Search results for "Vasospasm"

Changes in the cerebrovascular effects of endothelin-1 and nicardipine after experimental subarachnoid hemorrhage.

1993

The role of endothelium-related factors in the pathogenesis of cerebral vasospasm after subarachnoid hemorrhage (SAH) has gained interest since the discovery of endothelin-1 (ET-1). We have examined, before and after SAH, the responsiveness of the cerebrovascular bed of the goat to ET-1, the sources of Ca2+ in ET-1-induced responses, and the ability of the Ca2+ entry blocker nicardipine to counteract them. Before SAH, injection of ET-1 into the cerebral circulation increased cerebrovascular resistance, thereby producing dose-dependent reductions in cerebral blood flow (CBF), which were prevented by nicardipine. In isolated middle cerebral arteries, ET-1 induced concentration-dependent contr…

Effect of Intra-Arterial Infusion of Papaverine Hydrochloride on Brain Tissue Oxygen Pressure in the Management of Severe Vasospasm Following Aneurys…

2001

Despite considerable advances in diagnostic, surgical and interventional techniques, the overall outcome for patients with aneurysmal subarachnoid hemorrhage remains poor. Concerning perioperative course, cerebral ischaemia is one of the major factors causing secondary brain demage. The aim of all therapeutic interventions is the stabilization and maintance of cerebral blood flow and tissue oxygenation in order to prevent cerebral ischaemia and consecutively brain infarction [1].

ERYTHROPOIETIN FOR THE TREATMENT OF SUBARACHNOID HEMORRAGE: A FEASIBLE INGREDIENT FOR A SUCCESS MEDICAL RECIPE

2015

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 morbidity and mortality. Cerebral vasospasm occurs in more than half of all patients after aneurysm rupture and is recognized as the leading cause of delayed cerebral ischemia after SAH. Hemodynamic strategies and endovascular procedures may be considered for the treatment of cerebral vasospasm. In recent years, the mechanisms contributing to the development of vasospasm, abnormal reactivity of cerebr…

Ruolo dell'eritropoietina nel trattamento del vasospasmo cerebrale: stato dell'arte. SINCH

2012

New cerebral protection strategies.

2005

PURPOSE OF REVIEW This article presents an overview of the most recent and important strategies to reduce secondary brain damage. RECENT FINDING There is currently no magic bullet available to protect the brain after neuronal injury. This is related to the complex pathophysiology of cerebral ischemia, which makes it unlikely that a single pharmacological intervention results in sustained neuroprotection. Analyses of clinical studies reveal that acute physiologic derangements (e.g. fever, hypertension and hypotension, hypoxemia, hypercapnia, hyperglycemia) are the most important predictors of unfavorable outcome after brain injury and have to be treated. The effectiveness of anesthetic agent…

Impairment of the modulatory role of nitric oxide on the endothelin-1-elicited contraction of cerebral arteries: a pathogenetic factor in cerebral va…

1997

OBJECTIVE: Nitric oxide (NO) and endothelin-1 (ET-1) are two endothelium-derived factors probably involved in the pathogenesis of cerebral vasospasm after subarachnoid hemorrhage (SAH). Our aim was twofold, i.e., to ascertain whether endothelial and nonendothelial NO modulates the contractile response of cerebral arteries to ET-1 and to analyze whether this relationship might be impaired after experimental SAH. METHODS: Rings of middle cerebral artery from goats in the control group and from goats with SAH were set up for isometric tension recordings. SAH was induced 3 days before the experiments by infusion of 10 ml of autologous arterial blood through a catheter previously inserted into t…

Management of aneurysmal subarachnoid hemorrhage: State of the art and future perspectives

2017

Background: Aneurysmal subarachnoid hemorrhage (SAH) accounts for 5% of strokes and carries a poor prognosis. It affects around 6 cases per 100,000 patient years occurring at a relatively young age. Methods: Common risk factors are the same as for stroke, and only in a minority of the cases, genetic factors can be found. The overall mortality ranges from 32% to 67%, with 10–20% of patients with long-term dependence due to brain damage. An explosive headache is the most common reported symptom, although a wide spectrum of clinical disturbances can be the presenting symptoms. Brain computed tomography (CT) allow the diagnosis of SAH. The subsequent CT angiography (CTA) or digital subtraction …

Comparing the Outcomes of Different Agents to Treat Vasospasm at Microsurgical Anastomosis during the Papaverine Shortage.

2017

Letter to Editor

Executive summary of the joint position paper on renal denervation of the Cardiovascular and Interventional Radiological Society of Europe and the Eu…

2016

Renal denervation (RDN) was reported as a novel exciting treatment for resistant hypertension in 2009. An initial randomized trial supported its efficacy and the technique gained rapid acceptance across the globe. However, a subsequent large blinded, sham arm randomized trial conducted in the USA (to gain Food and Drug Administration approval) failed to achieve its primary efficacy end point in reducing office blood pressure at 6 months. Published in 2014 this trial received both widespread praise and criticism. RDN has effectively stopped out with clinical trials pending further evidence. This joint consensus document representing the European Society of Hypertension and the Cardiovascular…

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

2004

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 arteries and cerebral ischemia after SAH have been intensively investigated in recent years. It has been suggested that the pathogenesis of vasospasm is related to a number of pathological processes, including endothelial damage, smooth muscle cell contraction resulting from spasmogenic substances generated during lyses of subarachnoid blood clots, changes in vascular responsiveness and inflamma…