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1.
蛛网膜下腔出血后脑血管痉挛实验研究   总被引:6,自引:5,他引:1  
目的 在兔蛛网膜下腔出血 (SAH)模型上 ,尝试建立经颅多普勒超声 (TCD)及血管造影 ,监测椎基动脉脑血管痉挛 (CVS)的新方法。方法 兔枕大池一次性注血 ,同时行逆行颈总动脉插管椎基动脉造影及开骨窗TCD监测。结果 逆行性脑血管造影能清晰显示椎基底动脉系统 ,注血前后血管直径差异明显 (P <0 .0 5 ) ,平均血流速度注血后明显增快 ,但中、重度痉挛之间基底动脉血流速度变化无明显差异。结论 一侧颈总动脉逆行插管椎基动脉造影 ,操作简便 ,结果可靠。采取开骨窗以提高TCD超声频率的方法 ,可获得兔基底动脉稳定的频谱图并易于重复。  相似文献   
2.
The aim of the study was to explore whether the biphasic time course of the vasospastic response following experimental subarachnoid hemorrhage is associated with any concomitant changes in the amount of cerebral dopamine beta-hydroxylase in the noradrenergic central nervous system. A single-hemorrhage animal model was used. Rabbits were sacrificed from day 1 to day 8 after subarachnoid hemorrhage. Intimal corrugation of the basilar artery and the amount of cerebral dopamine beta-hydroxylase in the hypothalamus and brain stem were measured each day. Vasospastic changes occurred in the biphasic manner following subarachnoid hemorrhage. More profound vasospastic corrugation occurred in the acute phase, followed by a slightly less intense corrugation in the chronic phase (between days 5 and 8 after the subarachnoid hemorrhage). Simultaneously, a clear concomitant biphasic time course developed in the form of an increased amount of dopamine-beta-hydroxylase in the noradrenergic nervous system of the rabbit hypothalamus and brain stem during the acute and chronic phases after the subarachnoid hemorrhage. Statistically significant correlation between basilar artery corrugation and the amount of dopamine beta-hydroxylase was found. These results suggest the possible role of the central sympathetic system in the pathogenesis of vasospasm. At the same time, this study demonstrates the chronological similarity of the vasospastic development after subarachnoid hemorrhage in the animal experimental model with the human time course of vasospasm.  相似文献   
3.
Computed tomography (CT) perfusion imaging is a technique for the measurement of cerebral blood flow, cerebral blood volume, and time-to-peak or mean transit time. The technique involves the administration of a single-bolus dose of iodinated contrast material, followed by spiral CT imaging during the passage of the contrast bolus through the cerebral vasculature. CT perfusion is a fast and inexpensive brain imaging modality for use in the management of patients with various neurological disorders, ranging from acute stroke to subarachnoid hemorrhage. This article reviews the technique of CT perfusion and presents several illustrative cases in which this imaging modality was used effectively in the critical care of patients with neurological disorders.  相似文献   
4.
Introduction: Cerebral vasospasm in aneurysmal subarachnoid hemorrhage (SAH) is associated with poor outcome. The safety and feasibility of continuous high-dose intravenous magnesium sulfate (MgSO4) for the prevention of cerebral vasospasm and ischemic cerebral injury has not been well studied. Methods: Patients presenting to our center within 72 hours of aneurysmal SAH (confirmed by computed tomography [CT] scanning and cerebral angiography) between June 2001 and October 2002 were enrolled in a prospective pilot study in which they received MgSO4 as an adjunct to standard SAH management. Study patients received an intravenous infusion of 12 g of MgSO4 in a 500-mL solution of 0.9% NaCl administered at a rate of 4.06 mM (or 0.5 g) every hour over a 24-hour period for 10 days to achieve a target predetermined serum Mg range of more than 1.5 to less than 4.0 mM/L. The effect of MgSO4 on clinical examination, heart rate, and blood pressure was measured every 2 hours; serum glucose and phenytoin levels were monitored daily. Outcome measures included evidence of vasospasm on clinical examination, transcranial Doppler study ((TCD); velocity ≥100 cm/s), or repeat cerebral angiogram obtained within 10 days of SAH; and Glasgow Outcome Scale (GOS) score assessment and CT scan evidence of ischemic infarction at 30 days. Results: Nineteen patients (mean age: 55 years; range: 39–84 years; 11 males, 8 females) were enrolled in the study. Presenting Hunt & Hess grade was II or higher; mean Fisher grade was 3. Vasospasm was observed in nine patients (by clinical examination in two, TCD in five, and angiogram in nine). The mean serum Mg level was 2.7 mM/L (standard deviation: ±0.37) and was maintained during the infusion period. No clinical adverse effects, hemodynamic changes, or fluctuations in serum glucose or phenytoin levels were observed. None of the patients died; no CT evidence of ischemic infarction was present; and most had good outcomes (GOS 5 in 10 patients; GOS 4 in 8 patients). Conclusion: Our study confirmed the safety and feasibility of a continuous infusion of high-dose intravenous MgSO4 in patients with aneurysmal SAH. Randomized controlled trials are required to confirm the promising results.  相似文献   
5.
The phenomenon of reversible cerebral arterial segmental vasoconstriction has been associated with several conditions, including pregnancy and puerperium (“postpartum angiopathy”), thunderclap headache, and use of vasoconstrictive medications. Patients with cerebral vasoconstriction typically present with sudden, severe, and recurrent (“thunderclap”) headaches and can develop strokes. Cerebral vasoconstriction syndromes are under-recognized, are poorly characterized, and are frequently misdiagnosed as primary cerebral vasculitis. This article presents an illustrative case report and reviews the historical aspects, clinical and imaging characteristics, etiology, differential diagnosis, management, and prognosis of cerebral vasoconstriction syndromes.  相似文献   
6.
Neurogenic pulmonary edema (NPE) is a well-known complication of acute brain injury. Neurogenic stunned myocardium (NSM) occurs clinically in a significant subset of patients with NPE. A 49-year-old woman developed refractory cerebral vasospasm requiring angioplasty following a subarachnoid hemorrhage. During angioplasty, NPE with NSM manifested as acute pulmonary edema associated with elevated pulmonary artery occlusion pressure and reduced cardiac output. Evaluations disclosed a right insular infarction, cardiac wall motion abnormalities, and electrocardiographic characteristics of NSM. The NSM completely resolved, and the neurological outcome was good. A 56-year-old woman developed NPE during complicated coil embolization of an internal carotid artery aneurysm. Cardiac function was normal, and the NPE resolved with a brief period of mechanical ventilation and diuresis. The delayed appearance of NSM and NPE during endovascular therapy in these patients implies a degree of risk for sympathetically mediated cardiopulmonary dysfunction during complex intracranial endovascular procedures.  相似文献   
7.
Some of the neurological deficits that emerge after aneurysmal subarachnoid hemorrhage (SAH) in humans are presumably caused by ischemic brain damage consequential to SAH-induced delayed cerebral vasospasm. This vasospasm probably results from an imbalance among vasoactive factors released from both the clot formed by extravasated blood and adjacent tissues, and in particular from a decrease in the endothelium-derived relaxing factor nitric oxide (NO). Brain ischemia is also known to elevate brain production and deposition of β-amyloid, and to induce a delayed increase in total NO synthase (NOS) activity due to induction of expression of so-called induced NOS isoform, phenomena that may secondarily contribute to SAH-related brain damage. The aim of this study was to investigate the effects of treatment with the intracellular NO donor hydroxylamine on: (i) basilar arterial wall that remained in a direct contact with the clot, (ii) formation of the β-amyloid precursor protein (β-APP), (iii) total brain NOS activity, and (iv) neurological outcome in a ‘two-hemorrhage' rat SAH model. Intraperitoneal (i.p.) administration of 0.18 mmol/kg hydroxylamine hydrochloride (12.5 mg/kg) twice daily for 7 days beginning immediately after the first ‘hemorrhage' (intracisternal blood injection) reduced basilar arterial wall damage and attenuated post-SAH neurological deficit. It also reduced the SAH-related increases in hippocampal and cortical β-APP immunoreactivities and hippocampal NOS activity measured 24 h after commencement of the treatment. These results indicate that intracellular NO donors that yield NO through the action of widely distributed enzymes in brain cells (cytochromes, catalase) can attenuate detrimental effects of SAH.  相似文献   
8.
This study was conducted to investigate whether the intraparenchymal and extraparenchymal portions of small cerebral arteries show different histopathological changes after subarachnoid hemorrhage (SAH). SAH was produced in dogs by a two-hemorrhage method, and the dogs were perfusion-fixed at 7 and 14 days after SAH. Normal untreated animals were also examined to determine whether or not the histological and morphological changes in the perforating arteries were affected by the perfusion pressure during perfusion-fixation. Control dogs, which received cisternal injection of saline, and untreated normal dogs, which were divided into two groups depending on the perfusion pressure during perfusion-fixation, were also examined. Microvascular corrosion casts produced by arterial injection of polyester resin were examined by scanning electron microscopy (SEM) with morphometric analysis of the caliber of the small perforating arteries. Slices sectioned parallel to the pontine surface were examined by SEM and by light microscopy with morphometric analysis of the luminal diameter and wall thickness of the small perforating arteries. Corrosion casts showed irregular width with folds in the perforating arteries 7 days after SAH. Sectioned slices showed an increased wall thickness of the perforating arteries with intimal corrugation 7 days after SAH. Morphometric analysis revealed that the extraparenchymal portion of the perforating arteries showed no significant differences between any of the groups tested; however, the intraparenchymal portion showed a significant decrease of luminal diameter 7 days after SAH, and a significant increase of wall thickness 7 and 14 days after SAH. The perfusion pressure during perfusion-fixation did not affect the histological changes in the perforating arteries. The results of this study showed that the vasoconstrictive response of the perforating arteries to SAH was different between the extraparenchymal and the intraparenchymal portion, and showed that the intraparenchymal portion of the perforating arteries constrict after SAH, which may affect cerebral ischemia during cerebral vasospasm by increasing total cerebrovascular resistance. Received: 26 November 1998 / Revised, accepted: 1 March 1999  相似文献   
9.
Trapidil对蛛网膜下腔出血后脑血管痉挛作用的实验研究   总被引:1,自引:0,他引:1  
目的 探讨蛛网膜下腔出血(SAH)后脑血管痉挛的发生机制及其可能的治疗方法。方法 利用家兔枕大池内注血构建SAH模型,观察血小板衍生生长因子(PDGF)拮抗剂trapidil对脑基底动脉的影响。结果 脑基底动脉于SAH后48h明显变细;静脉或动脉内持续灌注trapidil 15min(1.5mg/min)后,数字减影脑血管造影(DSA)显示痉挛血管已明显扩张变粗,30min时达高峰。结论 PDGF可能参与脑血管痉挛发生的病理过程,PDGF拮抗剂trapidil可有效缓解实验性SAH后脑血管痉挛,有望成为脑血管痉挛的治疗药物。  相似文献   
10.
Summary Changes in intracellular calcium levels in canine basilar arterial smooth muscle were semiquantitatively measured by an electron microscopic cytochemical technique using a combined oxalate-pyroantimonate method. Measurements made after subarachnoid hemorrhage were compared with those made after contraction induced by prostaglandin F2. Fifteen minutes after topical application of the drug, when the basilar artery was constricted by 20%, 15% of smooth muscle cells contained a large amount of intracellular calcium. One hour later, the diameter of the basilar artery and intracellular calcium precipitation returned almost to control levels. Fifteen minutes after the first intracisternal injection of autologous blood, when acute vasospasm was angiographically evident, 13% of smooth muscle cells contained a large amount of calcium. After 1 h, when acute vasospasm had already abated, the number of smooth muscle cells containing a large amount of calcium markedly increased to 37% and some smooth muscle cells showed early degenerative findings such as intracytoplasmic vacuoles including calcium accumulation. After 48 h, when delayed vasospasm had already started, the calcium deposits and early degenerative changes had decreased significantly. After 49 h and 4 days (1 h and 48 h after the second injection of blood), the change in the amount of calcium was the same as at 1 h and 48 h after the first injection, respectively, but degeneration of smooth muscle cells increased. Therefore, acute vasospasm after subarachnoid hemorrhage may be caused by an initial elevation of intracellular calcium levels, as is the case with drug-induced contraction. Delayed vasospasm may be initiated by an excessive influx of calcium accompanied by early degeneration of cells within a few hours after subarachnoid hemorrhage. This may be followed by persistent contraction of smooth muscle cells in a low concentration of intraccllular calcium and by progressive structural derangement.  相似文献   
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