spasmogenic/ischemia

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Spasmogenic Effects of the Proteasome Inhibitor Carfilzomib on Coronary Resistance, Vascular Tone and Reactivity.

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BACKGROUND Carfilzomib (CFZ) is a new proteasome inhibitor used for the treatment of multiple myeloma. Besides heart failure, angina and myocardial ischemia occurred following administration of CFZ, which is not contraindicated in patients with recent myocardial infarction/unstable angina excluded

The three phases of vasospasm.

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We propose the theory that prolonged cerebral vasospasm involves three phases: (1) the initial muscular contraction of the arterial wall; (2) a secondary injury to the artery that consists of endothelial desquamation with adherence of platelets to te denuded internal elastic lamina and mural

Prevention of ventricular fibrillation, acute myocardial infarction (myocardial necrosis), heart failure, and mortality by bretylium: is ischemic heart disease primarily adrenergic cardiovascular disease?

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It is widely, but mistakenly, believed that ischemic heart disease (IsHD) and its complications are the sole and direct result of reduced coronary blood flow by obstructive coronary artery disease (CAD). However, cardiac angina, acute myocardial infarction (AMI), and sudden cardiac death (SCD) occur

Effects of barbiturates, phencyclidine, ketamine and analogs on cerebral circulation and cerebrovascular muscle.

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Although barbiturates are often effective as therapeutic agents in several types of brain ischemia, there is no consensus as to their mechanisms of action. Exactly why other intravenous anesthetics such as ketamine are not effective therapies in brain ischemia is not known. Structural analogs of

Physiopathological criteria of vasospasm treatment.

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Cerebral vasospasm following aneurysmal subarachnoid hemorrhage is one of the most important causes of cerebral ischemia, and is the leading cause of death and disability after aneurysmal rupture. The optimal treatment of vasospasm awaits development of agents for blocking or inactivating

An overview of new pharmacological treatments for cerebrovascular dysfunction after experimental subarachnoid hemorrhage.

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Cerebral vasospasm and the resulting cerebral ischemia occurring after subarachnoid hemorrhage (SAH) are still responsible for the considerable morbidity and mortality in patients affected by cerebral aneurysms. Mechanisms contributing to the development of vasospasm, abnormal reactivity of cerebral

Mechanisms of magnesium-induced vasodilation in cerebral penetrating arterioles.

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We investigated in cerebral penetrating arterioles the signaling mechanisms and dose-dependency of extracellular magnesium-induced vasodilation and also its vasodilatory effects in vessels preconstricted with agonists associated with delayed cerebral vasospasm following SAH. Male rat penetrating

[Spasm of the renal and digestive arteries. Radiologic aspect].

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Spasms of the mesenteric and renal arteries are of great concern to the radiologist specialized in angiography. In most cases, they appear to be of iatrogenic origin, due to difficulties in selective catheterization and especially in superselective catheterization of the mesenteric and renal

New perspectives on the function of coronary artery spasm in acute myocardial infarction: the thromboischemic reentry mechanism. A review of 10 years research on the pathophysiology of AMI.

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Research during the last ten years into the pathophysiology of acute myocardial infarction (AMI) has made it gradually clearer that this is a phasic event. A number of independent authors have made this conclusion quite obvious. The authors of this review suggest that the alternating sequence of

Expression of vascular endothelial growth factor (VEGF) in rat brain after subarachnoid haemorrhage and endothelin receptor blockage with BQ-123.

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Cerebral vasospasm is one of the most severe complications of subarachnoid haemorrhage (SAH), leading to pathological changes in the vessel wall itself and in the nervous tissue, due to ischaemia of endothelial cells and neurones. Amongst the known substances inducing vasospasm, the most potent

Erythropoietin for the treatment of subarachnoid hemorrhage: A feasible ingredient for a successful medical recipe.

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Subarachnoid hemorrhage (SAH) following aneurysm bleeding accounts for 6% to 8% of all cerebrovascular accidents. Although an aneurysm can be effectively managed by surgery or endovascular therapy, delayed cerebral ischemia is diagnosed in a high percentage of patients resulting in significant

Cerebrovascular reactivity: role of endothelium/platelet/leukocyte interactions.

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In the last two decades, a tremendous amount of knowledge has been accumulated in various fields of biomedical research that discloses mechanisms of platelet/leukocyte/endothelium interactions. Occupying a strategically important location between circulating blood and underlying tissues, the

Vascular KCNQ (Kv7) potassium channels as common signaling intermediates and therapeutic targets in cerebral vasospasm.

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Cerebral vasospasm after subarachnoid hemorrhage (SAH) is characterized by prolonged severe constriction of the basilar artery, which often leads to ischemic brain damage. Locally elevated concentrations of spasmogenic substances induce persistent depolarization of myocytes in the basilar artery,

Endothelin and subarachnoid hemorrhage: an overview.

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BACKGROUND Delayed cerebral vasospasm occurring after subarachnoid hemorrhage (SAH) is still responsible for a considerable percentage of the morbidity and mortality in patients with aneurysms. It has been suggested that the pathogenesis of delayed cerebral vasospasm is related to a number of

Cysteinyl leukotriene signaling aggravates myocardial hypoxia in experimental atherosclerotic heart disease.

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BACKGROUND Cysteinyl-leukotrienes (cys-LT) are powerful spasmogenic and immune modulating lipid mediators involved in inflammatory diseases, in particular asthma. Here, we investigated whether cys-LT signaling, in the context of atherosclerotic heart disease, compromises the myocardial

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