Biomedical subjects
N Borges
Publications and source records attributed to N Borges.
Changes in brain microvessel endothelial cell monolayer permeability induced by adrenergic drugs.
Brain microvessel endothelial cell monolayers have been shown to be a suitable blood-brain barrier in vitro system to study adrenergic regulation of permeability. We tested adrenergic drugs on bovine brain microvessel endothelial cell monolayer permeability to a biomembrane impermeant molecule, sodium fluorescein. Endogenous catecholamines noradrenaline and adrenaline were tested as well as the alpha-adrenoceptor agonist phenylephrine, the beta-adrenoceptor agonist clenbuterol and the alpha-adrenoceptor antagonist prazosin. Results showed an alpha-adrenoceptor mediated increase and a beta-adrenoceptor mediated decrease in monolayer permeability. Both alpha- and beta-adrenoceptor mediated changes in permeability were abolished by inhibiting fluid-phase pinocytosis, either by vincristine or by avoiding bovine brain microvessel endothelial cell's energy utilization. The reverse transport (i.e., from brain to blood side) was also influenced by adrenergic drugs; alpha- or beta-adrenoceptor stimulation induced a permeability-reducing effect. We conclude that alpha-adrenoceptor stimulation increases bovine brain microvessel endothelial cell monolayer permeability and that beta-adrenoceptor stimulation has the opposite effect. Reverse transport results obtained with beta-adrenoceptor stimulation seem controversial and deserve further study. These results also support in vivo findings that demonstrated adrenergic influences on blood brain barrier permeability.
Influence of electrical stimulation of locus coeruleus on the rat blood-brain barrier permeability to sodium fluorescein.
The role of central adrenergic innervation of the brain capillaries is still a matter of discussion. The hypothesis that these nerves control the blood-brain barrier permeability was tested by electrically stimulating the locus coeruleus, the major central adrenergic nucleus, in the anaesthetized rat. Frequencies of 5, 15, and 30 Hz were used. A frequency dependent increase in blood-brain barrier permeability to sodium fluorescein was verified. Prior administration of the alpha-adrenoceptor antagonist phenoxybenzamine (10 mg/kg i.p., 24 h before electrical stimulation) totally blocked the effect of 15 Hz stimulation. The same dose of pindolol (a beta-adrenoceptor antagonist) given 1 h before electrical stimulation potentiated the effect of 5 Hz stimulation. Thus, blood-brain barrier permeability is increased, in a frequency dependent manner, by electrical stimulation of the locus coeruleus. The results obtained with phenoxybenzamine and pindolol suggest an opposite effect of alpha and beta-adrenoceptors on the control of sodium fluorescein transport through the blood-brain barrier.
Age-induced nerve cell loss in the myenteric plexus of the small intestine in man.
We examined the number of nerve cells of the myenteric plexus and the thickness of the smooth muscle in the small intestine in autopsy material of 6 young and 6 old persons. Neurons in the myenteric plexus have been visualised by a nonhistochemical method (Giemsa) in laminar preparations of the muscularis externa. Significant reductions of at least 34% in the number of neurons in the ganglia of the myenteric plexus of the old subjects were recorded in all regions of the small intestine, especially in the duodenum where the number of neurons decreased by over 38%. However, there was no significant correlation between nerve cell count and thickness of intestinal smooth muscle since no difference was found in thickness of intestinal smooth muscle between young and old subjects. The decrease in the neuron density with age could affect the potential of the enteric nervous system to influence control over several small intestinal functional parameters.
Effects of nebivolol stereoisomers on the action of adrenaline on blood pressure, heart rate and blood levels of noradrenaline and DOPEG.
1. Nebivolol (a new beta 1-adrenoceptor blocking drug) has particular effects on the cardiovascular system, i.e. it induces hypotension without affecting cardiac function or increasing peripheral vascular resistances. In this study, we aimed to evaluate the effects of nebivolol and its stereoisomers on the actions of adrenaline (AD) at the cardiovascular level as well as at the prejunctional level (as ascertained by modification of noradrenaline (NA) and dihydroxyphenylglycol (DOPEG) plasma levels in the anaesthetized dog. 2. AD infusion (0.1 micrograms kg-1 min-1) did not induce statistically significant changes in mean blood pressure and heart rate; it caused a pronounced and sustained rise of AD levels, no significant alterations in NA levels and a marked, progressive and sustained increase in DOPEG levels. 3. Mean blood pressure was not affected by any of the nebivolol isomers. d- and dl-nebivolol in the two doses used (0.3 and 0.03 mg kg-1 in 15 min) caused a significant and dose-dependent decrease in heart rate. Plasma levels of AD and NA were not changed by any of the nebivolol isomers tested. However, all of them significantly reduced the increase in plasma levels of DOPEG induced by adrenaline infusion. 4. We conclude (1) that AD infusion in the dog facilitates NA release and that DOPEG is a good index of this effect; and (2) nebivolol appears to act at the prejunctional level, reducing the increase in NA release induced by adrenaline, as shown by the effect on DOPEG plasma levels.
Adrenergic influences on the control of blood-brain barrier permeability.
The central adrenergic innervation of the cerebral microvessels may play a role in the control of blood-brain barrier permeability. To pursue the study of this hypothesis we investigated the effect of noradrenaline on both the permeability of the blood-brain barrier to sodium fluorescein and on the pinocytotic activity of cerebral endothelial cells in the rat. Noradrenaline, stereotactically injected in the right lateral cerebral ventricle, significantly increased the cerebral extraction ratio of sodium fluorescein in a dose-dependent way. The same effect was induced by phenylephrine. Prostaglandin F2 alpha had no significant effect on the passage of sodium fluorescein through the blood-brain barrier. The effect of noradrenaline (150 micrograms) on the cerebral extraction ratio of sodium fluorescein was totally blocked by phenoxybenzamine (25 mg/kg i.p., 24 h before noradrenaline). Noradrenaline (150 micrograms) significantly increased the pinocytotic activity of cerebral endothelial cells. Phenoxybenzamine (as above) reduced the effect of noradrenaline on pinocytosis. It is concluded that noradrenaline increases the blood-brain barrier's permeability to sodium fluorescein, most probably through an effect on alpha adrenoceptors. The increase induced in the blood-brain barrier's permeability by noradrenaline seems to be due, at least in part, to an increase in the pinocytotic activity of endothelial cells.
[Radiological clinical aspects of a leiomyosarcoma of the stomach].
Explore the source record for details and available documents.