Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of the current study was to examine the effects of 10 degrees reverse Trendelenburg position (rTp) on subdural intracranial pressure (ICP), cerebral perfusion pressure (CPP), and dural tension. Additionally, the relationship between preoperative Hunt and Hess (H and H) grade and the subdural ICP in patients scheduled for cerebral aneurysm surgery was investigated. Twenty-eight consecutive patients with a cerebral aneurysm were subjected to craniotomy in propofol/fentanyl or propofol/remifentanil anesthesia. Subdural ICP was measured after opening of the bone flap and exposure of dura. After reference measurements of subdural ICP and mean arterial blood pressure (MABP), the measurements were repeated during 10 degrees rTp. No significant differences between the anesthetic groups were disclosed. During 10 degrees rTp, a significant decrease in MABP, ICP, and jugular bulb pressure was observed whereas CPP remained unchanged. In H and H 0 patients (unruptured aneurysm), the ICP decreased from 2.9 +/- 2.6 mmHg to 0.4 +/- 2.2 mmHg at 10 degrees rTp. In H and H I to II patients, the ICP decreased from 9.3 +/- 3.8 mmHg to 4.6 +/- 3.3 mmHg at 10 degrees rTp. A significant difference in the mean baseline subdural ICP and DeltaICP (change in ICP) was found between patients with unruptured aneurysm and patients with subarachnoid hemorrhage (H&H I and II). Furthermore, the relationship between the subdural ICP at neutral position and DeltaICP was significant. In patients without intracranial hypertension, 10 degrees rTp decreases subdural ICP and dural tension in patients with ruptured as well as patients with unruptured cerebral aneurysm; CPP is unchanged.
 ...
PMID:The effects of 10 degrees reverse Trendelenburg position on subdural intracranial pressure and cerebral perfusion pressure in patients subjected to craniotomy for cerebral aneurysm. 1636 35

Despite advances in surgical techniques and improvements in perioperative care, the incidence of perioperative strokes has not decreased, reflecting the aging of the population and the increased number of patients with complication. We investigated the cases who were consulted due to perioperative stroke. From April, 2004 to March, 2007, a total of 102 patients were referred for neurological evaluation because of perioperative stroke. Types of planned or performed surgery, risk factors, types of stroke and timing of the events were analyzed. Sixty-seven cases were consulted preoperatively for history or risk factors of stroke. Forty-seven cases had ischemic risk factors and cerebral vascular recanalization was carried out in four patients who experienced severe cerebral hypoperfusion. The other patients with ischemic risk factors were treated to avoid dehydration or hypotension perioperatively. Nine cases with hemorrhagic risk factors, such as cerebral aneurysm, were treated to avoid significant hypertension during surgery. The types of planned surgery were cardiovascular surgery in 29 cases, abdominal surgery in 13, cervical surgery in 7, and thoracic surgery in 6. Except for one case, who suffered cerebral embolism due to cardiac surgery, those who were consulted preoperatively did not experience stroke. Neurological events had occurred in 35 patients and they were consulted postoperatively. The surgical procedures were cardiovascular surgery in 19 patients, thoracic surgery in 6, abdominal surgery in 6. The types of stroke were cerebral infarction in 20 cases, hypoxic brain in 8, and transient ischemic attack in 5. The cause of the cerebral infarction was considered as cerebral embolism in 19 cases. Those who were consulted preoperatively were treated to prevent intraoperative stroke and did not suffer neurological complication. Most stoke in patients undergoing surgery were not related to hypoperfusion but due to embolism.
 ...
PMID:[Etiologic mechanism and prevention of perioperative stroke]. 1851 58

In development of intracranial aneurysms contribute genetic factors together with smoking, hypertension, diabetes mellitus. Epidemiology studies suggest that as many as 5% of people harbour a cerebral aneurysm by age 75. Rupture of cerebral aneurysm is the most frequent cause of spontaneous subarachnoid haemorrhage (up to 80%.) Annual incidence of SAH is 10-14/100 000, but only 15-20% of aneurysms will rupture, and that will happen probably between 40-60 years. The morbidity and mortality of aneurismal subarachnoid (SAH) continues to be high. It is not possible to predict who has aneurysm and is it going to bleed or not, but it is possible to reveal high risk groups (polycystic kidney disease, Ehlers-Danlos sy, Marphan sy, family history of cerebral aneurysms, suspect de novo aneurysm formation in patients with prior history of cerebral aneurysm). Reviewing data from literature and reporting cases from each group with high risk, that have been screened and aneurysms discovered, authors wish to focus interest on this matter and propose screening program for these groups of patients. The mortality and morbidity in cases treated before rupture is significantly lower than after SAH, so screening programs could save many lives. According to our preliminara data, mostly based on control angiographies after 8-10 zears in patients previouslz operated for intracranial aneurysmas, from 15 angipgraphies 4 revealed new aneurysms (26% in 10 years period) with total number of 6 de novo formed aneurysms, which is not valid due to small number of patients but strongly suggests the importancy of screening program for risk groups.
 ...
PMID:[Screening of risk groups for discovering intracranial aneurysms before rupture]. 1879 72

The coexistence of internal carotid artery (ICA) stenosis and intracranial aneurysm, although uncommon, can be a therapeutic dilemma. We present a case of a 73-year-old woman with a history of arterial hypertension and diabetes who had a severe symptomatic ICA stenosis (>90%) and an incidental ipsilateral cerebral aneurysm. The carotid stenosis was treated with angioplasty and stenting using a distal cerebral protection system. The patient was anticoagulated and maintained on antiplatelet therapy according to a standard protocol. Microcoil embolization of the aneurysm was performed 5 months after an intracranial stent was implanted. No growth has been observed in the aneurysm of the arterial lumen since the carotid intervention. There were no complications after the procedures during the postoperative period. This case shows that the incidental presence of an ipsilateral intracranial aneurysm does not appear to be a contraindication for the endovascular treatment of a carotid artery stenosis.
 ...
PMID:Endovascular treatment of carotid stenosis associated with incidental intracranial aneurysm. 1954 89

Activation of the renin-angiotensin (Ang)-aldosterone system is involved in the pathology of vascular diseases. Although the blockade of the mineralocorticoid receptor protects against vascular diseases, its role in cerebral aneurysms remains to be elucidated. We treated female rats subjected to renal hypertension, increased hemodynamic stress, and estrogen deficiency for 3 months with the mineralocorticoid receptor blocker eplerenone (30 or 100 mg/kg per day) or vehicle (vehicle control). Eplerenone reduced the incidence of cerebral aneurysms and saline intake without lowering of the blood pressure. In the aneurysmal wall, the production of Ang II and nitrotyrosine was increased. The mRNA levels of Ang-converting enzyme 1 and NADPH oxidase subunits NOX4, Rac1, monocyte chemoattractant protein 1, and matrix metalloproteinase 9 were increased. Eplerenone brought about a reduction in these molecules, suggesting that mineralocorticoid receptor blockade suppresses cerebral aneurysm formation by inhibiting oxidative stress, inflammatory factors, local renin-Ang system activation, and saline intake. Other female rats implanted with pellets of the mineralocorticoid receptor agonist deoxycorticosterone acetate manifested a high incidence of cerebral aneurysm formation and the upregulation of molecules related to oxidative stress, inflammatory factors, and the local renin-Ang system; their saline intake was increased. We demonstrate that mineralocorticoid receptor activation at least partly contributes to the pathogenesis of cerebral aneurysms.
Hypertension 2009 Sep
PMID:Role of mineralocorticoid receptor on experimental cerebral aneurysms in rats. 1962 May 12

Fasudil (a Rho-kinase inhibitor) has been shown to attenuate abdominal aortic aneurysm development, but any preventive effect against development of cerebral aneurysms is unclear. The effect of fasudil on the development of cerebral aneurysms was investigated in 55 female Sprague-Dawley rats divided into 4 groups: Group 1 (n=10) was the control group without treatment. Groups 2-4 (n=15 each) were subjected to cerebral aneurysm induction procedures plus 1% NaCl in the drinking water. Groups 3 and 4 were also treated with 0.5 or 1.0mg/mL of fasudil in the drinking water, respectively. Vascular corrosion casts of the cerebral arteries were prepared and examined using a scanning electron microscope after 2 months. No significant differences were observed in the degree of induced hypertension between Groups 2, 3 and 4. No aneurysms were found in Group 1. Examination of the left anterior cerebral-olfactory artery junction, which is the most susceptible site for aneurysm development, found significantly fewer aneurysmal lesions in Groups 3 (60%) and 4 (53%) compared to Group 2 (100%) (P<0.02). This study suggests that fasudil attenuated induction of cerebral aneurysms in the rat model.
 ...
PMID:Fasudil, a Rho-kinase inhibitor, attenuates induction and progression of cerebral aneurysms: experimental study in rats using vascular corrosion casts. 2004 78

An acute subdural hematoma is commonly regarded as a complication of a head injury, and bleeding is associated with contusion or laceration of the bridging vein in the subdural space. Occasionally, reports describe non traumatic acute subdural bleeding from the rupture of cerebral aneurysm or vascular malformation. However, acute spontaneous subdural hematomas (ASDH) of arterial origin, without any traumatic history or vascular anomaly, are rarely reported in literature. Here we describe two cases who presented with acute signs of intracranial hypertension secondary to a spontaneous acute subdural hematoma in which spontaneous bleeding from a small cortical artery was seen during operation.
 ...
PMID:Acute spontaneous subdural hematoma: an unusual form of cerebrovacular accident. 2022 Jul 41

Craniotomy sometimes causes pseudoankylosis of the mandible, i.e., limited mouth opening, leading to a difficult airway. We describe a case of difficult airway due to pseudoankylosis of the mandible after craniotomy, in which orotracheal intubation was successfully performed with an AirWay Scope (AWS). A 60-year-old woman was scheduled for clipping of an unruptured cerebral aneurysm. She had undergone emergency clipping of a ruptured cerebral aneurysm under frontotemporal craniotomy on the other side three weeks previously. In the previous anesthesia, she had presented normal mouth opening, and orotracheal intubation had been easily performed. Preoperative examination for the second surgery, however, revealed that she had a limited mouth opening with 1.8 cm of interincisor distance, resulting in a class 4 Mallampati view. A difficult airway was anticipated. In order to avoid the risk of hypertension caused by sedated-awake fiberoptic intubation, we planned orotracheal intubation under general anesthesia with AWS. After careful induction with fentanyl and propofol, the blade was inserted smoothly. Her glottic opening was easily visualized, and her trachea was intubated without any difficulty or any distinct hemodynamic disturbance. Careful assessment of the interincisor distance is essential in patients who have previously undergone craniotomy.
 ...
PMID:[Case of pseudoankylosis of the mandible after craniotomy]. 2042 Jan 38

Cerebral hyperperfusion syndrome is a rare but well-described complication following carotid endarterectomy or stenting. Clinical signs are ipsilateral, throbbing, unilateral headache with nausea or vomiting, seizures, and neurological deficits, with or without intracerebral abnormalities on CT scan, such as brain edema or intracerebral hemorrhage. Subarachnoidal hemorrhage is rarely described especially if it occurs isolated. We describe a 74-year-old man with a history of high blood pressure, hypercholesterolemia, atrioventricular block with pacemaker, and ischemic cardiopathy with coronary bypass. He underwent right carotid endarterectomy for a 90% NASCET asymptomatic stenosis. Four days after surgery, he complained of unusual headaches with right, throbbing hemicrania. Nine days after surgery, he presented with left hemiplegia and a partial motor seizure. He had fluctuant altered consciousness, left hemiplegia, and left visual and sensory neglect. Brain CT showed right frontal subarachnoidal hemorrhage without parenchymal bleeding. Cerebral angiography found no cerebral aneurysm, no vascular malformation, but a vasospasm of the left middle cerebral artery. Transcranial Doppler confirmed this vasospasm. Evolution was favorable with no recurrence of seizures but with an improvement of the neurological deficits and vasospasm. Physicians should bear in mind this very rare complication of endarterectomy and immediately perform neuroimaging in case of unusual headache following endarterectomy or angioplasty.
 ...
PMID:Isolated Subarachnoidal Hemorrhage following Carotid Endarterectomy. 2067 62

The rupture of cerebral aneurysm (CA) and subsequent subarachnoid hemorrhage can cause fatal results. Recent experimental findings have suggested that the mechanism of CA formation is based on chronic inflammation in arterial walls by hemodynamic force. Endothelial nitric oxide synthase (eNOS) protects arterial walls from vascular inflammation by relieving hemodynamic force through nitric oxide (NO) production. Thus, the expression and protective role of eNOS in CA formation have been investigated in this study. In this study, experimental induced rodent CA models by carotid ligation and systemic hypertension were used. The expression of eNOS was examined in rat CA models and revealed that it was decreased at the site of CA formation. Next, CA was induced in eNOS(-/-) mice to clarify the role of eNOS in CA formation. In eNOS(-/-) mice, the incidence of CA formation was similar to that found in wild-type mice. In CA walls of eNOS(-/-) mice, the expression of neuronal nitric oxide synthase (nNOS) was upregulated compared with that in wild-type mice, suggesting the compensatory effect of nNOS. Hence, eNOS(-/-) nNOS(-/-) mice were generated, underwent CA induction and confirmed that eNOS(-/-) nNOS(-/-) mice exhibited an increased incidence of CA formation accompanied by accelerated macrophage infiltration. These results suggested that the deficiency of eNOS could be compensated by nNOS upregulation in cerebral arteries and that the eNOS and nNOS complementarily had the protective role in CA formation. The results of this study will provide us with new insight about the mechanisms of CA formation and the functional redundancy between eNOS and nNOS in cerebral arteries.
 ...
PMID:Complementary inhibition of cerebral aneurysm formation by eNOS and nNOS. 2132 33


<< Previous 1 2 3 4 5 6 7 8 Next >>