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Biomedical subjects

J E Hardebo

Publications and source records attributed to J E Hardebo.

124 records · Page 7Linked to original sources
PubMed1977

Regional brain uptake of noradrenaline following mechanical or osmotic opening of the blood-brain barrier.

The passage of noradrenaline from the cerebrovascular circulation into the brain (vessel walls and parenchyma) was studied quantitatively and regionally by a modification of Oldendorf's technique for determination of brain uptake index. Using 14C-ethanol as the highly diffusible internal standard, the index for noradrenaline varied between 2.7 and 4.5% in different regions, confirming the poor penetration of this neurotransmitter. The barrier was impaired transiently as evidenced by Evans blue extravasation, through osmotic opening by internal carotid injection of a hyperosmolar urea solution or mechanical disruption by a short-lasting elevation of the intracarotid hydrostatic pressure. This resulted in a 3-4-fold increase in the passage of noradrenaline from the circulation into the brain.

Animals↗
PubMed1977

Quantitative evaluation of the blood-brain barrier capacity to form dopamine from circulating L-DOPA.

The ability of the blood-brain barrier to form dopamine from increasing doses of systemically administered L-DOPA has been studied in rats by a combination of chemical determination of dopamine, and histochemical and cytofluorometric measurements of L-DOPA and dopamine. The break-through of L-DOPA from the circulation into the brain parenchyma via the enzymatic blood-brain barrier was estimated by comparing the amount of newly formed dopamine in the caudate nucleus-putamen and in the cerebellum. The capillaries were found to efficiently trap L-DOPA in their walls, and an upper limit was reached (at an administered i.p. dose of 100 mg/kg of L-DOPA). It could be estimated that approximately 3% of the total dose of L-DOPA given was decarboxylated by the blood-brain barrier. The possible influence by the regional differences in perfusion of the two regions seen after administration of L-DOPA was ruled out in measurements of local cerebral blood flow using the 14C-ethanol technique.

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PubMedDate not supplied

Interaction between cerebrovascular sympathetic, parasympathetic and sensory nerves in blood flow regulation.

Morphological and pharmacological findings support that different cerebrovascular nerve types have close relationships in the vessel wall and that interactions may contribute to the control of vascular tone. This study in rat investigates whether interaction in blood flow regulation occurs between sympathetic, parasympathetic and sensory nerves in the cerebral vessels. Cortical blood flow (CBF) was measured with a laser-Doppler flowmeter during electrical stimulation of one of the nerves, with or without prior denervation of one or two of the other nerves. Unilateral sympathetic stimulation significantly decreased CBF ipsilaterally. The response was unaffected in magnitude and time course by parasympathetic or sensory denervation. Sensory nerve stimulation did not significantly affect CBF, even after sympathetic denervation. Parasympathetic nerve stimulation caused a marked increase in CBF, which was similar in magnitude in the presence or absence of sympathetic innervation. However, the return to the basal CBF level after parasympathetic stimulation was prolonged after sympathetic denervation. Thus, activation of the sympathetic nerves may contribute to a rapid normalization of the enhanced CBF during parasympathetic nerve stimulation, whereas the reverse phenomenon, parasympathetic normalization of the sympathetically induced CBF reduction, does not occur.

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PubMedDate not supplied

Adenine compounds: cerebrovascular effects in vitro with reference to their possible involvement in migraine.

Adenosine and adenine compounds (AMP, cyclic AMP, ADP and ATP) markedly dilated feline and human pial arteries in vitro, the effect being more prominent with increasing tone of the vessel (active tonic contraction induced by prostaglandin F 2 alpha or serotonin). In contrast, the various adenine compounds were unable to produce any dilation of extracranial arteries tested (branches of lingual, external maxillary, and superficial temporal arteries). The degree of dilatation depended upon the perivascular potassium concentration, so that low potassium increased Emax and reduced ED50 values. Possible involvement of adenine compounds in the vasodilatory phase of the migraine attack is discussed.

Adenosine↗
PubMedDate not supplied

Moderate homocysteinemia--a possible risk factor for arteriosclerotic cerebrovascular disease.

Highly elevated concentrations of homocysteine measured as homocysteine or cysteine-homocysteine mixed disulfide (MDS) are found in plasma and urine in subjects with inherited abnormalities of the methionine metabolism. These subjects have a high incidence of arteriosclerotic vascular complications during childhood. Homocysteine causes endothelial cell injury and cell detachment that initiates the development of arteriosclerosis. The present study demonstrates a significantly elevated mean plasma MDS concentration in 19 patients with arteriosclerotic cerebrovascular disease compared to 17 controls. Our findings suggest that moderate homocysteinemia might be a risk factor for arteriosclerotic cerebrovascular disease.

Adult↗
PubMedDate not supplied

Characterization of the contractile and dilatory responses to electrical field stimulation in guinea-pig and monkey isolated pial arteries.

Changes in vascular tone brought about by electrical field stimulation were studied in isolated guinea-pig and monkey pial arteries, using stimulus intensities similar to, or weaker than, those usually utilized by other investigators. In the guinea-pig, excitation of the smooth muscle cells was easily induced, even at low intensity stimulus parameters. This contraction faded upon repeated stimulation. Certain characteristics indicated that the response was neurogenic with excitation of perivascular sympathetic nerve terminals, despite the fact that it persisted after treatment with guanethidine and phentolamine and was only little reduced by tetrodotoxin; surgical sympathectomy or pretreatment with reserpine abolished the response, whereas removal of endothelium or mast cell degranulation was without effect. Attempts were made to further characterize the substance released. It was probably not noradrenaline, neuropeptide Y, adenosine triphosphate, serotonin, histamine or acetylcholine. In the monkey, similar low intensity stimulus parameters induced a fully tetrodotoxin-sensitive contractile response, attributable to the release of noradrenaline alone. By a minor increase in stimulus intensity, tetrodotoxin-resistant contractions, probably due to direct smooth muscle activation, could easily be obtained in pial arteries from both species. Tests were also performed to elucidate whether a dilatation, caused by a neurogenic transmitter release, could be obtained in these vessels. In both species, however, only a tetrodotoxin-resistant response was found, even at weak stimulus intensities, in agreement with previous observations in vessels from several other species. The present data illustrate the need for a careful choice of stimulus parameters when vascular tonic responses upon electrical field stimulation are used as an index for neurogenic release. They also demonstrate that such a response may, indeed, be neurogenic despite marked resistance to tetrodotoxin.

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