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coronary vasospasm/tyrosine
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6 risultati
Coronary artery spasms due to tyrosine kinase inhibitors used in chronic myeloid leukemia.
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Tyrosine kinase inhibitors (TKIs) have changed the landscape of treatment for patients with chronic myeloid leukemia (CML) leading to a life expectancy comparable to the general population. Side effects commonly encountered during TKI treatment are pleural effusion due to use of dasatinib and
Hypoxia-reoxygenation triggers coronary vasospasm in isolated bovine coronary arteries via tyrosine nitration of prostacyclin synthase.
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The role of peroxynitrite in hypoxia-reoxygenation-induced coronary vasospasm was investigated in isolated bovine coronary arteries. Hypoxia-reoxygenation selectively blunted prostacyclin (PGI2)-dependent vasorelaxation and elicited a sustained vasoconstriction that was blocked by a cyclooxygenase
Proteinase-activated receptors 1 and 2 and the regulation of porcine coronary artery contractility: a role for distinct tyrosine kinase pathways.
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OBJECTIVE
Because angiotensin-II-mediated porcine coronary artery (PCA) vasoconstriction is blocked by protein tyrosine kinase (PYK) inhibitors, we hypothesized that proteinase-activated receptors (PARs), known to regulate vascular tension, like angiotensin-II, would also cause PCA contractions via
Sorafenib-associated multivessel coronary artery vasospasm.
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Cardiotoxicity associated with cancer treatment is an important field of interest especially as the new class of VEGF signaling pathway inhibitors (VSP) continues to grow. Small molecule tyrosine kinase inhibitors such as sorafenib, sunitinib, and pazopanib inhibit the downstream pathways of all
Endothelin-1--induced enhancement of coronary smooth muscle contraction via MAPK-dependent and MAPK-independent [Ca(2+)](i) sensitization pathways.
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Endothelin-1 (ET-1) has been implicated in coronary vasospasm by enhancing coronary vasoconstriction to vasoactive eicosanoids, and a role for protein kinase C (PKC) activation has been suggested. However, the cellular mechanisms downstream from PKC activation are unclear. We investigated whether
Phosphorylation in coronary artery cold-induced contraction in the newborn lamb.
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Myocardial dysfunction after hypothermic protection has been linked to various mechanisms. Coronary vasospasm in particular may be responsible for ischemic injury during reperfusion. Herein we hypothesized that coronary arteries (CA) sustain a cold-induced contraction during hypothermia mediated by
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