alpha prostaglandin f 2/hypoxia

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Cloprostenol, a prostaglandin F(2alpha) analog, induces hypoxia in rat placenta: BOLD contrast MRI.

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Blood oxygen level dependent (BOLD) contrast was used to monitor hypoxia induced by cloprostenol, a prostaglandin F(2alpha) (PGF(2alpha)) analog, in the rat embryo-placental unit (EPU). It is shown that administration of cloprostenol (0.025 mg/rat) at mid-gestation (day 16) reduced EPU oxygenation,

Protective effects of a prostaglandin oligomer on rats exposed to hypoxia.

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To study the protective effects of a prostaglandin E1 oligomer against hypoxia, hypoxia was induced in artificially ventilated rats by replacing the air with 100% nitrogen under anesthesia. Parameters such as survival rate, blood pressure, electrocardiogram, blood lactate, glucose, pH, PO2, PCO2,

Effect of graded hypoxia on activin A, prostaglandin E2 and cortisol levels in the late-pregnant sheep.

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The aim of the present study was to determine whether activin A concentrations are dependent on feto-placental oxygen availability and to investigate the temporal relationship of activin A with prostaglandin (PG) E(2) and cortisol. Nine fetal sheep (six hypoxic and three control) were instrumented

Cyclooxygenase-2 inhibition and hypoxia-induced pulmonary hypertension: effects on pulmonary vascular remodeling and contractility.

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Pulmonary arterial hypertension (PAH) is a significant disease process characterized by elevated pulmonary vascular resistance leading to increased right ventricular afterload and ultimately progressing to right ventricular dysfunction and often death. Irreversible remodeling of the pulmonary

Role of prostaglandins in mediating differences in human internal mammary and radial artery relaxation elicited by hypoxia.

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The effects of hypoxia-reoxygenation on internal mammary (IMA) and radial (RA) arteries used for coronary artery bypass grafting (CABG) were examined to identify mechanisms regulating contractile function and differences that could contribute to vasospasm. Isolated endothelium-intact IMA and RA

Prostaglandin mediated relaxation of coronary artery strips under hypoxia.

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Strips of beef coronary branch arteries, maintained in vitro, respond to decreased PO2 in the bathing medium with relaxations which are much attenuated by pretreatment with indomethacin or aspirin. It was determined that these hypoxia-induced relaxations are sustained until strips are returned to an

Potentiation by hypoxia of contractions caused by angiotensin II in dog and monkey cerebral arteries.

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OBJECTIVE Hypoxia alters the responsiveness to endogenous substances of cerebral arteries, possibly resulting in the modulation of blood supply to ischemic brain regions. The present study was undertaken to analyze the mechanism of potentiation by hypoxia of angiotensin II-induced cerebroarterial

Feto-placental hypoxemia regulates the release of fetal activin A and prostaglandin E(2).

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The evaluation of the role of critical hypoxia in unexplained fetal death in utero has been hampered by the lack of a physiological marker. Here we report the novel observation that feto-placental hypoxemia is an acute trigger for increased activin secretion from the feto-placental unit in late

Anoxia-induced release of prostaglandins in rabbit isolated hearts.

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We investigated the relationship between prostaglandin release and the coronary vasodilation evoked by anoxia. Isolated rabbit hearts were perfused via the aorta with Krebs-Ringer's solution. The coronary effluent was bioassayed continuously in terms of prostaglandin E2 for prostaglandinlike

IL-1 beta depresses respiration and anoxic survival via a prostaglandin-dependent pathway in neonatal rats.

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IL-1 beta has been proposed to be an important mediator linking infection, apnea, and sudden infant death syndrome. We hypothesized that IL-1 beta acts in this capacity by depressing brainstem respiratory neurons via a prostaglandin-dependent pathway. For studying the effects of IL-1 beta on

Absence of cyclooxygenase-2 exacerbates hypoxia-induced pulmonary hypertension and enhances contractility of vascular smooth muscle cells.

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BACKGROUND Cyclooxygenase-2 (COX-2) is upregulated in pulmonary artery smooth muscle cells (PASMCs) during hypoxia and may play a protective role in the response of the lung to hypoxia. Selective COX-2 inhibition may have detrimental pulmonary vascular consequences during hypoxia. RESULTS To

Mitochondrial dysfunction during anoxia and acute cell injury.

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Mitochondrial function is closely linked to the maintenance of mitochondrial integrity. During short-term anoxia, ion-transport systems in the inner membrane are inhibited to protect against loss of the promotive force and associated osmotic imbalance that can cause irreversible loss of

Hypoxia induced activin secretion by the fetoplacental unit: differential responses related to gestation.

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OBJECTIVE To determine whether activin A levels reflect oxygen availability in basal and hypoxic conditions in the late pregnant fetus and newborn lamb. METHODS In vivo animal experimental study. METHODS Department of Physiology, Monash University. METHODS Chronically catheterised fetal sheep in

Thrombospondin-1 null mice are resistant to hypoxia-induced pulmonary hypertension.

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OBJECTIVE Chronic hypoxia induces pulmonary hypertension in mice. Smooth muscle cell hyperplasia and medial thickening characterize the vasculature of these animals. Thrombospondin-1 null (TSP-1(-/-)) mice spontaneously develop pulmonary smooth muscle cell hyperplasia and medial thickening. In

Effects of hypoxia and recovery on brain eicosanoids and carbohydrate metabolites in rat brain cortex.

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The effects of hypoxia (respiration of 5% O2 for 30 min) and recovery (respiration of air up to 30 min) on brain levels of carbohydrate metabolites, of free arachidonate (FAA) and of several eicosanoids (E) were studied in the rat. Animals were sacrificed before or after 30 min of hypoxia, and

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