; Oxytocin; Perfusion; Platelet Activating Factor; Platelet Membrane Glycoproteins; Receptors, G-Protein-Coupled; Uterine Contraction; Uterus; Visceral Pain

Sleep apnea is a common sleep disorder characterized by intermittent periods of low blood oxygen levels. The risk for sleep apnea increases with age and is more prevalent in men than women. A common comorbidity of sleep apnea includes male sexual dysfunction, but it is not clear if a causal relationship exists between sleep apnea and sexual dysfunction. Possible mechanisms that link these two disorders include oxidative stress and testosterone. Oxidative stress is elevated in clinical patients with sleep apnea and in rodents exposed to chronic intermittent hypoxia (CIH), an animal model for apnea-induced hypopnea. Further, oxidative stress levels increase with age. Therefore, age may play a role in sleep apnea-induced sexual dysfunction and oxidative stress generation. To investigate this relationship, we exposed gonadally intact 3 (young) and 12 (middle-aged) month old male F344/BN F1 hybrid male rats to 8 days of CIH, and then examined male sexual function. Plasma was used to assess circulating oxidative stress and hormone levels. Middle-aged male rats had lower testosterone levels with increased sexual dysfunction and oxidative stress, independent of CIH. However, CIH decreased testosterone levels and increased sexual dysfunction and oxidative stress only in young gonadally intact male rats, but not in gonadectomized young rats with physiological testosterone replacement. In sum, CIH had a greater impact on younger gonadally intact animals, with respect to sexual behaviors, testosterone, and oxidative stress. Our data indicate CIH mimics the effects of aging on male sexual behavior in young gonadally intact male rats.

Topics: Aging; Animals; Corticosterone; Follicle Stimulating Hormone; Hypoxia; Luteinizing Hormone; Male; Orchiectomy; Oxidative Stress; Oxytocin; Rats; Sexual Behavior; Sleep Apnea Syndromes; Testosterone

The paraventricular nucleus of the hypothalamus (PVN) contributes to both autonomic and neuroendocrine function. PVN lesion or inhibition blunts cardiorespiratory responses to peripheral chemoreflex activation, suggesting that the PVN is required for full expression of these effects. However, the role of efferent projections to cardiorespiratory nuclei and the neurotransmitters/neuromodulators that are involved is unclear. The PVN sends dense projections to the nucleus tractus solitarii (nTS), a region that displays neuronal activation following hypoxia. We hypothesized that acute hypoxia activates nTS-projecting PVN neurons. Using a combination of retrograde tracing and immunohistochemistry, we determined whether hypoxia activates PVN neurons that project to the nTS and examined the phenotype of these neurons. Conscious rats underwent 2 h normoxia (21% O

Topics: Animals; Corticotropin-Releasing Hormone; Hypothalamus; Hypoxia; Male; Neurons; Oxytocin; Paraventricular Hypothalamic Nucleus; Rats, Sprague-Dawley; Solitary Nucleus

Traumatic brain injury (TBI) is a common cause of mortality and long-term morbidity in children and adolescents. Posttraumatic stress disorder (PTSD) frequently develops in these patients, leading to a variety of neuropsychiatric syndromes. Currently, few therapeutic strategies are available to treat juveniles with PTSD and other developmental neuropsychiatric disorders. In the present investigation, postnatal day 14 (P14) Wistar rats were subjected to TBI induced by a controlled cortical impact (CCI) (velocity = 3 m/s, depth = 2.0 mm, contact time = 150 ms). This TBI injury resulted in not only cortical damages, but also posttrauma social behavior deficits. Three days after TBI, rats were treated with intracranial transplantation of either mouse iPSC-derived neural progenitor cells under normal culture conditions (N-iPSC-NPCs) or mouse iPSC-derived neural progenitor cells pretreated with hypoxic preconditioning (HP-iPSC-NPCs). Compared to TBI animals that received N-iPSC-NPCs or vehicle treatment, HP-iPSC-NPC-transplanted animals showed a unique benefit of improved performance in social interaction, social novelty, and social transmission of food preference tests. Western blotting showed that HP-iPSC-NPCs expressed significantly higher levels of the social behavior-related genes oxytocin and the oxytocin receptor. Overall, HP-iPSC-NPC transplantation exhibits a great potential as a regenerative therapy to improve neuropsychiatric outcomes after juvenile TBI.

Topics: Animals; Astrocytes; Brain Injuries, Traumatic; Cell- and Tissue-Based Therapy; Cells, Cultured; Hypoxia; Induced Pluripotent Stem Cells; Male; Mice; Nerve Regeneration; Neural Stem Cells; Oxytocin; Rats; Rats, Wistar; Receptors, Oxytocin; Social Behavior; Stress Disorders, Post-Traumatic

Hypertension is a common outcome associated with obstructive sleep apnea (OSA), a prevalent yet poorly treated cardiovascular disease. Recent studies showed oxytocin (OXT), released from hypothalamic paraventricular nucleus (PVN) neurons, activates cardiac vagal neurons in the dorsal motor nucleus of the vagus (DMNX) and may blunt cardiovascular responses to stress. This study tests whether the release of OXT from PVN fibers in the DMNX is diminished with chronic intermittent hypoxia-hypercapnia (CIH/H) exposure, an animal model of OSA, and whether activation of PVN OXT neurons restores OXT release in the DMNX and prevents the hypertension resulting from CIH/H. To assess OXT release from PVN fibers, Chinese hamster ovarian (CHO) cells were engineered to be highly sensitive to OXT by stable expression of the human recombinant OXT receptor and the calcium indicator R-GECO1. PVN fibers in the DMNX were selectively photoactivated in vitro by expression of channelrhodopsin. The release of OXT onto CHO cells in the DMNX was blunted in rats exposed to 21 days of CIH/H. Chronic activation of PVN OXT neurons in vivo, using designer receptors exclusively activated by designer drugs, restored the release of OXT onto CHO cells in the DMNX. Chronic PVN OXT neuron activation in vivo also prevented the hypertension that occurred in conscious unrestrained telemetry-equipped sham rats exposed to 3 wk of CIH/H. These results demonstrate that chronic activation of OXT neurons restores the release of OXT from PVN fibers in the DMNX and prevents the hypertension that occurs with 3 wk of CIH/H exposure.

Topics: Animals; Biosensing Techniques; Blood Pressure; Channelrhodopsins; CHO Cells; Chronic Disease; Cricetulus; Disease Models, Animal; Hypercapnia; Hypertension; Hypoxia; Male; Neurons; Optogenetics; Oxytocin; Paraventricular Hypothalamic Nucleus; Rats, Sprague-Dawley; Receptors, Oxytocin; Signal Transduction; Telemetry; Time Factors; Transfection

For successful birth, contractions need to become progressively stronger. The underlying mechanisms are unknown, however. We have found that a novel mechanism, hypoxia-induced force increase (HIFI), is switched on selectively, at term, and is essential to strengthening contractions. HIFI is initiated as contractions cyclically reduce blood flow and produce repeated hypoxic stresses, with associated metabolic and transcriptomic changes. The increases in contractility are a long-lasting, oxytocin-independent, intrinsic mechanism present only in the full-term pregnant uterus. HIFI is inhibited by adenosine receptor antagonism and blockade of cyclooxygenase-2 signaling, and partially reproduced by brief episodes of acidic (but not alkalotic) pH. HIFI explains how labor can progress despite paradoxical metabolic challenge, and provides a new mechanistic target for the 1 in 10 women suffering dysfunctional labor because of poor contractions.

Topics: Acids; Adaptation, Physiological; Adenosine; Adenosine Triphosphate; Animals; Biomechanical Phenomena; Calcium; Cyclooxygenase 2; Female; Humans; Hydrogen-Ion Concentration; Hypoxia; In Vitro Techniques; Labor, Obstetric; Myometrium; Oxygen; Oxytocin; Pregnancy; Rats, Wistar; Receptor, Adenosine A1; Receptors, Purinergic P2X7; Stress, Physiological; Uterine Contraction

We present the case of a parturient diagnosed with primary ciliary dyskinesia with secondary bronchiectasis who developed significant hypoxemia following administration of intravenous oxytocin during Cesarean delivery under spinal anesthesia. This case suggests that oxytocin can affect pulmonary vascular tone and interfere with the protective effects of hypoxic vasoconstriction.. A 35-yr-old primigravida at 37 weeks gestation presented for a scheduled Cesarean delivery due to breech positioning and fetal abnormalities. The patient had a diagnosis of primary ciliary dyskinesia and had undergone a right middle lobectomy seven years earlier for resultant bronchiectasis. Pulmonary function testing in the month prior to delivery showed a 4% decline in her baseline FEV1 to 1.06 L (32% of predicted value) but she was functionally well. The patient initially had an uneventful spinal anesthetic and maintained an oxygen saturation of 97% on room air in the supine position until delivery of her baby. An intravenous infusion of oxytocin for uterine contraction was started following removal of the placenta. The patient then became acutely hypoxemic with a drop in room air saturation to 84% but with no other accompanying hemodynamic instability. Maternal oxygen saturation did not improve with the addition of supplemental oxygen, and the patient had a significant arterial-alveolar oxygen gradient suggesting an intrapulmonary shunt. No supporting clinical, radiologic, or laboratory evidence of a thrombotic, air, or amniotic fluid embolism or mucous plug was detected. The patient remained hypoxemic during the postoperative period with gradual improvement back to baseline saturation in approximately 48 hr.. The vasodilatory effects of intravenous oxytocin on the pulmonary vasculature may worsen shunting and interfere with hypoxic pulmonary vasoconstriction, producing clinically significant hypoxemia in patients with comorbid lung disease. Oxytocin should be used with caution in patients with compromised lung function.

Topics: Acute Disease; Adult; Ciliary Motility Disorders; Female; Humans; Hypoxia; Infusions, Intravenous; Oxytocin; Pregnancy; Vasoconstriction

Oxytocin (OT) has been reported to have a potential protective effect on stress-induced functional gastrointestinal disorders. This study determined whether colonic contraction in adults was affected by antenatal maternal hypoxia, and whether OT is involved in antenatal maternal hypoxia induced colonic contraction disorder. Isometric spontaneous contractions were recorded in colonic longitudinal muscle strips in order to investigate colonic contractions and the effects of exogenous OT on the contraction in antenatal maternal hypoxia and control mice. Both high potassium and carbachol-induced contractions of proximal colon but not distal colon were reduced in antenatal maternal hypoxia mice. Exogenous OT decreased the contractions of proximal colonic smooth muscle strips in control mice, while it increased contractions in antenatal maternal hypoxia mice. OT increased the contractions of distal colonic smooth muscle strips in both antenatal maternal hypoxia and control mice. Hexamethonium blocked the OT-induced potentiation of proximal colon but not distal colon in antenatal maternal hypoxia mice. These results suggest that exogenous oxytocin reverses the decrease of proximal colonic smooth muscle contraction in antenatal maternal hypoxia mice via ganglia.

Topics: Animals; Animals, Newborn; Colon; Female; Ganglia; Gastrointestinal Motility; Hypoxia; Mice; Mice, Inbred BALB C; Muscle Contraction; Muscle, Smooth; Oxytocin; Pregnancy

The purpose of this study was to determine whether the increased expression of tyrosine hydroxylase (TH), the first and limiting enzyme in catecholamine synthesis in vasopressin (VP) neurons of the human neonate, represents a primary developmental phenomenon or reflects a secondary phenomenon related to the activation of VP systems due to perinatal hypoxia. Using immunohistochemistry, we investigated TH expression in the supraoptic nucleus (SON) of 15 human neonates at autopsy in relation to the age and severity/duration of hypoxic injury that was estimated on the basis of neuropathological criteria. Increased expression of TH was observed selectively in VP-synthesizing neurons of neonates who experienced prolonged perinatal hypoxia; was not related to the age, body weight/percentile, brain weight, or head perimeter of the subjects but depended on the neuropathological grade of the hypoxic injury (p < 0.01); and was found in VP-synthesizing neurons with increased cellular and nuclear size, that is, neurons with histological evidence of activation. Taken together, these observations indicate that increased expression of TH in VP neurons of SON is not developmentally determined but represents a response to hypoxic stress. We propose that increased TH expression in SON neurons of the human neonate may serve as a neuropathological marker of prolonged perinatal hypoxia in autopsy material.

Topics: Autopsy; Female; Gene Expression Regulation, Developmental; Humans; Hypoxia; Immunophilins; Infant; Male; Neurons; Oxytocin; Severity of Illness Index; Statistics as Topic; Supraoptic Nucleus; Tyrosine 3-Monooxygenase; Vasopressins

To explore middle cerebral artery (MCA) and anterior cerebral artery (ACA) blood flow responses to superimposed acute hypoxemia in growth-restricted fetuses with and without established brain-sparing flow during basal conditions.. 47 term fetuses suspected of growth restriction were exposed to an oxytocin challenge test with simultaneous cardiotocography and Doppler velocimetry in the umbilical artery, MCA and ACA. The MCA-to-ACA pulsatility index (PI) ratio was calculated during basal conditions, contractions and relaxations. Basal brain-sparing flow was defined as an MCA-to-umbilical artery PI ratio of<1.08, de novo brain-sparing flow in the MCA as an MCA PI decrease with> or =1 standard deviation during uterine contractions or relaxations compared with basal measurements, and de novo brain-sparing flow in the ACA as an ACA PI decrease with > or =1 standard deviation. Non-parametric statistical tests were used with P<0.05 considered significant.. MCA and ACA PI were both significantly lower in the brain-sparing flow group (N=8) during basal conditions (P< or =0.01). During the oxytocin challenge test, MCA and ACA PI both decreased in the non-brain-sparing flow group (N=39) (P< or =0.02) but not in the brain-sparing flow group (P> or =0.4). The MCA-to-ACA PI ratio remained unchanged in both groups. de novo brain-sparing flow calculations revealed no preferential flow to any cerebral artery.. Cerebral circulatory responses to acute hypoxemia are synchronized in the middle and anterior cerebral arteries without any preferential regional flow distribution.

Topics: Adult; Anterior Cerebral Artery; Cerebrovascular Circulation; Female; Fetal Growth Retardation; Humans; Hypoxia; Middle Cerebral Artery; Oxytocin; Pregnancy; Regional Blood Flow; Telencephalon; Ultrasonography, Doppler; Ultrasonography, Prenatal; Uterine Contraction

Insufficient tissue oxygenation is a likely contribution to weak, inco-ordinate human uterine contractile activity characteristic of prolonged, dysfunctional labour. However, the direct effects of hypoxia on human myometrial contractility has, surprisingly, not yet been detailed. Therefore, we report the influence of hypoxia on spontaneous and agonist-induced carbachol, prostaglandin (PGF2alpha), and oxytocin contractions of myometria from nonpregnant and pregnant women.. Uterine biopsies were obtained from pregnant women at term undergoing elective Caesarean section and nonpregnant women undergoing hysterectomy. Myometrial strips were equilibrated at 37 degrees C in normoxic physiological salt solution (95% air/5% CO(2)) and the influence of hypoxia (95% N(2)/5% CO(2)) on contractility was investigated.. Hypoxia resulted in a significant reduction in spontaneous contractile function; nonpregnant tissue was less resistant to the deleterious effects of hypoxia. Agonist-induced contractions, while being more resistant to hypoxia than spontaneous contractions, were also significantly inhibited. In myometria of pregnant women the PGF2alpha- or oxytocin-induced contractility was more resistant to hypoxia than carbachol. Finally, the inhibitory actions of hypoxia were exacerbated with repeated oxytocin administration with a more severe effect on contractile integral than on initial phasic contraction amplitude.. We detail, for the first time, the effects of hypoxia on contractility of human myometria from nonpregnant and pregnant women. Physiologically important uterotonic agents are more resistant to the effects of hypoxia than spontaneous contractions although repeated stimulation with oxytocin during hypoxia results in progressively less force. The results indicate that if significant hypoxia occurs in vivo then it is a likely contributory factor to the pathways underlying prolonged dysfunctional labour.

Topics: Adult; Carbachol; Cesarean Section; Cholinergic Agonists; Dinoprost; Female; Humans; Hypoxia; Hysterectomy; Middle Aged; Oxygen; Oxytocics; Oxytocin; Parturition; Pregnancy; Tissue Culture Techniques; Uterine Contraction

Brain natriuretic peptide (BNP) levels are used in the evaluation of patients with heart disease, yet there is little understanding of the effect of hypoxia on natriuretic peptide secretion. Furthermore, recent data suggest that oxytocin may mediate stretch-induced atrial natriuretic peptide (ANP) secretion.. Ten patients with cyanotic congenital heart defects and 10 control subjects were studied. N-terminal proatrial natriuretic peptide and N-terminal probrain natriuretic peptide levels were 4-fold (P=0.02) and 12-fold (P=0.03) greater in cyanotic patients than in control subjects. Cyanotic patients had reduced body water compared with control subjects, although the difference did not reach statistical significance (P=0.22). In a separate group of patients, cardiac myocytes were isolated from the right atrial appendage during CABG. The amount of oxygen in the buffered saline was varied to simulate hypoxia. Isolated hypoxic atrial myocytes had 43% fewer dense surface secretory granules compared with normoxic myocytes (P<0.0001). Immunohistochemical staining demonstrated decreased ANP and BNP in hypoxic compared with normoxic right atrial tissue. Isolated myocytes also degranulated when incubated with oxytocin (P<0.0001), but there was no difference in oxytocin levels in cyanotic patients compared with control subjects (P=0.49).. ANP and BNP are markedly elevated in adults with cyanotic congenital heart disease despite reduced body water. Our results show that hypoxia is a direct stimulus for ANP and BNP secretion in human cardiac myocytes. These findings may have implications for the interpretation of BNP levels in the assessment of patients with heart and lung disease.

Topics: Adult; Atrial Appendage; Atrial Natriuretic Factor; Body Water; Cell Hypoxia; Cells, Cultured; Cyanosis; Cytoplasmic Granules; Female; Heart Defects, Congenital; Humans; Hypoxia; Male; Myocytes, Cardiac; Natriuretic Peptide, Brain; Oxygen; Oxytocin; Secretory Rate

Magnocellular neuroendocrine cells of the supraoptic nucleus of the hypothalamus produce and release the hormones vasopressin and oxytocin in response to a variety of stimuli to regulate body water and salt as well as and parturition and lactation. The aim of the present study was to estimate oxytocin release into the blood dialysate outflowing from the vicinity of the cavernous sinus and from the femoral vein after NMDA (N-methyl-D-aspartic acid) infusion or acute hypoxia.. The samples of dialysates of venous blood outflowing from the vicinity of the cavernous sinus and, for comparison, from the femoral vein were collected in anesthetized rats. Oxytocin was determined in the sample of dialysates by radioimmunoassay.. NMDA acid infusion or acute hypoxia caused an increase of oxytocin concentration in the blood dialysate outflowing from the vicinity of the cavernous sinus of the sella turcica and from the femoral vein. A blockade of the NMDA receptors by specific and non-specific antagonists significantly inhibited the increase in the blood dialysate oxytocin concentration.. The results indicate the involvement of excitatory amino acid or acute hypoxia in the control of oxytocin release into the blood.

Topics: Animals; Cavernous Sinus; Femoral Vein; Hypoxia; Male; N-Methylaspartate; Oxytocin; Quinoxalines; Rats; Rats, Wistar; Receptors, N-Methyl-D-Aspartate

Previous studies from our laboratory demonstrated that long-term hypoxia (LTH) altered in vitro contractile responses to oxytocin in full-thickness myometrial strips from pregnant sheep. The present study was designed to determine, first, if the reduced contractile response to oxytocin following LTH is the result of combined effects on longitudinal and circular smooth muscle or if the effect is specific to a single muscle layer and, second, if the reduced contractile response to oxytocin following LTH is caused by changes in oxytocin-receptor protein. Pregnant ewes were maintained at high altitude (3820 m) from Day 30 to Days 137-142 of gestation, when the ewes were killed for collection of myometrial tissue. Tissue was also collected from age-matched, normoxic controls. Longitudinal and circular layers were separated, length-tension curves generated to determine optimal resting tension, and all strips exposed to increasing half-log doses of oxytocin ranging from 10-12 to 10-6.5 M. The expression of oxytocin-receptor protein was measured using Western blot analysis. We found that LTH did not affect KCl-induced contraction of either smooth muscle layer, whereas the sensitivity of both myometrial layers to oxytocin was altered. A decreased maximum contractile response of the circular layer to oxytocin was also observed. Additionally, LTH decreased expression of oxytocin-receptor protein in the circular layer and increased levels in the longitudinal layer. Results from the present study indicate that LTH alters contractile responses and oxytocin-receptor protein expression in a layer-specific manner in the pregnant sheep myometrium.

Topics: Animals; Blotting, Western; Dose-Response Relationship, Drug; Female; Hypoxia; Muscle Contraction; Muscle, Smooth; Myometrium; Oxytocin; Pregnancy; Pregnancy, Animal; Receptors, Oxytocin; Sheep; Uterine Contraction

This study examined the effects of increased myometrial contracture frequency from 96 to 131 days' gestation on ovine fetal oxygen transport and physiologic response to acute hypoxemia.. Ten pregnant ewes received either saline solution (control, n = 5) or long-term administration of oxytocin (600 microU. kg-1. min-1) in 5-minute pulses every 20 minutes to the maternal jugular vein beginning at 96 days' gestation (n = 5). Maternal tracheal tubes, fetal carotid artery and jugular vein catheters, and electrocorticographic and electromyographic electrodes were placed with the animals under halothane general anesthesia at 122 days' gestation. At 131 days' gestation fetal hypoxemia was induced for 1 hour. Maternal and fetal arterial blood gas samples were obtained at 60, 15, and 5 minutes before the start of hypoxemia and at 5, 10, 20, 30, 40, 60, and 120 minutes after the start of hypoxemia.. Baseline PO2 before hypoxemia was significantly lower and oxygen content was significantly higher in fetuses in the long-term oxytocin group than in control fetuses. At the end of hypoxemia the fetal pH, oxygen saturation, and oxygen content were significantly higher in the long-term oxytocin group than in the control group, although PO2 did not differ between groups. The fetal blood oxygen dissociation curve was shifted to the left in the long-term oxytocin group. During hypoxemia the absolute fetal blood pH was higher and the blood pH variation was lower in long-term oxytocin group than in the control group. Lower baseline and hypoxia-induced fetal plasma cortisol concentrations were observed in fetuses in the long-term oxytocin group than in fetuses of control ewes.. Increased contracture frequency during a period of 35 days shifts the fetal oxygen dissociation curve toward the left and alters fetal response to acute hypoxemia.

Topics: Adrenocorticotropic Hormone; Animals; Female; Fetal Blood; Fetal Diseases; Gestational Age; Hydrocortisone; Hydrogen-Ion Concentration; Hypoxia; Kinetics; Oxygen; Oxytocin; Pregnancy; Sheep; Uterine Contraction

The state of hypothalamic oxytocin-synthesizing system in Wistar rats were investigating. The morphometric measurements and immunocytochemical detection of oxytocin-containing cells was used for determining of the functional state of supraoptic nucleus, anterior and posterior-medialis magnocellular subdivisions of paraventricular nucleus. It was established intermittent hypoxic training exert positive influence on rats with experimental diabetes mellitus. This effects depending on increasing synthesis and secretion of hypothalamic oxytocin. Intermittent hypoxic training elevate contents of immunoreactive oxytocin without changing morphometric characteristics in neurons of supraoptic and paraventricular nuclei and median eminence of hypothalamus. In comparison oxytocin contents in these neurons elevade less significance in diabetic rats, but it was observed increasing of nucleolus volume in hypothalamic oxytocin-synthesizing neurons. Intermittent hypoxic training of diabetic rats stimulate more significance elevating oxytocin contents in hypothalamic neurons and median eminence that evidence high level activity of hypothalamic oxytocin-synthesizing system.

Topics: Animals; Atmosphere Exposure Chambers; Diabetes Mellitus, Experimental; Fluorescent Antibody Technique; Hypothalamus; Hypoxia; Neurons; Oxytocin; Rats; Rats, Wistar; Time Factors

We designed the present study to determine: (1) if phenoxybenzamine can be used as an irreversible blocker for oxytocin receptors, and as such to determine oxytocin affinity, (2) if prolonged hypoxic exposure alters oxytocin receptor coupling efficacy of oxytocin receptors to post-receptor mediated mechanisms in the rat myometrium. Rats were exposed to room air (control), or to continuous hypoxia (10.5% O2) from day 19 through day 21 (2-day exposure). On day 21, one uterine horn was removed and used for in vitro study of myometrial contractile responses to oxytocin, while the other was used for oxytocin receptor analysis. In normoxic tissues, phenoxybenzamine (20 microM) decreased the maximum contractile response (EMAX) to oxytocin (155+/-17 vs. 66+/-19 g s/cm2) and oxytocin binding sites (BMAX: 253+/-35 vs. 114.9+/-21.3 fmol/mg protein). A similar degree of reduction in EMAX and BMAX were observed in hypoxic tissues. The oxytocin dissociation constant (KA) in the normoxic rat was 2.8+/-0.7 nM, which was not different from the chronic hypoxic rat (3.3+/-0.9 nM). Analysis of receptor occupancy-response curves indicated no oxytocin receptor reserve in both normoxic and hypoxic myometrium. However, for a given fraction of the total oxytocin receptors occupied, hypoxic tissue elicited a lower contractile response to oxytocin. We conclude that: (1) phenoxybenzamine is a useful tool to functionally study oxytocin receptor kinetics, (2) prolonged hypoxic exposure does not affect the oxytocin affinity, (3) no spare receptors for oxytocin are present in the rat myometrium, and (4) prolonged exposure to hypoxia decreases oxytocin receptor-effector coupling efficiency in rat myometrium.

Topics: Animals; Female; Hypoxia; In Vitro Techniques; Kinetics; Muscle Contraction; Myometrium; Oxytocin; Phenoxybenzamine; Pregnancy; Pregnancy, Animal; Protein Binding; Radioligand Assay; Rats; Rats, Sprague-Dawley; Receptors, Oxytocin; Vasodilator Agents

The mechanism causing peripheral oedema in hypoxaemic chronic obstructive pulmonary disease has not been established. Vasopressin, a powerful antidiuretic hormone involved in salt and water homeostasis, is released in response to acute hypoxia. However, the effect of prolonged hypoxaemia on hypothalamic and pituitary release of the magnocellular hypothalamic hormones, vasopressin and oxytocin, has not previously been studied.. Male Wistar rats were randomly allocated to either normobaric, hypoxic (10% O2) or control (21% O2) environmental chambers. An initial series of experiments examined plasma vasopressin concentration, osmolality, sodium concentration, packed cell volume (PCV), and weight gain at weekly intervals (n = 4-6) for six weeks. The maximum increase in plasma vasopressin concentration and PCV occurred after five weeks. In a second experiment vasopressin and oxytocin concentrations in the hypothalamus, pituitary gland, and plasma were measured in eight control and eight hypoxic rats after five weeks in the environmental chambers.. In rats exposed to environmental hypoxia PCV increased (p < 0.001) and weight gain decreased (p < 0.05) compared with controls. The plasma vasopressin concentration increased progressively from a baseline of 1.36 (0.2) pmol/l (n = 6) to a maximum of 4.38 (0.8) pmol/l (n = 6; p < 0.01) during the first five weeks of environmental hypoxia (difference 3.02 (95% CI 1.18 to 4.86)). Plasma osmolality and sodium concentration were unchanged in hypoxic rats compared with controls during the six week period. The hypothalamic vasopressin concentration was increased (p < 0.001) after five weeks of environmental hypoxia (91.6 (4.8) pmol/ hypothalamus) compared with controls (57.4 (5.1) pmol/hypothalamus), the difference being 34.2 pmol/hypothalamus (95% CI 21.6 to 46.5). The pituitary vasopressin concentration was unchanged. In hypoxic rats hypothalamic oxytocin (59.6 (3.2) pmol/hypothalamus) was greater (p < 0.01) than in controls (42 (3.8) pmol/hypothalamus), a difference of 17.6 pmol/ hypothalamus (95% CI 8.7 to 26.5). Similarly, the plasma oxytocin concentration was increased (p < 0.05) in hypoxic rats (6.78 (1.2) pmol/l) compared with controls (3.3 (0.8) pmol/l), a difference of 3.48 pmol/l (95% CI 0.89 to 6.07). The pituitary oxytocin concentration was unchanged in the two groups.. These results demonstrate an increase in hypothalamic production of vasopressin and oxytocin in rats during prolonged hypoxaemia. Increased plasma concentrations of neurohypophysial hormones would be expected to impair sodium and water homeostasis in patients with hypoxaemia. However, the absence of change in the plasma osmolality and sodium concentrations in this study and previous clinical investigations suggests that compensatory mechanisms modulate the actions of both vasopressin and oxytocin. A reduction in renal blood flow or decreased renal responsiveness to the neurohypophyseal hormones may be involved.

Topics: Animals; Hematocrit; Hypothalamus; Hypoxia; Male; Osmolar Concentration; Oxygen; Oxytocin; Pituitary Gland; Random Allocation; Rats; Rats, Wistar; Sodium; Vasopressins; Weight Gain

In light of our previous finding that chronic hypoxia decreases the myometrial contractile response to oxytocin in the near-term pregnant rat, we designed the current study (1) to investigate the effect of duration of hypoxic exposure on the contractile response to oxytocin and oxytocin binding sites and (2) to examine the effect of prolonged hypoxia on the contractile response to aluminum fluoride.. Rats were exposed to room air (control) or to continuous hypoxia (10.5% oxygen) from day 19 through day 21 (48-hour exposure), from day 20 through day 21 (24-hour exposure), or midday 20 through day 21 of gestation (12-hour exposure). On day 21 the uterine horns were used for oxytocin receptor analysis and for in vitro study of myometrial contractile responses to cumulative doses of oxytocin (10(-10) to 10(-6) mol/L) or aluminum fluoride (0.5 to 4.0 mmol/L sodium fluoride in 10 mumol/L aluminum chloride).. The maximal contractile tensions for the control and 12-hour exposure showed no difference. In contrast, 24-hour hypoxic exposure resulted in a reduction of the maximal contractile tension from 143 +/- 11 (control) to 116 +/- 7 gm x sec/cm2. By 48 hours the maximal contractile tension was reduced even further, to 44 +/- 13 gm x sec/cm2. Oxytocin binding sites followed a similar trend with values changing from 256.9 +/- 34.9 for control to 122.9 +/- 26.1 and 84.9 +/- 21.3 fmol/mg protein for the 24- and 48-hour exposure groups, respectively (p < 0.01, analysis of variance), with no change in the 12-hour group. The contractile responses to aluminum fluoride were not altered.. The suppression in the myometrial contractile response to oxytocin and oxytocin binding sites depends on the duration of hypoxic exposure. Chronic hypoxic exposure did not affect the myometrial response to aluminum fluoride.

Topics: Aluminum Compounds; Animals; Binding Sites; Dose-Response Relationship, Drug; Female; Fluorides; GTP-Binding Proteins; Hypoxia; Myometrium; Oxytocics; Oxytocin; Pregnancy; Rats; Rats, Sprague-Dawley; Receptors, Oxytocin; Sodium Fluoride; Time Factors; Uterine Contraction

Mechanisms involving the timing of normal parturition are not well understood in most animal species. To gain a greater understanding of the mechanisms, we employed hypoxia to perturb the normal system of parturition. The present study was designed to investigate the effects of chronic hypoxia on myometrial contractility in the near-term pregnant rat. Rats were exposed to room air (control) or to continuous hypoxia (10.5% O2) either from experimental days 19 through 21 (2-day exposure) or from experimental days 15 through 21 (6-day exposure). On day 21, blood was collected for hormone assays, and the uterine horns were collected from each dam. One horn was snap-frozen in liquid nitrogen for oxytocin (OT) receptor analysis, and the other was used for in vitro assessment of myometrial contractile responses to cumulative doses of OT or arginine vasopressin (AVP). Hypoxic exposure resulted in approximately 60% reduction of the maximal myometrial contractile response to OT and a significant reduction in OT binding sites from 256.9 +/- 34.9 to 84.9 +/- 21.3 fmol/mg protein (P<0.01). In contrast, the contractile response to AVP was unaffected after exposure to chronic hypoxia (P> 0.05). Additionally, we observed no difference in the plasma concentrations of estrogen, progesterone, and corticosterone. We conclude that chronic hypoxia decreased the effectiveness of OT-specific contractile mechanisms, at least partially through a decrease in OT binding sites.

Topics: Animals; Arginine Vasopressin; Corticosterone; Estrogens; Female; Hypoxia; In Vitro Techniques; Myometrium; Oxytocin; Pregnancy; Pregnancy Complications; Progesterone; Rats; Rats, Sprague-Dawley; Receptors, Oxytocin; Reference Values; Time Factors; Uterine Contraction

Hypothalamic mechanisms of neurohormone regulation of endocrine pancreas in diabetes mellitus, adaptation to hypoxia and their combination were studied on Wistar rats. To evaluate the condition of supraoptic nucleus (SON) secretory function, paraventricular subnuclei (PVH) of hypothalamus and endocrine pancreas, we used radioimmunoassay, immunocytochemical, morphometrical and histochemical methods. Hyperglycemia, hypoinsulinemia, glucagon and somatostatin synthesis and secretion intensification in diabetes mellitus is accompanied by marked reorganization of hypothalamic neurohormones (CRF, vasopressin, oxytocin) secretion with corresponding signs of activity increase of synthesizing their hypothalamus nuclei and subnuclei and also ACTH, corticosterone, cortisol rise in blood. Adaptation to hypoxia caused hypoglycemia, activated insulin biosynthesis, changed glucagon and somatostatin synthesis and secretion. CRF concentration, corticosterone and cortisol, ACTH in blood was not changed, vasopressin concentration lowered, oxytocin in median eminence of hypothalamus increased to a higher degree than in diabetes. Adaptation to hypoxia corrected impaired hormone balance and state of Langerhans islets (beta-cells destruction process inhibition, insulin biosynthesis stimulation, glucagon and somatostatin secretion decrease) in diabetes mellitus, hypothalamic neurohormones participating in this process.

Topics: Adaptation, Physiological; Animals; Blood Glucose; Corticotropin-Releasing Hormone; Diabetes Mellitus, Experimental; Glucagon; Hypothalamus; Hypoxia; Insulin; Islets of Langerhans; Oxytocin; Rats; Rats, Wistar; Somatostatin; Vasopressins

Low amplitude, long-lasting epochs of myometrial activity, contractures, occur throughout the majority of pregnancy in all species studied to date. Contractures are associated with a fall in fetal oxygenation and changes in fetal behavioral state. In the present study we observed that contractures produced by the administration of 70 mU oxytocin iv to the pregnant ewe at 125-139 days gestational age (term 145-150 days) result in a fall in fetal carotid arterial PO2 of approximately 2.5 mm Hg and are followed by a rise in fetal carotid arterial plasma ACTH of 16.3 +/- 9.6 pg.ml-1 (mean +/- SEM). When the contracture-induced fall in fetal arterial PO2 was prevented by administration of oxygen to the ewe, fetal ACTH did not rise after the contracture. In conclusion, these observations demonstrate that the relatively small fall in fetal PO2 that accompanies a contracture can be sensed by the fetus and is an essential part of the stimulus to the increased secretion of fetal ACTH that accompanies a contracture. These findings support the view that myometrial activity is one of the factors that influence fetal ACTH secretion.

Topics: Adrenocorticotropic Hormone; Animals; Carbon Dioxide; Female; Fetal Blood; Gestational Age; Hypoxia; Myometrium; Oxygen; Oxytocin; Partial Pressure; Sheep; Uterine Contraction

Acute and chronic pulmonary and systemic hemodynamic responses to arginine vasopressin (AVP) were examined in 4-wk hypoxia-adapted and air control rats. AVP, administered intravenously as bolus injections or sustained infusions, produced major dose-dependent V1-receptor-mediated reductions in mean pulmonary arterial pressure in hypoxia-adapted rats. These effects were comparable in pentobarbital-anesthetized, thoracotomized animals and in conscious, intact rats. Chronic infusions of AVP induced a sustained reduction in mean pulmonary arterial pressure and partially prevented the development of pulmonary hypertension without changing systemic arterial pressure. AVP induced significant decreases in cardiac output in both groups; the cardiac output response was not significantly different in hypoxia-adapted and air control animals. AVP induced almost no change in MPAP in air control rats. Furthermore the systemic pressor effects of AVP were significantly blunted in hypoxia-adapted rats compared with air controls. We conclude that the pulmonary depressor and blunted systemic pressor effects of AVP observed in hypoxia-adapted rats may be related to release of a vasodilator, such as endothelium-derived relaxing factor, vasodilator prostaglandins, or atrial natriuretic peptides. Further study is needed to elucidate these mechanisms and assess the usefulness of AVP and/or its analogues in the treatment and prevention of hypoxia-induced pulmonary hypertension.

Topics: Adaptation, Physiological; Anesthesia; Animals; Arginine Vasopressin; Blood Pressure; Cardiac Output; Chronic Disease; Consciousness; Hemodynamics; Hypoxia; Male; Oxytocin; Pulmonary Artery; Rats; Rats, Inbred Strains

The effect of hypoxemia on arginine vasopressin (AVP) and oxytocin (OT) release was investigated in the chronically catheterized fetus and ewe. During 30 min of 10% maternal oxygen delivery, mean (+/- SEM) arterial PO2 decreased from 105 +/- 10.6 to 48 +/- 3.5 mm Hg in the ewe and from 21 +/- 1.3 to 12 +/- 0.8 mm Hg in the fetus (each P less than 0.001). Arterial PCO2 decreased from 35 +/- 4.4 to 29 +/- 1.0 mm Hg in the ewe, whereas fetal PCO2 decreased from 43 +/- 2.3 to 35 +/- 3.5 mm Hg (P less than 0.05). Blood pH increased from 7.44 +/- 0.03 to 7.56 +/- 0.04 in the ewe (P less than 0.01) and from 7.36 +/- 0.004 to 7.40 +/- 0.006 in the fetuses (P less than 0.01). Baseline mean AVP levels were identical in ewes and fetuses (0.7 +/- 0.1 microU/ml). After 30 min of hypoxia, plasma AVP levels remained unchanged in the ewes (0.9 +/- 0.1), but increased dramatically in the fetuses (47 +/- 21 microU/ml) (P less than 0.001). There was a highly significant correlation between the duration of hypoxia and log fetal AVP concentrations (r = 0.85). The log fetal plasma AVP also was inversely correlated to the log fetal PO2 values (r = 0.83). Mean baseline fetal and maternal plasma OT levels were 2.6 +/- 0.5 microU/ml and 2.2 +/- 0.5 microU/ml, respectively. After 30 min of hypoxia fetal and maternal OT values were 2.9 +/- 0.8 microU/ml (not significant).

Topics: Animals; Arginine Vasopressin; Carbon Dioxide; Female; Fetal Hypoxia; Hydrogen-Ion Concentration; Hypercapnia; Hypoxia; Maternal-Fetal Exchange; Oxygen; Oxytocin; Pituitary Gland, Posterior; Pregnancy; Pregnancy Complications; Sheep

The role of hyperthermia in the absence of infection has been investigated in the pregnant baboon. Twenty-three near term animals were used. Catheters were placed in maternal and fetal arteries and thermocouples implanted in maternal colon and fetal esophagus. Maternal temperature was raised to between 41 and 42 degrees Centigrade (C.), by applying external heat. The temperature gradient between fetus and mother (delta T F-M) was 0.47 degree C. under steady-state conditions with maternal temperature at 38 degrees C. and rose to 0.75 degree C. at 42 degrees C. Hyperthermia caused a twofold increase in uterine activity; a metabolic acidosis developed in the mother and a profound acidosis and hypoxia developed in the fetus. There was also a marked fall in blood pressure and an increase in heart rate in both mother and fetus; late deceleration of the fetal heart rate occurred at a higher oxygen level and pHa than has been observed under normothermic conditions.

Topics: Acidosis; Animals; Arrhythmias, Cardiac; Body Temperature; Female; Fetal Death; Fetal Diseases; Fetal Heart; Fever; Haplorhini; Heart Rate; Hypotension; Hypoxia; Labor, Obstetric; Oxytocin; Papio; Pregnancy; Pregnancy Complications; Vasopressins

In our series of vaginal breech deliveries the morbidity from hypoxia and acidosis showed no difference to the same type of morbidity in our series of breech deliveries by Caesarean section. The correct selection of cases, intensive monitoring during labour and the management of the second stage of labour as outlined in our paper are the most important perequisites which permit to plan and justify a vaginal breech delivery in present obstetric practice.

Topics: Acidosis; Birth Injuries; Birth Weight; Breech Presentation; Cephalometry; Cesarean Section; Delivery, Obstetric; Dystocia; Extraction, Obstetrical; Female; Humans; Hypoxia; Infant Mortality; Infant, Newborn; Labor Presentation; Oxytocin; Paralysis, Obstetric; Pelvic Bones; Pelvimetry; Pregnancy; Radiography; Ultrasonography; Umbilical Cord

Topics: Adolescent; Adult; Anesthesia, Epidural; Anesthesia, Obstetrical; Bupivacaine; Female; Fetal Diseases; Humans; Hydrogen-Ion Concentration; Hypoxia; Infant, Newborn; Lactates; Oxytocin; Pregnancy; Pyruvates

Topics: Action Potentials; Adrenal Glands; Anesthesia; Animals; Electrophysiology; Estrus; Female; Hypercapnia; Hypophysectomy; Hypotension; Hypothalamus; Hypoxia; Methohexital; Neurons; Organ Size; Ovary; Oxytocin; Periodicity; Pituitary Gland; Pregnancy; Rats; Urethane; Uterus

Topics: Bilirubin; Birth Weight; Delivery, Obstetric; Female; Fetal Diseases; Germany, West; Gestational Age; Humans; Hypoxia; Infant, Newborn; Infant, Premature; Jaundice, Neonatal; Labor, Induced; Natural Childbirth; Oxytocin; Pregnancy; Pregnancy Complications

Topics: Female; Humans; Hypoxia; Infusions, Parenteral; Isoenzymes; L-Lactate Dehydrogenase; Labor, Induced; Lactates; Oxytocin; Pregnancy; Pyruvates

Topics: Cytodiagnosis; Female; Fetal Diseases; Humans; Hypoxia; Labor, Induced; Methods; Oxytocin; Pregnancy; Pregnancy Complications; Pregnancy, Prolonged

Topics: Animals; Electric Stimulation; Ganglia, Autonomic; Glucagon; Glycogen; Hexoses; Histocytochemistry; Hydrocortisone; Hypoxia; Insulin; Microscopy, Electron; Neurons; Oxytocin; Rats; Vasopressins

Topics: Chlorpromazine; Extraembryonic Membranes; Female; Fetal Death; Fetus; Histamine H1 Antagonists; Humans; Hypoxia; Labor Presentation; Labor, Obstetric; Maternal Mortality; Meperidine; Muscles; Natural Childbirth; Obstetric Labor, Premature; Oxytocin; Pregnancy; Uterine Inertia

Topics: Birth Injuries; Brain Injuries; Cesarean Section; Female; Fetal Death; Humans; Hyaline Membrane Disease; Hypoxia; Infant Mortality; Infant, Newborn; Labor Presentation; Obstetric Labor Complications; Oxytocin; Parity; Pregnancy; Pulmonary Atelectasis; Statistics as Topic; Vitamin K Deficiency Bleeding

Topics: Animals; Arginine Vasopressin; Biological Transport; Biological Transport, Active; Bombyx; Chlorthalidone; Cholinesterase Inhibitors; Dinitrophenols; Epinephrine; Hypoxia; Intestinal Absorption; Iodoacetates; Ion Transport; Ouabain; Oxytocin; Pharmacology; Potassium; Research; Sodium; Sulfides; Sulfonamides; Vasopressins

Topics: Acetylcholine; Adaptation, Physiological; Animals; Birds; Blood Circulation; Coronary Vessels; Dibenzylchlorethamine; Epinephrine; Hexamethonium Compounds; Hyperemia; Hypoxia; Isoproterenol; Norepinephrine; Oxytocin; Vasopressins

Topics: Amniotic Fluid; Female; Fetal Diseases; Fetal Distress; Humans; Hypoxia; Labor, Obstetric; Oximetry; Oxygen; Oxytocin; Pregnancy

Synthetic oxytocin (Syntocinon) can be shown to reduce or abolish ST-T changes induced experimentally by hypoxaemia alone, by hypoxaemia and ergometrine, by vasopressin, and by a new procedure involving injection of small doses of picrotoxin into the lateral cerebral ventricle. Ventricular fibrillation induced by picrotoxin can also be reversed by oxytocin. These effects suggest a probable metabolic action of oxytocin against cardiac anoxic changes, and its possible therapeutic usefulness as an antagonist of myocardial ischaemia. It is speculated that this might be a physiological action of the hormone.

Topics: Animals; Arginine Vasopressin; Electrocardiography; Ergonovine; Hypoxia; Myocardial Ischemia; Oxytocics; Oxytocin; Rabbits; Vasopressins