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At least 325 records · Page 18Linked to original sources
PubMed1987

Effects of a calcium entry blocker on cerebral circulation in essential hypertension.

The acute effects of the calcium entry blocker, nifedipine, on cerebral circulation were studied in 22 patients (56 +/- 5 years) with essential hypertension (EHT, WHO I-II) and 12 age-matched normal subjects. Cerebral effects were reevaluated in sixteen EHT patients after 8 weeks of treatment. The cerebrovascular resistance (Rp), cerebral capacitance (Cp), carotid velocity, and flow volume were measured by a newly developed ultrasonic volume flow meter coupled with a built-in computer which calculates Rp and Cp based on a simulated model. In EHT, acute administration of nifedipine (10 mg orally) decreased Rp from 13.5 +/- 1.8 to 8.0 +/- 0.3 (p less than 0.01) and increased Cp from 22.8 +/- 3.3 to 54.9 +/- 5.2 mFc (p less than 0.01). The carotid blood flow and velocity increased by 25.7% and 22.9%, respectively (p less than 0.05) in the face of lowered arterial pressure. In normal subjects, nifedipine also decreased Rp and increased Cp but to a lesser degree compared with EHT. The acute changes in cerebrovascular circulation in EHT were maintained at 8 weeks of treatment. These results suggest that nifedipine reduces Rp, possibly as the consequence of systemic hypotension and direct vasodilation of the cerebral arteries. This may be beneficial for hypertensive patients.

Adult↗
PubMed2006

Moyamoya disease--magnetic resonance imaging and magnetic resonance angiographic features.

A rare case of moyamoya disease in a 9-year-old female presented with behavioural disturbances and recurrent hemiparetic attacks is reported. Moyamoya disease is an uncommon form of arteritis which affects the cerebrovascular circulation. Magnetic resonance angiography is a non-invasive technique for evaluation of the carotid and vertebrobasilar circulation. The magnetic resonance angiography findings are typical and characteristic of this disease.

Cerebrovascular Circulation↗
PubMed1984

Effect of indomethacin on cerebral blood flow, carbon dioxide reactivity and the response to epoprostenol (prostacyclin) infusion in man.

Cerebral blood flow (CBF) has been measured using a non-invasive Xenon133 clearance technique in six normal subjects after 2 days pretreatment with oral indomethacin at a dose of 100 mg/day. The results were compared with placebo given in a double blind balanced cross-over design. Indomethacin was found to result in a reduction in resting CBF of about 25% but the reactivity of the cerebrovascular circulation to carbon dioxide was preserved at normal levels. Infusions of epoprostenol (prostacyclin, PGI2) at a dose of 5 ng/kg/min resulted in a reduction of CBF of about 10% after placebo but no significant change in CBF after indomethacin. The results suggest that prostaglandins are involved in the maintenance of cerebrovascular tone but not in the mechanism of cerebral vasodilation accompanying hypercapnia. The combination of indomethacin and PGI2 has been proposed as a treatment of cerebral artery spasm and the findings suggest that the combination therapy would not be accompanied by undesirable intracerebral steal.

Adult↗
PubMed1985

Eicosanoids in the central nervous system.

All mammalian tissue investigated to date is capable of eicosanoid biosynthesis in response to various activating stimuli. While the importance of these metabolites as major mediators of many normal physiological processes and some pathophysiological conditions has not been proven, it is evident that these compounds are at least important modulators of many cellular and organ system functions. This review is intended to provide the reader with a brief overview of eicosanoid biology, with specific reference to the neurosciences. The increasing knowledge about the role of the eicosanoids in neurobiology may contribute to the understanding and treatment of many neurological diseases. The eicosanoids comprise several groups of biologically active unsaturated fatty acids: the "primary" prostaglandins, the cyclic endoperoxides, the prostanoids, the leukotrienes, and other acid lipids. This article includes a review of the enzymatic pathways of biosynthesis and metabolism of eicosanoids in man, and the pertinent structural nomenclature. The general basic and clinical pharmacological effects of the more important compounds on vascular perfusion, platelet function, intracellular enzyme activity, and interactions with other mediators of cellular activity are reviewed. A more detailed review of the actions of eicosanoids as mediators or modifiers of central nervous system physiology and pathophysiology is presented. Recent animal and human studies on the use and alterations of the eicosanoid metabolites is summarized, specifically where they relate to several clinical problem areas of interest to the neurosurgeon and neurobiologist. These areas include cerebrovascular circulation physiology, cerebral ischemia, cerebral vasospasm following subarachnoid hemorrhage, migraine headaches, hypothalamic function, neurotransmission, and nociception. A bibliography of 92 articles for further review is also included.

Central Nervous System↗
PubMed1998

[The usefulness of carotid artery ultrasonography in patients with Binswanger's encephalopathy].

Carotid artery ultrasonography (B-mode and Duplex method) was conducted in 49 cases of Binswanger's encephalopathy (group B) to compare with 189 cases of lacunar infarction (group L). With B-mode method, there was no significant difference in the amount of plaque between group B and group L, but the inner diameter of the common carotid artery was greater in group B. Using Duplex method, we measured maximum systolic flow velocity (Max), minimum diastolic flow velocity (Min) and time velocity integral (TVI). We found that those data were consistently lower in group B than in group L, with a correlation to the severity of mental impairment. The decrease in Max in group B, which has diffuse arteriosclerosis, indicates a decline in cardiac function, while the decrease in Min indicates an increase of intracranial small vessel resistance. The lower TVI in group B is thought to reflect a loss of velocity in cerebrovascular circulation due to the decrease in Max and Min. Carotid artery ultrasonography thus proved useful in evaluating the pathogenesis and progression of the disease.

Aged↗
PubMed2005

Permissive contributions of NO and prostacyclin in CO-induced cerebrovascular dilation in piglets.

Endogenously produced CO is an important dilator in newborn cerebrovascular circulation. CO dilates cerebral arterioles by activating Ca2+-activated K+ channels, but modulatory actions of other effectors and second messenger inputs are unclear. Specifically, the mechanisms behind the obligatory permissive roles of prostacyclin and NO are uncertain. Therefore, the present study was performed using acutely implanted, closed cranial windows in newborn pigs to address the hypothesis that the permissive roles of NO and prostacyclin in cerebrovascular dilation in response to CO involve a common mechanism. The NO donor sodium nitroprusside restored dilation in response to CO after inhibition of that dilation with the prostaglandin cyclooxygenase inhibitor indomethacin. The stable prostacyclin analog iloprost restored CO-induced dilation blocked by the NO synthase inhibitor Nomega-nitro-L-arginine. Restoration of dilation in response to CO by the cGMP-dependent phosphodiesterase inhibitor zaprinast and blockade of CO dilation by the guanylyl cyclase inhibitor 1H-[1,2,4]oxadiazole-[4,3-a]quinoxalin-1-one (ODQ) suggests involvement of the cGMP/PKG pathway. Iloprost or the cAMP-dependent dilator isoproterenol restored dilation in response to CO after ODQ administration. However, CO-induced dilation blocked by the cGMP-dependent PKG inhibitor Rp-8-[(4-chlorophenyl)thio]-cGMPS triethylamine could not be reversed by administration of sodium nitroprusside, iloprost, or isoproterenol. Conversely, PKA inhibition did not block dilation in response to CO. Overall, data indicate that activation of PKG is the predominant mechanism of the permissive actions of NO and prostacyclin for CO-induced pial arteriolar dilation.

Animals↗
PubMed2003

Normalization of endothelial and inducible nitric oxide synthase expression in brain microvessels of spontaneously hypertensive rats by angiotensin II AT1 receptor inhibition.

Inhibition of angiotensin II AT1 receptors protects against stroke, reducing the cerebral blood flow decrease in the periphery of the ischemic lesion. To clarify the mechanism, spontaneously hypertensive rats (SHR) and normotensive control Wistar Kyoto (WKY) rats were pretreated with the AT1 receptor antagonist candesartan (0.3 mg. kg.(-1) d(-1)) for 28 days, a treatment identical to that which protected SHR from brain ischemia, and the authors studied middle cerebral artery (MCA) and common carotid morphology, endothelial nitric oxide synthase (eNOS) and inducible nitric oxide synthase (iNOS) messenger RNA (mRNA), and protein expression in cerebral microvessels, principal arteries of the Willis polygon, and common carotid artery. The MCA and common carotid artery of SHR exhibited inward eutrophic remodeling, with decreased lumen diameter and increased media thickness when compared with WKY rats. In addition, there was decreased eNOS and increased iNOS protein and mRNA in common carotid artery, circle of Willis, and brain microvessels of SHR when compared with WKY rats. Both remodeling and alterations in eNOS and iNOS expression in SHR were completely reversed by long-term AT1 receptor inhibition. The hemodynamic, morphologic, and biochemical alterations in hypertension associated with increased vulnerability to brain ischemia are fully reversed by AT1 receptor blockade, indicating that AT1 receptor activation is crucial for the maintenance of the pathologic alterations in cerebrovascular circulation during hypertension, and that their blockade may be of therapeutic advantage.

Angiotensin Receptor Antagonists↗
PubMed2002

T-786C polymorphism in endothelial NO synthase gene affects cerebral circulation in smokers: possible gene-environmental interaction.

Effects of smoking on white matter lesions, such as lacunar infarction and leukoaraiosis, are still controversial. We hypothesized that the endothelial NO synthase (eNOS) genotype was a modulating factor for the effect of smoking on cerebral circulation. We took a cross-sectional population from the participants of a health examination to study the effects of smoking and a single-nucleotide polymorphism in the eNOS gene, T-786C. Smokers and nonsmokers were defined as having a smoking index (cigarettes per day times years) of >/=200 and 0, respectively. One hundred sixty-six male nonsmokers and 344 male smokers were recruited. Cerebral blood flow was measured by the (133)Xe inhalation method. Genotyping of T-786C was performed by using a newly developed allele-specific polymerase chain reaction. Smokers were exposed to greater oxidative stress, as estimated by urinary F(2)-isoprostane excretion. In smokers, CC homozygotes of T-786C showed a significant decrease of cerebral blood flow (56.6+/-13.3, 57.6+/-11.5, and 44.0+/-7.2 mL/min per 100 g tissue for TT, TC, and CC, respectively; P=0.03 by ANOVA) and a significant increase of cerebrovascular resistance, whereas the eNOS genotype did not affect these parameters in nonsmokers. This result indicated that the eNOS genotype could modify cerebrovascular circulation in a general population by potentiating the adverse effect of smoking.

Analysis of Variance↗
PubMedDate not supplied

Transcranial Doppler ultrasound assessment of intracranial hemodynamics in patients with type 2 diabetes mellitus.

BACKGROUND: Diabetics have a 3-fold risk for cardiovascular diseases compared with non-diabetics. This study was designed to evaluate cerebral hemodynamic changes related to type 2 diabetes mellitus (DM) with transcranial Doppler ultrasonography (TCD). TCD is a highly sensitive and specific method of quick bedside assessment of cerebrovascular circulation hemodynamics. PATIENTS AND METHODS: In a prospective study, we compared a group of 100 patients with the diagnosis of type 2 diabetes mellitus (aged 48 to 67 years) and an age- and sex-matched control group of 100 healthy subjects without diabetes mellitus. We measured flow velocities (Vm) and the Gosling pulsatility index (PI) of the middle cerebral artery (MCA). RESULTS: The rate of TCD abnormalities was significantly higher in diabetic patients than in healthy control subjects (55% vs. 11%, P < 0.05). The PI was significantly higher in diabetic patients than in healthy controls (P < 0.001). Atherosclerotic changes were found in 34.0% and 71.4% of patients suffering from diabetes for <5 and > or =5 years, respectively. CONCLUSION: This study suggests that TCD is a useful marker for the detection of diabetic cerebrovascular changes. The duration and type of diabetes were found to have an impact on the development of pathologic cerebrovascular changes.

Aged↗
PubMed1992

Cerebral blood flow, cerebral blood volume, and cerebrovascular reactivity after severe head injury.

Traumatic brain injury (TBI) often causes disturbances of the cerebrovascular circulation, which contribute to the infliction of secondary injury, although the complex nature of the mechanisms involved is not fully understood. First, the role of ischemia in TBI is still controversial. Despite experimental and pathologic data suggesting important interactions between ischemia and trauma, evidence for posttraumatic ischemia with CBF measurements in patients so far had eluded most investigators. Recent data, however, indicate that low CBF and ischemia probably only occur within the first few hours after injury, yet have important impact on neurologic status and outcome. Similarly, the clinical significance of posttraumatic hyperemia is unclear. A relationship between raised intracranial pressure (ICP) and hyperemia has been suspected, but reports have not been consistent, possibly due to a dissociation between CBF and CBV in head-injured patients. Measurements of CBV in the acute stage of severe head injury now have confirmed this concept, and also suggest that increased CBV may contribute to brain stiffness and elevated ICP. Impairment of cerebrovascular CO2 reactivity and autoregulation often occurs after TBI. Although no correlation with the severity of injury or outcome has been established, it is obvious that diminished adaptive responses of the cerebral vasculature render the brain more vulnerable to additional systemic insults, such as derangements of blood pressure, altered rheology, or hypoxia. The posttraumatic status of vascular reactivity and autoregulation also has important implications with regard to the treatment of high ICP, in particular for the use of hyperventilation and pharmacologic management of blood pressure, which are discussed in detail.

Adult↗
PubMed1994

Vascular grafts in head and neck reconstructive surgery.

The best management of advanced head and neck tumors invading the carotid artery utilizes a collaborative, anticipatory approach. Preoperative characterization of the anatomy and extent of tumor involvement, coupled with the physiologic assessment of the cerebrovascular circulation through the variety of adjunctive studies, facilitates operative planning. Careful preoperative evaluation allows the surgeon to make the most informed decision regarding extracranial carotid artery reconstruction, should carotid artery resection be required for adequate tumor removal. When the preoperative evaluation indicates that adequate cerebral perfusion or collateral reserve will not be maintained with carotid artery occlusion, carotid artery reconstruction needs to accompany any resection of this vessel. Autogenous saphenous vein remains the graft conduit of choice, but prosthetic materials may be used. Graft patency and healing require appropriate concomitant soft-tissue coverage of any overlying mucosal or cutaneous defects.

Blood Vessel Prosthesis↗
PubMed1992

Cerebrovascular stability during isoflurane anaesthesia in children.

The aims of this study were firstly, to determine the effect of various concentrations of isoflurane on cerebrovascular circulation and secondly, to examine the time-response characteristics of the drug on cerebral blood flow velocity in anaesthetized children. Thirty-two ASA physical status I or II patients aged one to eight years and scheduled for urological surgery were studied. Anaesthesia was induced with thiopentone 5 mg.kg-1 and fentanyl 2 micrograms.kg-1. Muscle relaxation was provided with vercuronium 0.1 mg.kg-1. Tracheal intubation was performed in all cases. Anaesthesia was maintained with isoflurane in a mixture of air and oxygen to produce an inspired oxygen fraction (FIO2) of 0.3. Ventilation was adjusted to maintain normocapnia. A caudal or lumbar epidural catheter was inserted before skin incision and a continuous bupivacaine, without epinephrine, infusion established. During the first part of this study, the initial isoflurane concentration for 24 patients was randomized and age-adjusted to 0.5 MAC, 1.0 MAC, or 1.5 MAC. After steady-state was reached, the subsequent isoflurane MAC concentration was randomized by either raising or lowering it from the initial concentration. In the second part of this study, the time-response effect of isoflurane was examined. Eight patients received 1.0 MAC isoflurane over 90 to 150 min. Temperature, heart rate, and systolic blood pressure were unchanged throughout the study. Cerebral blood flow velocity (CBFV) and resistance index (RI+), a measure of cerebrovascular resistance, were measured in the M1 segment of the middle cerebral artery (MCA) with a 2 MHz transcranial Doppler monitor.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Inhalation↗
PubMed1993

Evidence for increased noradrenaline release from subcortical brain regions in essential hypertension.

OBJECTIVE: To test whether the activation of the sympathetic nervous system that is common in essential hypertension derives from subcortical noradrenergic neuronal excitation. DESIGN AND METHODS: We performed a radionuclide cerebral venous sinus scan, using technetium-99m, to establish which internal jugular vein predominantly drained the cortical (the major jugular vein) and which the subcortical (minor jugular vein) brain regions. Blood samples were then collected simultaneously from catheters placed percutaneously in the brachial artery or radial artery and high in the internal jugular vein in 11 untreated hypertensive patients and 18 normotensive subjects, for determination of the plasma concentrations of noradrenaline, its precursor dihydroxyphenylalanine (DOPA) and its metabolite dihydroxyphenylglycol (DHPG) to calculate their rates of overflow into the cerebrovascular circulation. RESULTS: In normotensive subjects blood flow determined by thermodilution was significantly higher in the major than in the minor jugular vein. The noradrenaline spillovers into the major and minor jugular veins calculated during infusions of L-[3H]-7-noradrenaline were similar in healthy subjects. The noradrenaline spillover from subcortical regions into the minor jugular vein was significantly higher in the hypertensives than in the normal subjects, as was the overflow of DHPG. In contrast, cortical noradrenaline and DHPG overflows into the major jugular vein were similar in hypertensive and normotensive subjects. Overflow of DOPA into the minor jugular vein, which derives largely from precursor turnover in dopaminergic neurons, was similar in hypertensive and normotensive subjects. Subcortical noradrenaline spillover correlated with neurochemical indices of sympathetic nervous system activity, with total body noradrenaline spillover (r = 0.56, P < 0.05) in normal and hypertensive subjects combined, and with renal noradrenaline spillover in the six hypertensive patients tested (r = 0.91, P < 0.05). CONCLUSION: These results suggest that increased subcortical noradrenaline release is a possible cause of peripheral sympathetic activation in essential hypertension.

Adult↗
PubMed2000

Nitric oxide redox species exert differential permeability effects on the blood-brain barrier.

Excessive production of nitric oxide (NO) in the central nervous system is suspected to contribute to neurodegenerative diseases. Previous studies showed that excessive central nervous system NO increased the permeability of the blood-brain barrier (BBB) during experimental meningitis. The present work hypothesizes that the various NO redox forms (NO(*), NO(+), NO(-)) differentially mediate disruption of the BBB. Pharmacological agents that release NO redox forms (i.e., NO prodrugs) were selected based on the rate of NO release and the liberated NO redox form. An in situ rodent brain perfusion preparation was used to administer NO prodrugs into the cerebrovascular circulation, followed by brain perfusion with [(14)C]sucrose, a marker of BBB integrity. Cerebrovasculature infusion of certain NO prodrugs caused a significant, 2- to 5-fold BBB permeability increase in all forebrain regions (P <.01). The NO prodrug rank order of BBB disruption was S-nitroso-N-acetylpenicillamine-beta-cyclodextrin (releases NO(*), NO(+), and NO(-)) > Angeli's salt (NO(*), NO(-)) > MAHMA NONOate approximately diethylamine NONOate (NO(*)) > spermine NONOate (NO(*)) > DETA NONOate approximately Piloty's acid (negligible NO redox release) approximately saline. When normalized to BBB disruption caused by hyperosmotic mannitol (100%), S-nitroso-N-acetylpenicillamine-beta-cyclodextrin (NO(*), NO(+), and NO(-)) elicited approximately 45% disruption, Angeli's salt (NO(*), NO(-)) elicited approximately 18% disruption, and the NONOates (NO(*)) ranged from approximately 0 to 8% disruption. Cerebral blood flows and intracranial pressures were within normal limits for each tested NO prodrug, thereby suggesting that BBB disruption was not secondary to altered cerebral perfusion. Collectively, the results of this work identify that NO(*) alone exerts modest BBB disruption compared with the specie combination of NO(*) and NO(-), and the greatest disruption is exerted by the combination of NO(*), NO(-), and NO(+).

Animals↗
PubMed2000

Pulmonary function affects the quantification of rCBF by non-invasive xenon methods.

Estimates of regional cerebral blood flow (rCBF) by non-invasive xenon methods (133-xenon inhalation, xenon-enhanced computed tomography (Xe/CT) and 133-xenon iv injection) are frequently applied in the diagnosis and evaluation of patients suffering from diseases which cause disturbances in the cerebrovascular circulation. These methods all depend on an estimate of the arterial xenon concentration curve derived non-invasively from measurements of the end-tidal xenon concentration curve and used as brain input function in the Kety equation. We have studied the influence of impaired pulmonary gas exchange on the end-tidal and arterial xenon concentration curves in nine anaesthetized pigs by simultaneously measurements of both the end-tidal xenon and arterial xenon concentration curves. Computer simulations were performed to determine the deviations in the calculated rCBF values when using the end-tidal as compared to the arterial xenon concentration curve as brain input function. The results indicated that impairment of the pulmonary gas exchange caused a significant further 'delay' in the arterial xenon concentration curve in comparison to the end-tidal xenon concentration curve. The time constants of arterial curve delay were 11.9 s in the normal pulmonary group, 21 s in the right lung atelectasis group, and 19.7 s in the left pulmonary artery occlusion group. Accordingly, computer simulations indicated a statistically significant 'underestimation' of rCBF due to: (1) pulmonary gas exchange; (2) high or low levels of rCBF; (3) partition coefficient (lambda) of gray and white matter; and (4) xenon inhalation protocols. Our results indicate that quantitative measurements of rCBF by non-invasive xenon methods are markedly affected by deviations between the end-tidal and arterial xenon concentration curve, so that estimates of flow thresholds for infarction are problematic under conditions of impaired pulmonary gas exchange.

Animals↗
PubMed1996

Stimulation of alpha 2 adrenoceptors dilates the rat middle cerebral artery.

BACKGROUND: Because alpha 2 adrenoceptor agonists are used as adjuncts to anesthetics, their effects on the cerebrovascular circulation are of prime importance. We studied changes in the diameter of rat middle cerebral arteries after stimulation of alpha 2 adrenoceptors with UK14,304. METHODS: Rat middle cerebral arteries were isolated, cannulated at each end with a glass micropipette, and pressurized to 85 mmHg. The middle cerebral arteries were immersed in a bath (37 degrees C) containing physiologic saline solution, and luminally perfused with physiologic saline solution (100 microliters/ min). Changes in vessel diameter were measured after magnification with a microscope. RESULTS: Resting diameter of the middle cerebral arteries was 239 +/- 13 microns (n = 8) for the first study. A dose-dependent dilation was produced by addition of UK14,304 to the extraluminal bath; a 10-15% increase in diameter occurred at a concentration of 10(-4)M. The dilations produced by UK14,304 were blocked with selective alpha 2-antagonists, idazoxan and rauwolscine, but not by the selective alpha 1-antagonist, prazosin. The dilations could be blocked by removal of the endothelium, or the nitric oxide synthase inhibitor, N-nitro-L-arginine methyl ester (10(-5) M). The inhibitory effects of N-nitro-L-arginine methyl ester were reversed with the addition of 10(-3) M L-arginine, but not 10(-3) M D-arginine. Furthermore the dilation produced by UK14,304 was completely abolished with pertussis toxin (100 ng/ml). CONCLUSIONS: It was concluded that the stimulation of alpha 2 adrenoceptors with UK14,304 produced a dilation in the rat middle cerebral artery that (1) was dependent on intact endothelium, (2) involved nitric oxide, and (3) acted via a pertussis toxin-sensitive G protein.

Animals↗