prostaglandin/hypoxia

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Hypoxia upregulates cyclooxygenase-2 and prostaglandin E(2) levels in human peritoneal fibroblasts.

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OBJECTIVE To determine the levels of COX-1, COX-2, and prostaglandin (PG) E(2) in human fibroblasts isolated from normal peritoneal and adhesion tissues. METHODS Prospective experimental study. METHODS University medical center. METHODS Fibroblast cultures from both peritoneum and adhesion tissues

Hypoxia Induces Macrophage tnfa Expression via Cyclooxygenase and Prostaglandin E2 in vivo.

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Macrophage phenotypes are poorly characterized in disease systems in vivo. Appropriate macrophage activation requires complex coordination of local microenvironmental cues and cytokine signaling. If the molecular mechanisms underpinning macrophage activation were better understood,

[The role of the prostaglandin system in the cardioprotective effect of adaptation to hypoxia in stress].

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The adaptation to periodic altitude hypoxia is known to have cardioprotective and antiarrhythmic effects in stress-induced and ischemic lesions. The effects are assumed to be associated with the enhanced activity of the body's stress-limiting systems, including prostaglandins (PG). Wistar rats were

The effect of acute hypoxia on prostaglandin release in perfused human fetal placenta.

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The release of prostaglandin E2 and F2 alpha, thromboxane B2 and 6-keto-prostaglandin F1 alpha was measured in isolated human placental cotyledons perfused under high- and low-oxygen conditions. Also the effect of reoxygenation on prostaglandin production was studied. During the high-oxygen period,

The effect of hydrogen peroxide on hypoxia, prostaglandin F2 alpha and potassium chloride induced contractions in isolated rat pulmonary arteries.

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We have investigated the action of the product of the enzyme NADPH oxidase; hydrogen peroxide (H2O2), on the first phase of the hypoxic contraction, prostaglandin F2 alpha (PGF2 alpha)-induced contractions and potassium chloride (KCl)-induced contractions, in isolated rat pulmonary arteries in a

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

Contribution of prostaglandins in hypoxia-induced vasodilation in isolated rabbit hearts. Relation to adenosine and KATP channels.

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The mechanism of hypoxia-induced coronary vasodilation was studied in isolated, saline-perfused rabbit hearts under constant flow conditions. Reduction in the perfusion solution PO2 (from 520 +/- 6 to 103 +/- 9 mm Hg) under control conditions halved the coronary resistance and was accompanied by a

Hypoxia modifies the vasodilatory effects of nitroglycerin, prostaglandin E1, and hydralazine on isolated porcine coronary arteries.

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To evaluate the potency of vasodilatory drugs in hypoxia, we studied the effects of nitroglycerin (NTG), prostaglandin E1 (PGE1), and hydralazine on porcine coronary artery constricted with endothelin-1 (ET-1) in both oxygenated and hypoxic conditions. Removal of endothelium potentiated NTG-induced

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,

Regulation of rat intrapulmonary arterial tone by arachidonic acid and prostaglandin E2 during hypoxia.

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OBJECTIVE Arachidonic acid (AA) and its metabolites, prostaglandins (PG) are known to be involved in regulation of vascular homeostasis including vascular tone and vessel wall tension, but their potential role in Hypoxic pulmonary vasoconstriction (HPV) remains unclear. In this study, we examined

Does hypoxia selectively stimulate the generation of prostaglandin E1 by the isolated rat uterus?

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The contractile activity of uterine horns maintained for 90 to 120 minutes under normal oxygenation (carbogen or 100% O2) became undetectable. When in this condition the gassing was stopped one or two minutes later, regular phasic contractions appeared super-imposed on a small increment of the basal

Inhibitory effect of hydrocortisone on the release of prostaglandins from dog's brain in hypoxia and cerebral embolism.

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Cerebral hypoxia and embolism evoke the release of prostaglandin (PG)-like substances, predominantly of E type, into cerebral venous blood. This has been shown by bioassay used for monitoring the level of PG-like substances in sagittal sinus blood (ssb) in dogs. Hypoxia was induced by inhalation of

Protective effect of prostaglandins D2, E1 and I2 against cerebral hypoxia/anoxia in mice.

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The protective effect of prostaglandins (PGs) against cerebral hypoxia/anoxia was investigated with a variety of experimental models in relation to their CNS depressant effects in mice. Furthermore, the effect of PGs on the changes of cerebral energy metabolites and cyclic nucleotide was examined in

Prostaglandin content in blood and lung tissue during alveolar hypoxia.

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The aim of the present work was to investigate whether prostaglandins (PGs) are synthetized and released from isolated blood-perfused rat and cat lungs secondary to vasoconstriction induced by alveolar hypoxia. The lungs were perfused with autologous blood with constant volume inflow via the

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