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Biomedical subjects

G Rothacher

Publications and source records attributed to G Rothacher.

6 recordsLinked to original sources
PubMed1994

Intra- and extracerebral blood flow changes and flushing after intravenous injection of human corticotropin-releasing hormone.

To study facial flush after systemic administration of human corticotropin-releasing hormone (hCRH) we injected 100 micrograms hCRH intravenously to ten healthy young men. The increase in facial temperature was measured by infrared camera. A significant increase in facial temperature of 1.39 degrees C +/- 0.3 was found within 7 min in all patients, which lasted up to 60 min, although facial flushing was visible in only 50% (5/10) of the probands. In a second experiment 100 micrograms hCRH was then administered to seven other healthy young men. Intra- and extracerebral blood flow velocity changes in the medial cerebral artery (MCA) and external carotid artery (ECA) were measured after hCRH administration by use of Doppler sonography. We found a decrease of intracerebral blood flow which was caused by hyperventilation and was reversible following 6% CO2 hyperventilation during a second injection of 100 micrograms hCRH. Blood flow velocity in the ECA increased by 111.5 +/- 32.9% (compared to baseline level), lasted up to 60 min after hCRH injection, and was not reversible by 6% end-tidal CO2 ventilation. We thus demonstrated that the direct vasodilatory effect of hCRH involves the ECA-supplied vascular territory only. The intracerebral vasoconstrictory effect represents the result of hyperventilation following hCRH injection. The data thus clearly suggest an interaction of hCRH and the vascular endothelium of the ECA, causing a marked blood flow velocity increase and facial flushing.

Adult↗
PubMed1994

Control for carbon dioxide-related changes in flow velocity by transcranial Doppler monitoring.

Transcranial Doppler ultrasonography can monitor changes in intracranial blood flow velocity over time in a variety of experimental and clinical settings with excellent temporal resolution. Alterations in arterial carbon dioxide pressure exert a profound influence on blood flow velocity. Such changes exhibit important individual fluctuation depending on respiratory status. This limits the ability of transcranial Doppler to accurately study subtle changes in blood flow velocity, independent of the respiratory state of the subject. Suggested here is a method to control for the respiration artifact on blood flow velocity. The middle cerebral artery of 7 healthy male volunteers was studied with transcranial Doppler under resting conditions, monitoring end-tidal carbon dioxide concentration and blood flow velocity. Hyperventilation was performed both voluntarily and with pharmacological induction by human corticotropin-releasing hormone. These studies were carried out both with and without the use of counterregulation of the end-tidal carbon dioxide concentration via a respiration unit, with an adjustable carbon dioxide-oxygen gas supply preventing significant changes in end-tidal carbon dioxide. The blood flow velocity in the middle cerebral artery during maximal voluntary hyperventilation decreased from baseline values of 100% to 44.4 +/- 4.3% (a 55.6% decrease), and with human corticotropin-releasing hormone-induced involuntary hyperventilation, to 65.1 +/- 5.3% (a 34.9% decrease). With the control method, blood flow velocities during voluntary and pharmacological hyperventilation were 100 +/- 1.6% and 100 +/- 2.8%, respectively. This method allows for control of respiration-induced artifacts during transcranial Doppler monitoring, and can be used to assess the effect of direct or indirect blood flow velocity stimuli independent of respiratory status.

Adult↗
PubMed1992

EEG changes in patients during the introduction of carbamazepine.

This study evaluates the EEG changes during the standardized introduction of carbamazepine in 16 previously untreated neurological patients and their relationship to serum levels of carbamazepine and carbamazepine-10,11-epoxide. Therapy was started with a dosage of 400 mg carbamazepine b.i.d. and remained unchanged during the whole study period of 35 days. Frequency analysis of serial EEG records was performed by Fast Fourier Transformation. In comparison to the pretreatment period (1) the mean values of the total power and relative powers of the theta and delta bands increased and (2) the mean values of the relative power of the alpha band and the center frequency decreased. These changes were already established 3 days after the beginning of the treatment and remained constant during the observation period. There were marked interindividual differences. (3) There was no statistically significant correlation between serum levels of carbamazepine or carbamazepine-10,11-epoxide and the EEG parameters. Our results demonstrate that the degree of EEG change primarily reflects individual susceptibility to carbamazepine and its metabolite during the early stage of carbamazepine exposure and is not dose related.

Adolescent↗
PubMed1989

[Carotid dissections].

In younger patients, the clinical symptoms of sudden unilateral headache and facial pain, often combined with Horner syndrome and the cerebrovascular symptoms of TIAs or stroke, should indicate the diagnosis of spontaneous carotid dissection. Angiographic findings can verify this diagnosis, showing various signs of eccentric, narrowing stenosis, false lumen, pseudoaneurysms, or complete occlusion. An addition to noninvasive Doppler ultrasonography, B-mode and Duplex investigations, although more or less nonspecific, give some indications of the diagnosis; modern imaging techniques, especially MRI, can image the intramural hematoma directly. As the hematoma is the source of the intracranial emboli, the therapy of choice in this rarely diagnosed disease should be anticoagulation.

Adult↗
PubMed1986

On the opioid receptor subtype inhibiting the evoked release of 3H-noradrenaline from guinea-pig atria in vitro.

Guinea-pig isolated atria were incubated and loaded with 3H-(-)-noradrenaline. The intrinsic nerves were stimulated with trains of 5 or 35 field pulses (4 Hz), and the evoked efflux of 3H-noradrenaline and of total tritium was determined in the presence of atropine, corticosterone, desipramine, and phentolamine by liquid scintillation spectrometry. Ethylketocyclazocine (1.4 nmol/l, IC50), MR 2033 (9.1 nmol/l), dynorphin A (1-13) (25 nmol/l, peptidase inhibitors present), etorphine (71 nmol/l), and [D-Ala2, D-Leu5]-enkephalin (greater than 10 mumol/l, peptidase inhibitors present) inhibited the stimulation-evoked efflux of 3H-noradrenaline in a concentration-dependent manner, but not morphine up to 10 mumol/l. The inhibition by ethylketocyclazocine, MR 2033, and etorphine was antagonized by naloxone 1 mumol/l. Similarly, the MR 2033 effect was antagonized by SKF 10047 1 mumol/l. All antagonists investigated failed to affect the evoked 3H-noradrenaline efflux when present in the absence of exogenous agonists. Arunlakshana-Schild plots were calculated for the antagonism between ethylketocyclazocine and a pair of stereoisomers, (-)-MR 2266 (20 nmol/l-5 mumol/l) and (+)-MR 2267 (0.3-10 mumol/l) at the presynaptic opioid receptor, and pA2 values were estimated. The isomeric affinity ratio was 60, with pA2 values of (-)-MR 2266, 9.06, and (+)-MR 2267, 7.28, respectively. The results show that the 3H-noradrenaline release can be inhibited via activation of presynaptic opioid receptors. Under the conditions presently investigated endogenous opioids do not modulate the evoked transmitter release. The results favour the idea that a single population (presumably of the kappa-subtype) of opioid receptors is present at guinea-pig atrial noradrenergic nerves.

Animals↗