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At least 235 records · Page 13Linked to original sources
PubMed1994

[Evaluation of cerebral circulation and cerebrovascular CO2 reactivity with transcranial Doppler ultrasonography].

We examined the cerebrovascular CO2 reactivity (K) determined by measurements of the middle cerebral artery blood flow velocity (Vm) with transcranial Doppler ultrasonography (TCD) in 24 anesthetized patients. The relationship between Vm and mean arterial blood pressure (mBP) showed a linear regression in each constant level of PaCO2. The exponential curve with an exponent of 0.0399 mmHg-1 was found to be the best fit to the plotted data of Vm against PaCO2 during normotension of 90 mmHg. The following equation was used to evaluate K from the two flow values, because the calculated K value would be logically constant, i.e., an exponent of Vm/PaCO2 exponential curve: K (mmHg-1) = delta lnVm/delta PaCO2 = (lnVm(1) - lnVm(2)/(PaCO2(1) - PaCO2(2)). The validity of K values could be enhanced under conditions of the delta PaCO2 > or = 12.5 mmHg and the variation in arranged mBP < or = 30 mmHg. This methodology with TCD can be used to correlate changes in cerebral blood flow and provide much benefit for the evaluation of cerebrovascular CO2 reactivity.

Adult↗
PubMed2001

Studies on improved model for cerebrovascular blood circulation.

For the elastic cavity model adopted in the existing cerebrovascular hemodynamics analyzers was too simple, we developed the improved model for cerebrovascular blood circulation to describe more exactly the physiologic nature of both sides cerebrovascular blood circulation and the relation between them (Willis Circle). It was a network consisting of 2 inputs, 9 arteries and 4 terminal flow resistances. For two cases, constant flow and pulsating flow, the further improved models for calculability were analyzed and the mathematical equations describing the model was obtained; some algorithms were given to solve the positive and negative problems to the mathematical functions; the physiologic means to parameters in the model were defined; at last, the possible applications of the models in basic research and clinic about cerebrovascular disease were stated as well. In the paper, we compared our portable cerebrovascular hemodynamics analyzer with the improved model to other analyzers with the elastic cavity model, and concluded that because of providing additional M-style ultrasonic detector for measuring the diameters of blood vessels and improving the Doppler ultrasonic detector for measuring the velocity of blood flow of the internal carotid artery we could accept the improved model to obtain more exact and more details and the relation about cerebrovascular blood circulation and hemodynamics.

Algorithms↗
PubMedDate not supplied

[The effect of dimephosphon, sermion and piracetam on the reactivity of the cerebral vessels, on local cerebral blood flow and on oxygen tension in brain tissue].

The paper gives the results of experimental and clinical studies of the nootropic agents dimephosphone, sermion, and piracetam on local cerebral circulation, cerebrovascular responsiveness and O2 tension. The vasoactivity of the parameters studied has been shown to be displayed by their ability to normalize cerebrovascular responsiveness and it is associated with decreased brain tissue oxygen consumption when dimephosphone is applied and with its increased one when sermion and piracetam are used.

Adolescent↗
PubMed1991

[Radiological examination of cerebral circulation in cerebrovascular disorders].

The authors provide the results of radiological examinations of cerebral circulation in 215 patients aged 16 to 67 years with different periods of cervical osteochondrosis. The intensity of hemispheric hemocirculation derangement depends on the stage of osteochondrosis. At the same time cerebral circulation disorders running their course by the type of transitory disturbances are not specific for the given group of patients and can also be seen in patients suffering from other diseases of the brain.

Adolescent↗
PubMed1990

Racial differences in the anterior circulation in cerebrovascular disease. How much can be explained by risk factors?

The entry characteristics of 1367 patients enrolled into the Extracranial/Intracranial Bypass Study were examined to determine if site differences in intracranial and extracranial arterial lesions among racial groups could be explained by differences in risk factors. Blacks were more often hypertensive, diabetic, or cigarette smokers, while whites had higher systolic blood pressure and hemoglobin values. Orientals had the lowest prevalence of vascular risk factors. Despite these differences in risk factors, multivariate analysis showed race to be an independent and strong predictor of the location of cerebrovascular lesions. To our knowledge, this study is unique in documenting risk factors prospectively and systematically in three racial groups simultaneously. Although generalization is limited by possible biases related to patient selection, the results affirm previous tentative conclusions about the role of race in determining the location of cerebrovascular disease.

Asian People↗
PubMed1995

Posterior circulation infarction: anatomy, pathophysiology, and clinical correlation.

Posterior circulation cerebrovascular disease may be responsible for clinical syndromes that are determined by the vascular territory affected. An anatomic/topographic approach to the brain stem and cerebellum, relating the cross-sectional and functional anatomy to the vascular supply territories, is useful in the analysis of imaging studies of patients with posterior circulation cerebrovascular disease. Knowledge of the typical vascular distributions may be particularly useful for cases that do not show the classical clinical brain stem and cerebellar infarction syndromes. This approach may serve to improve our understanding of cerebrovascular disease in the posterior fossa.

Brain Stem↗
PubMed1991

[Effects of ethomersol on cerebrovascular blood circulation and oxygen metabolism of the brain in acute transient ischemia and recirculation].

Intravenous infusion of ethomersol (50 mg/kg during 60 min) decreased cerebral tissue hypoxia at the end of acute cerebral ischemia in cats (30-min occlusion of both carotid and both vertebral arteries). In recirculatory period ethomersol prevented the postischemic hypoperfusion and especially hypo-oxygenation. Ethomersol-induced reduction of Hb-affinity to O2 was demonstrated.

Acute Disease↗
PubMed1992

Increased norepinephrine spillover into the jugular veins in essential hypertension.

In essential hypertension sympathetic nerve firing is commonly increased. A central nervous system origin has been presumed but not tested directly. To estimate cerebral norepinephrine release in essential hypertension, spillover of norepinephrine into the cerebrovascular circulation was measured by isotope dilution, with high internal jugular venous sampling. Norepinephrine was released into the cerebrovascular circulation in both hypertensive patients and healthy volunteers and was present after administration of the ganglion blocker trimethaphan and in patients with sympathetic nervous failure, indicating that brain neurons and not cerebrovascular sympathetic nerves were the probable source. Although differing among hypertensive patients, norepinephrine spillover on average was higher in the hypertensive patients (153 +/- 41 pmol/min) than in healthy subjects (59 +/- 12 pmol/min; p less than 0.05), and was elevated in six of 17 patients, in whom the accompanying whole body norepinephrine spillover rate was higher than in the remaining 11 patients (p less than 0.01). To test for a possible link between brain norepinephrine release and human sympathetic nervous function, the effect of the tricyclic antidepressant desipramine (0.3 mg/kg i.v.) on both brain and whole body norepinephrine spillover was measured in healthy volunteers. Desipramine lowered the cerebrovascular spillover of norepinephrine, its precursor dihydroxyphenylalanine, and its metabolite dihydroxyphenylglycol by 50-80% and produced a mean fall of 35% in whole body norepinephrine spillover. One interpretation of these results is that human sympathetic nerve firing is dependent on norepinephrine release within the brain and that increased cerebral norepinephrine release may possibly be present in some patients with essential hypertension, underlying their higher sympathetic nerve firing rates.

Cerebrovascular Circulation↗
PubMed2005

The relationship between CSF circulation and cerebrovascular pressure-reactivity in normal pressure hydrocephalus.

OBJECTIVE: Previously, we documented association between CSF circulation and transcranial-Doppler derived autoregulation in non-shunted patients suffering from hydrocephalus. In the present study we sought to investigate the relationship between the resistance to CSF outflow and pressure-reactivity both in shunted and non-shunted NPH patients. MATERIAL AND METHODS: Sixty-eight patients (47 non-shunted and 21 shunted) with NPH have been examined as a part of routine diagnostic procedure. Resistance to CSF outflow (Rcsf) was measured using a ventricular constant rate infusion test. Cerebrovascular pressure-reactivity was assessed as a moving correlation coefficient (PRx) between coherent 'slow waves' of ICP and arterial blood pressure (ABP). This variable has previously been demonstrated to correlate with the autoregulation of CBF in patients following head injury. Results. In non-shunted patients cerebrovascular pressure-reactivity (PRx) was negatively correlated with Rcsf (R = -0.5; p < 0.0005). This relationship was inverted in shunted patients: a positive correlation between PRx and Rcsf was found (R = 0.51; p < 0.03). CONCLUSION: Cerebrovascular pressure-reactivity is disturbed in patients with normal resistance to CSF outflow, suggesting underlying cerebrovascular disease. This result confirms our previous finding where transcranial Doppler autoregulation was investigated. After shunting the pressure-reactivity strongly depends on shunt functioning and deteriorates when the shunt is blocked.

Aged↗
PubMed1996

[The pathophysiological mechanisms of disorders of cerebral circulation and the new directions in their prevention and treatment].

The contribution of Laboratory of Nervous System's Experimental Pathology (Institute of Neurology of Russian Academy of Medical Sciences) to cerebrovascular circulation investigations is described. The following questions were considered: cerebral circulation in cerebrovascular disturbances, collateral circulation in the "turned off" state of different brain arteries, and immunological brain alterations as the result of brain organic diseases. Results of the investigation of the damaging effect of acute increase in arterial pressure as well as individual sensitivity to brain ischemia and to drug administration were presented. The particular importance of researches of blood circulation biomechanics as well as of factors of its normalization were also emphasized.

Academies and Institutes↗
PubMed1991

Biochemical evidence of sympathetic hyperactivity in human hypertension.

Radiotracer measures of norepinephrine overflow to plasma are well suited for studying both human sympathetic nervous system responses to mental stress and sympathetic nervous pathophysiology in human hypertension. With an experimental laboratory stressor (cognitive challenge), we noted a preferential activation of the cardiac sympathetic outflow; however, in fainting reactions ("vasovagal syncope"), which occur infrequently during the course of central venous catheter placement under local anesthesia, the converse was seen--an almost total withdrawal of cardiac sympathetic activity. In primary human hypertension (particularly in younger patients), a differentiated activation of the sympathetic outflow to the heart and kidneys is present, based on measurements of norepinephrine spillover to plasma. It is uncertain whether this is attributable to behavioral factors and represents a component of the defense reaction. We previously reported overflow of norepinephrine into the cerebrovascular circulation (with high internal jugular venous sampling) in humans. Because this is resistant to ganglion blockade, brain neurons--not the cerebrovascular sympathetics--are the presumed source. In a preliminary study, we found higher rates of norepinephrine spillover into the cerebrovascular circulation in patients with essential hypertension than in healthy subjects, suggesting that an underlying increase in central nervous system norepinephrine turnover may be the basis for the increased sympathetic outflow.

Brain↗