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Biomedical subjects

Bernhard Rosengarten

Publications and source records attributed to Bernhard Rosengarten.

5 recordsLinked to original sources
PubMed2003

Control system analysis of visually evoked blood flow regulation in humans under normocapnia and hypercapnia.

OBJECTIVE: Among other factors, the cerebral blood flow (CBF) is regulated in accordance to the arterial CO(2) tension and the cortical activity. The CO(2) test is commonly used to measure the vascular reserve capacity. Most functional imaging studies rely on the activity-flow coupling (AFC). We aimed to combine both challenges in order to increase the insight into mechanisms of CBF regulation. METHODS: Fifteen healthy students underwent a functional transcranial Doppler test using a visual stimulation paradigm: firstly under normocapnia and secondly under conditions of hypercapnia. Hypercapnia was induced by breathing a carbogene gas mixture of 5% CO(2) and 95% O(2). The entire time course of flow velocity adaptation in the posterior cerebral artery (PCA) was analyzed mathematically using a control system approach. RESULTS: Resting CBF velocities increased by nearly 26% under conditions of hypercapnia, whereas the slight increase in arterial blood pressure (ABP) and the decrease in the Pourcelot-Pulsatility index (PI) were statistically not significant. From the control system parameters which were time delay, rate time, gain, attenuation and natural frequency, only the parameter rate time, indicative for the initial steepness of flow velocity increase, showed a statistically significant decrease, consistently for the peak systolic and enddiastolic flow velocity data. As concluded from the unchanged gain parameter the absolute amount of blood flow evoked by the same visual stimulus increased also by 26%. CONCLUSION: Evaluated by Doppler measurements hypercapnia seems to influence the AFC in two ways: It decreases the steepness of the initial increase in blood flow velocity and enhances the absolute amount of blood flow evoked by the same stimulus.

Adult↗
PubMed2003

Neuron-to-astrocyte signaling is central to the dynamic control of brain microcirculation.

The cellular mechanisms underlying functional hyperemia--the coupling of neuronal activation to cerebral blood vessel responses--are not yet known. Here we show in rat cortical slices that the dilation of arterioles triggered by neuronal activity is dependent on glutamate-mediated [Ca(2+)](i) oscillations in astrocytes. Inhibition of these Ca(2+) responses resulted in the impairment of activity-dependent vasodilation, whereas selective activation--by patch pipette--of single astrocytes that were in contact with arterioles triggered vessel relaxation. We also found that a cyclooxygenase product is centrally involved in this astrocyte-mediated control of arterioles. In vivo blockade of glutamate-mediated [Ca(2+)](i) elevations in astrocytes reduced the blood flow increase in the somatosensory cortex during contralateral forepaw stimulation. Taken together, our findings show that neuron-to-astrocyte signaling is a key mechanism in functional hyperemia.

Afferent Pathways↗
PubMed2003

Cerebrovascular reactivity in adolescents with migraine and tension-type headache during headache-free interval and attack.

BACKGROUND: Migraine is a common cause of headache in adolescents. Assuming that the cerebral vasculature is involved in the pathophysiology of migraine, we compared cerebral vasoreactivity in adolescents both during a migraine attack and a headache-free interval. METHODS: A functional transcranial Doppler test utilizing a visual stimulation paradigm was undertaken to measure the evoked flow velocity in the posterior cerebral artery of adolescents suffering from a migraine without aura or a tension-type headache. To serve as a control, data previously obtained from age-matched adolescents with no primary headache disorder were used. The flow curves were evaluated by determining the maximal flow velocity increase and by modeling their time course according to a control system analysis. In that analysis, the main dynamic features of the flow response were described mathematically in terms of a control system model of low order. The parameters were time delay, gain, attenuation, rate time, and natural frequency. RESULTS: The attenuation parameter (P<.005), indicative of an increased tone of the vessel, and the resting absolute flow velocity (P<.01) both showed a significant increase during an attack in the adolescents with migraine; the gain parameter showed a trend towards similar increase (P =.07). The maximal flow velocity did not increase significantly during an attack. CONCLUSIONS: The control system approach utilized here appears to be more sensitive for detecting migraine-associated changes in cerebral vasoreactivity than examination of the maximal flow velocities alone.

Adolescent↗
PubMed2002

A sudden arterial blood pressure decrease is compensated by an increase in intracranial blood volume.

BACKGROUND: A sudden decrease in arterial blood pressure (ABP) will cause the intracranial blood volume (IBV) to rise, despite the fact that arterial cerebral blood flow decreases. The aim of this study was to test the hypothesis that the increase in IBV is caused by a relative decrease of intracranial venous outflow. METHODS AND RESULTS: In 10 healthy volunteers we studied cerebral autoregulation (CA) by causing an ABP drop with bilaterally deflating leg cuffs. Blood flow velocities (BFV) in the middle cerebral artery and the straight sinus were monitored continuously with transcranial Doppler ultrasound, and the ABP with a non-invasive photoplethysmographic method. After transforming all variables in relative changes, the arterio-venous BFV difference was calculated. Allowing for diameter changes of the intracranial vessels of up to 10 %, and assuming a resting averaged cerebral blood flow of 55 to 60 ml per 100 g brain tissue per minute, an IBV increase of 9 to 10 ml could be calculated. CONCLUSIONS: In intact CA, a steep decrease of ABP results in an increase of intracranial blood volume. The transformation of our IBV data by means of the human intracranial pressure-volume relationship results in an excellent agreement with previously reported ICP increases of 10 mmHg. The increase in intracranial blood volume might be of clinical relevance in orthostatic dysregulation by increasing the ischemic tolerance of the brain before cerebral autoregulation becomes effective.

Adaptation, Physiological↗