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Biomedical subjects

A Villringer

Publications and source records attributed to A Villringer.

At least 91 records · Page 5Linked to original sources
PubMed1996

Cerebral oxygenation changes in response to motor stimulation.

We studied cerebral hemodynamic response to a sequential motor task in 56 subjects to investigate the time course and distribution of blood oxygenation changes as monitored by near-infrared spectroscopy (NIRS). To address whether response is modulated by different performance velocities, a group of subjects (n = 12) was examined while performing the motor task at 1, 2, and 3 Hz. The results demonstrate that 1) the NIRS response reflects localized changes in cerebral hemodynamics, 2) the response, consisting of an increase in oxygenated hemoglobin concentration [oxy-Hb] and a decrease in deoxygenated hemoglobin concentration ([deoxy-Hb]), is lateralized and increases in amplitude with higher performance rates, and 3) changes in [oxy-Hb] and [deoxy-Hb] differ in time course. Changes in [oxy-Hb] are biphasic, with a fast initial increase and a pronounced poststimulus undershoot. The stimulus-associated decrease in [deoxy-Hb] is monophasic, and response latency is greater. We conclude that NIRS is able to detect even small changes in cerebral hemodynamic response to functional stimulation.

Adult↗
PubMed1995

Nitric oxide modulates the CBF response to increased extracellular potassium.

The response of the regional cerebral blood flow (rCBF) to brain topical superfusion of 20 mM K+ was characterized in a closed cranial window preparation in barbiturate anesthetized and ventilated rats: Increasing K+ in the artificial cerebrospinal fluid (ACSF) induced a rCBF elevation (measured by laser-Doppler flowmetry) of +85 +/- 37% above baseline (n = 19). This elevation was stable for > 3 h with continuous superfusion of increased K+ (n = 5) and partially reversible to a level of +18 +/- 19% above baseline when returning to a physiological K+ concentration. Nitric oxide synthase (NOS) inhibition by brain topical superfusion with N omega-nitro-L-arginine (L-NA) revealed (a) Addition of L-NA to high-potassium ACSF reduced the rCBF increase from +94 +/- 36% to +21 +/- 18% (p < or = 0.01, n = 7). (b) When L-NA was superfused for 60 min before increasing K+, rCBF decreased to -17 +/- 7% below baseline. Subsequent coapplication of L-NA and increased K+ induced only an elevation of +7 +/- 4% above baseline (n = 4). (c) When the NO donor S-nitroso-N-acetylpenicillamine (SNAP) was added during NOS inhibition to restore basal tissue NO levels, the resultant level of rCBF was +28 +/- 54% above baseline. Subsequent increase of K+ in the presence of NOS inhibition and SNAP elevated rCBF to +137 +/- 89% above baseline (n = 4).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Global cerebral ischemia in the rat: online monitoring of oxygen free radical production using chemiluminescence in vivo.

Using online in vivo chemiluminescence (CL), we studied for the first time continuously the production of reactive oxygen species (ROS) after global cerebral ischemia and the relationship of ROS production to CBF. In anesthetized rats equipped with a closed cranial window, the CL enhancer, lucigenin (1 mM), was superfused onto the brain topically. CL was measured through the cranial window with a cooled photomultiplier, and CBF was measured simultaneously with laser-Doppler flowmetry. Reperfusion after 10 min (n = 8) of global cerebral ischemia led to a CL peak to 188 +/- 77% (baseline = 100%) within 10 +/- 4 min. After 2 h of reperfusion, CL had returned to 102 +/- 28%. Reperfusion after 20 min (n = 8) of ischemia increased CL to 225 +/- 48% within 12 +/- 3 min. After 2 h, CL was still increased (150 +/- 44%, p < 0.05 compared with 10 min of ischemia). CL after 10 min of ischemia was neither affected by brain topical free CuZn-superoxide dismutase (SOD) (100 U/ml, n = 3) nor by i.v. administration of free CuZn-SOD (104 U/kg, followed by 104 U/kg/h, n = 3). The CBF hyperfusion peak on reperfusion preceded the CL peak in all experiments by several minutes. In additional in vitro experiments we investigated the source of CL: Intracellular loading of lucigenin was demonstrated in cultured CNS cells, and a very similar pattern of CL as in the in vivo preparation after ischemia developed in rat brain slices after 15 min of hypoxia, which was unaffected by free CuZn-SOD (100 U/ml) but strongly attenuated by liposome-entrapped CuZn-SOD. We conclude that lucigenin-enhanced CL is a promising tool to study ROS production continuously from the in vivo brain of experimental animals and brain slices, and that the CL signal most likely derives from the intracellular production of superoxide. The production of ROS is preceded by reperfusion, is burst-like, and is dependent on the duration of the ischemic interval.

Acridines↗
PubMed1995

Age dependency of changes in cerebral hemoglobin oxygenation during brain activation: a near-infrared spectroscopy study.

We used near-infrared spectroscopy (NIRS) to study noninvasively the influence of aging on changes in the local concentration of oxygenated hemoglobin ([HbO2]), reduced hemoglobin ([HbR]), and total hemoglobin ([HbT] = [HbR] + [HbO2]) during activation of brain function. Young subjects (n = 12; age, 28 +/- 4 years) performing calculation tasks showed an increase in [HbO2] [mean (arbitrary units) +/- SD, 2.36 +/- 1.07] and [HbT] (2.24 +/- 1.13) in the frontal cortex, while [HbR] (-0.11 +/- 0.48) decreased. Elderly subjects (n = 17; age, 52 +/- 10 years) showed a significantly lower mean increase (p < 0.05) in [HbO2] and [HbT] levels (1.21 +/- 1.38 and 0.72 +/- 1.41, respectively). Regression analysis supports the hypothesis of an age-dependent decline in the activation-induced local increase in [HbO2] (y = -0.241x + 20.062; r = -0.431, p < 0.05) as well as [HbT] (y = -0.346x + 22.496; r = -0.568, p < 0.05). We conclude that NIRS is a promising approach for studying changes in Hb oxygenation during brain activation in physiological aging.

Adult↗
PubMed1995

Vasospastic amaurosis fugax in a patient with overlap collagenosis treated with nimodipine.

Vasospasm has been discussed as a less frequent cause of amaurosis fugax. Since its direct demonstration is difficult, its diagnosis is usually based on the exclusion of other causes and/or response to calcium entry blockers. We describe diagnosis and successful treatment of vasospastic amaurosis fugax in a patient with systemic autoimmune disease: A 54 year-old patient with an overlap collagenosis presented with relapsing episodes of transient monocular blindness. Angiography and transcranial Doppler scanning revealed a high-grade stenosis of the left ophthalmic artery. After administration of oral nimodipine the attacks ceased immediately and repeated Doppler examinations confirmed resolution of the stenosis. We infer that vasospasm of inflammatory altered cerebral vessels may contribute to focal neurological deficits in patients with systemic autoimmune disease. Calcium entry blockers should be discussed as a possible treatment in patients with systemic autoimmune disease and evidence of functional disturbances of cerebral blood flow.

Blindness↗
PubMed1995

Coupling of brain activity and cerebral blood flow: basis of functional neuroimaging.

The coupling of brain cell function to the vascular system is the basis for a number of functional neuroimaging methods relevant for human studies. These include methods as diverse as functional magnetic resonance imaging, positron emission tomography, single photon emission tomography, optimal intrinsic signals, as well as near infrared spectroscopy, a method that may have imaging capabilities in the near future. These methods map a specific localized brain activation through a vascular response, such as an increase in cerebral blood flow or a change in blood oxygenation. To understand these direct maps to obtain high resolution maps of localized functional brain activity, a precise knowledge of the specific underlying physiological mechanisms and methodological properties and restrictions is essential. In this article, these fundamental physiological and methodological aspects will be discussed. After reviewing how the techniques cited obtain maps of functional activity, we will discuss our current knowledge of the physiology of coupling with particular reference to the functional imaging techniques. Specifically, we will consider the function, the mediators, and the hemodynamic mechanisms of coupling and point out potential interference by diet, and neurological disease.

Brain↗
PubMed1994

Noninvasive assessment of cerebral hemodynamics and tissue oxygenation during activation of brain cell function in human adults using near infrared spectroscopy.

Near Infrared Spectroscopy (NIRS) was employed to noninvasively and continuously (temporal resolution 0.5 s) assess changes in cerebral hemodynamics and oxygenation during various functional states of the adult human brain. During cognitive stimulation (performing calculations) a frontal increase in local cerebral blood volume and oxygenated hemoglobin concentration was observed in most (10 of 12) subjects. During visual stimulation (observing a picture) this was demonstrated in the occipital region in all three subjects. Deoxygenated hemoglobin either decreased, remained unchanged or slightly increased during these procedures. Epileptic patients were examined during spontaneously occurring complex-partial seizures. During these seizures extremely large increases in blood volume and oxygenated hemoglobin concentration were measured. In conclusion, this feasibility study indicates that NIRS might become a useful and simple bedside tool to assess brain function.

Adult↗
PubMed1994

Coupling of cerebral blood flow to neuronal activation: role of adenosine and nitric oxide.

We studied the role and relationship of the putative mediators of coupling of cerebral blood flow (CBF) and neuronal activation, adenosine (Ado) and nitric oxide (NO). Topical brain application over the whisker barrel cortex of anesthetized rats (n = 24) of the Ado receptor antagonist theophylline (Theo, 5 x 10(-5) M) for 30 min reduced the CBF response to deflection of the contralateral whiskers from 17.9 +/- 3.0% of baseline to 10.6 +/- 2.7% (P < 0.05). Coapplication of Theo (5 x 10(-5) M) and the NO synthase blocker N omega-nitro-L-arginine (L-NNA, 10(-3) M) for 30 min led to a further reduction in the CBF response to whisker stimulation to 7.5 +/- 1.3% (P < 0.05 compared with Theo alone). The CBF effect of sodium nitroprusside (10(-5) M) was not affected by Theo-L-NNA coapplication (122 +/- 25 vs. 140 +/- 25%, n = 5). Application of adenosine deaminase (1 U/ml, n = 5) reduced the CBF response to whisker stimulation from 18.2 +/- 0.7 to 10.7 +/- 1.9% (P < 0.05). Superfusion of L-NNA (10(-3) M, 30 min, n = 7) attenuated the CBF response to application of Ado (10(-4) M) from 39.4 +/- 10.4 to 22.9 +/- 10.5% (P < 0.05). N omega-nitro-D-arginine did not affect the CBF response to Ado (n = 5). We conclude that 1) Ado is involved in coupling of CBF to neuronal activation, 2) NO is involved in this response as well, and 3) there is an interaction between the vasodilator pathways of Ado and NO.

Adenosine↗
PubMed1994

Capillary perfusion of the rat brain cortex. An in vivo confocal microscopy study.

Confocal laser-scanning microscopy was used to visualize subsurface cerebral microvessels labeled with intravascular fluorescein in a closed cranial window model of the anesthetized rat. In noninvasive optical sections up to 250 microns beneath the brain surface, plasma perfusion and blood cell perfusion of individual capillaries were studied. Under resting conditions, in all cerebral capillaries the presence of plasma flow as demonstrated by the appearance of an intravenously injected fluorescent tracer within 20 seconds after injection. Plasma flow was verified even in capillaries that contained stationary erythrocytes or leukocytes; 91.1% of the capillaries contained flowing blood cells, 5.2% contained stationary blood cells, and no blood cells were seen in 3.6%. Mean blood cell velocity was 498.3 +/- 443.9 microns/s, and the mean blood cell supply rate was 35.75 +/- 28.01 cells per second. When capillaries were continuously observed for 1 minute, "on" and "off" periods of blood cell flow were noted. During hypercapnia (increase of PCO2 from 33.25 to 50.26 mm Hg), mean blood cell flux increased from 38.6 +/- 17.2 to 55.5 +/- 12.2 per second (P < .005, paired t test of mean values in six animals), and blood cell velocity increased from 519.5 +/- 254.8 to 828.5 +/- 460.8 microns/s (P = .074, paired t test of mean values in six animals). Homogeneity of blood cell flux increased as indicated by the coefficient of variation decreasing from 44.6% to 22.0%, and the portion of poorly perfused capillaries (blood cell flux, < 40 per second) decreased from 59.2% to 22.4%.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Cortical hypoperfusion after global forebrain ischemia in rats is not caused by microvascular leukocyte plugging.

BACKGROUND AND PURPOSE: We tested the hypothesis that cerebral hypoperfusion after experimental global cerebral ischemia is caused by plugging of the microcirculation with activated leukocytes using in vivo microscopic observation of the behavior of leukocytes in the cortical microcirculation during the transition from postischemic hyperperfusion to hypoperfusion. METHODS: Anesthetized and ventilated rats (n = 24) were equipped with a closed cranial window. Physiological variables and cortical regional cerebral blood flow (laser-Doppler flowmetry) were measured continuously. Leukocytes were labeled intravitally with rhodamine 6G and visualized in the microcirculation of the brain surface and outer layers of the cortex with confocal laser scanning microscopy from preischemia to 4 hours after reperfusion that followed 10 minutes of global cerebral ischemia (rCBF < 10% of control). RESULTS: In controls (n = 8), there were no signs of leukocyte activation over the 4-hour observation period. In ischemic rats (n = 16), during the transition from hyperperfusion to hypoperfusion there was no change in the behavior of leukocytes. Most notably, no capillary pluggers were seen. In the postischemic period only a slight increase of the number of leukocytes rolling along or sticking to the venular endothelium was seen, and very few capillaries were plugged by leukocytes. Extravasation of leukocytes into the brain tissue was observed in 8 rats beginning 2 hours after ischemia with a variable degree between animals. CONCLUSIONS: Because there was only mild activation of leukocyte-endothelium interaction within the first hours of reperfusion after 10 minutes of global forebrain ischemia, because no leukocytes plugged superficial cortical capillaries during the transition from hyperperfusion to hypoperfusion, and because the regional cerebral blood flow transition was very rapid, we speculate that leukocyte plugging is not responsible for the early cortical hypoperfusion seen after brief global ischemia in rats.

Animals↗
PubMed1994

Dural sinus thrombosis: value of venous MR angiography for diagnosis and follow-up.

OBJECTIVE: The purpose of this study was to determine the value of venous MR angiography as the sole procedure for the diagnosis and follow-up of dural sinus thrombosis. MATERIALS AND METHODS: Forty-two patients with clinical findings suggestive of dural sinus thrombosis were examined with venous MR angiography and spin-echo MR imaging. Maximum-intensity-projection reconstructions and individual sections of the MR angiograms were examined for direct and indirect signs of dural sinus thrombosis by assessing flow signal from the major sinuses, the jugular bulb, upper jugular veins, ascending cortical veins (occlusion or increased flow due to formation of collaterals), diploe (emissary) veins and extracranial veins, and the deep subcortical veins (Galen's and internal cerebral veins). Direct signs of dural sinus thrombosis on MR angiograms included lack of typical high flow signal from a sinus that did not appear aplastic or hypoplastic on single sections from MR angiography and the frayed appearance of the flow signal from a sinus after recanalization. Indirect signs of dural sinus thrombosis included evidence of formation of collaterals, unusually prominent flow signal from deeper medullary veins, cerebral hemorrhage, visualization of emissary veins, and signs of increased intracranial pressure. When available, conventional angiograms were evaluated by analogous criteria as appropriate. Digital subtraction or cut-film angiograms were available for correlation in nine patients. In nine patients, MR angiography was repeated up to eight times during the course of follow-up. The results of MR angiography for all patients were compared with results in 10 control subjects. Confirmation of the diagnosis of dural sinus thrombosis was based either on conventional angiographic findings or on the changes seen in follow-up examinations. RESULTS: Dural sinus thrombosis could be ruled out in 25 of the 42 patients on the basis of clinical and MR angiographic findings. In 17 patients with MR angiographic findings that indicated dural sinus thrombosis, conventional angiography confirmed the diagnosis in nine patients, and changes seen on repeat MR angiograms during follow-up confirmed the diagnosis in nine patients as well (one patient's diagnosis was confirmed by both techniques). Individual frames from two-dimensional fast low-angle shot sequences allowed direct visualization of thrombus. Limited spin-echo sequences as performed here provided inconsistent findings and were insufficient for diagnosis. In the 10 control subjects, attenuation of flow signal was seen in the torcular Herophili in all studies; one subject had a nonpathologic variant of the sinojugular system. CONCLUSION: MR angiography is the technique of choice for diagnostic evaluation and follow-up of dural sinus thrombosis, and it is reliable as the sole examination for this condition. When MR angiographic findings are unremarkable and other abnormalities must be ruled out, routine spin-echo MR imaging should be performed.

Adult↗
PubMed1994

Pathophysiological aspects of cerebral sinus venous thrombosis (SVT).

In a series of 102 patients with angiographically proven cerebral sinus venous thrombosis (SVT) significant differences with arterial cerebrovascular disease were noted with respect to disease onset, reversibility of symptoms, occurrence of epileptic seizures and headache, cerebral blood flow under resting and stimulated conditions, occurrence of intracranial bleedings, and response to heparin therapy. From these findings pathophysiological differences are hypothesized: Whereas arterial cerebral ischemia usually is a monophasic abrupt thrombotic process and there is only a small penumbra, SVT is a continuing process of disequilibrium between prothrombotic and thrombolytic mechanisms; large areas of the brain are only functionally or metabolically disturbed but not irreversibly damaged. Intracranial bleeding in SVT is a consequence of increased venous and capillary pressure and thus occurs more frequently than in arterial thrombotic disease in which capillary pressure is reduced by the thrombosis and bleeding occurs during reperfusion of tissue damaged by ischemia. Heparin treatment in SVT is effective since it shifts the equilibrium away from the prothrombotic side and is able to save large areas of brain tissue that are only reversibly damaged. It improves venous outflow and thus decreases the risk of intracranial hemorrhage, in contrast with the arterial thrombotic disease where heparin increases the risk or at least the severity of intracranial bleedings.

Cerebral Angiography↗
PubMed1993

Near infrared spectroscopy (NIRS): a new tool to study hemodynamic changes during activation of brain function in human adults.

In healthy human adults, cerebral concentrations of oxygenated hemoglobin ([HbO2]) and deoxygenated hemoglobin ([HbR]) were assessed during brain activation using near infrared spectroscopy (NIRS). Measurements were made either in the frontal cortex (n = 10) during performance of cognitive tasks or in the occipital cortex (n = 6) during visual stimulation (flash-light exposure, picture observation). The typical findings during brain activation were an increase in [HbO2] and a decrease in [HbR]. We demonstrate that these findings are not due to alterations in skin blood flow. NIRS is a simple bedside technique for the assessment of hemodynamic alterations accompanying brain activation.

Adult↗
PubMed1993

Role of nitric oxide in the coupling of cerebral blood flow to neuronal activation in rats.

We tested the hypothesis that nitric oxide (NO) is a mediator in the coupling of cerebral blood flow to neuronal activation. The production of NO was blocked in anesthetized rats with the NO-synthase inhibitor N omega-nitro-L-arginine (L-NA). In controls, vibrissae stimulation for 60 s led to a fast (< or = 2 s), 17% increase in regional cerebral blood flow (rCBF) in the contralateral somatosensory cortex. Systemical (10 mg/kg) as well as topical (10(-3) M) application of L-NA reduced the response to stimulation by approximately 50%. Systemical application primarily attenuated the early component of the response, whereas topical application led to an attenuation throughout the whole 60-s stimulation interval. We conclude that NO is involved in rCBF coupling to neuronal activation.

Administration, Topical↗
PubMed1993

Applicability of laser-Doppler flowmetry for cerebral blood flow monitoring in neurological intensive care.

Laser Doppler flowmetry (LDF) is a technique for real-time assessment of cerebral blood flow (CBF) changes with potential clinical applicability. Experimental studies have validated that LDF allows accurate measurement of changes in CBF due to physiological and pathophysiological stimuli. Absolute quantitation of flow in ml/100 g min by LDF is not possible. The technique may be used in patients during open brain surgery and postoperatively for bedside CBF monitoring. Disadvantages of the technique are that the flow measurement is highly localized (about 1 mm3) and artifacts may be produced by movement, light or probe placement over large surface vessels. The fibre optic probes for LDF are small enough to be introduced into routinely used intraventricular pressure catheters. We suggest that simultaneous monitoring of CBF and intracranial pressure by such a device holds promise for improved management of patients with critical brain injury.

Blood Flow Velocity↗