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forskolin/krvarenje

Veza se sprema u međuspremnik
Stranica 1 iz 24 rezultatima
OBJECTIVE Compaction of extracellular matrix (ECM) lattices by cultured fibroblasts was accelerated by cerebrospinal fluid (CSF) from patients with subarachnoid hemorrhage (SAH). The rate of acceleration was significantly related to the clinical grade of vasospasm. However, the mechanism remains

The effect of subarachnoid hemorrhage on mechanisms of vasodilation mediated by cyclic adenosine monophosphate.

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OBJECTIVE This study was designed to determine whether subarachnoid hemorrhage (SAH) affects the function of the K+ channels responsible for relaxation of canine cerebral arteries in response to adenylate cyclase activation. METHODS The effect of K+ channel inhibitors on the arterial relaxation
Haemorrhagic diatheses due to platelet function defects are a heterogenous and poorly understood group of conditions. We report the investigation of a female with a lifelong history of epistaxes, haemarthroses, menorrhagia and persistent iron-deficiency anaemia. Although platelet numbers and

Reactive nitrogen species inhibit alveolar epithelial fluid transport after hemorrhagic shock in rats.

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Our recent experimental work demonstrated that a neutrophil-dependent inflammatory response in the lung prevented the normal up-regulation of alveolar fluid clearance by catecholamines following hemorrhagic shock. In this study, we tested the hypothesis that the release of NO within the airspaces of

Relaxation of subarachnoid hemorrhage-induced spasm of rabbit basilar artery by the K+ channel activator cromakalim.

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OBJECTIVE Cerebral vasospasm resulting from subarachnoid hemorrhage (SAH) is refractory to most vasodilators. However, despite evidence that a mechanism underlying the vasospasm may be smooth muscle cell membrane depolarization resulting from decreased K+ conductance, the ability of K+ channel
Calcitonin gene-related peptide (CGRP) is a potent vasodilator and a primary signaling molecule in neurovascular communication. In the present study, the authors examined cerebrovascular responses to CGRP and its related second messenger systems during cerebral vasospasm induced by subarachnoid

beta-adrenergic desensitization after burn excision not affected by the use of epinephrine to limit blood loss.

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BACKGROUND Burn patients have impaired myocardial function and decreased beta-adrenergic responsiveness. Further beta-adrenergic dysfunction from systemic absorption of topically administered epinephrine that is given to limit blood loss during burn excision could affect perioperative management.
We have examined platelet functional responses and characterized a novel signaling defect in the platelets of a patient suffering from a chronic bleeding disorder. Platelet aggregation responses stimulated by weak agonists such as adenosine diphosphate (ADP) and adrenaline were severely impaired. In

Molecular bases of defective signal transduction in the platelet P2Y12 receptor of a patient with congenital bleeding.

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We have identified structural attributes required for signal transduction through a seven-transmembrane-domain receptor. Platelets from a patient (AC) with a congenital bleeding disorder had normal shape change but reduced and reversible aggregation in response to 4 microM ADP, similar to normal
Choriocarcinoma (CC) is characterized by earlier blood metastasis compared with other female genital tumors and a high incidence of massive hemorrhage. Vasculogenic mimicry (VM) is highly associated with metastasis, and syncytiotrophoblast is involved in the formation of VM in CC. Forskolin is a
BACKGROUND Among the prostanoids, thromboxane (TX) A(2) is a potent stimulator of platelets, whereas prostaglandin (PG) I(2) inhibits their activation. The roles of PGE(2) in the regulation of platelet function have not been established, however, and the contribution of PGE(2) in hemostasis and

Measurement of adhesion of human platelets in plasma to protein surfaces in microplates.

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BACKGROUND Platelet adhesion is an initial, crucial and complex event for inhibiting blood loss upon vascular injury. Activation and adhesion of platelets also play a fundamental role in the development of thrombosis. A combination of exposed extracellular matrix proteins in the vascular wall and

Stimulation of contractions in human myometrium by serotonin is unmasked by smooth muscle relaxants.

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OBJECTIVE The aim of this study was to investigate the ability of serotonin to increase contractions in human myometrium. METHODS Isometric tension measurements were used to determine the effect of increasing doses of serotonin on strips of human myometrium obtained at the time of cesarean

Impaired adenylate cyclase activity of phenylhydrazine-induced reticulocytes.

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A method which involves Percoll gradient centrifugation, is described for separating rabbit reticulocytes from other blood cells, including erythrocytes. This permits a quantitative comparison of the adenylate cyclase activity of reticulocyte membranes which had been induced either by bleeding (30%

Rapid stimulation of human renal ENaC by cAMP in Xenopus laevis oocytes.

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Among the compensatory mechanisms restoring circulating blood volume after severe haemorrhage, increased vasopressin secretion enhances water permeability of distal nephron segments and stimulates Na(+) reabsorption in cortical collecting tubules via epithelial sodium channels (ENaC). The ability of
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