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Biomedical subjects

L Edvinsson

Publications and source records attributed to L Edvinsson.

At least 433 records · Page 24Linked to original sources
PubMed1979

Quantitative changes in regional cerebral blood flow of rats induced by alpha- and beta-adrenergic stimulants.

Cerebral blood flow was measured with the 14C-ethanol technique in 8 regions (frontal, parieto-temporal and occipital cortex, caudate nucleus, thalamus, cerebellum, mesencephalon, and pons) of rats. The highest flow values (83-89.5 ml/100 g/min) were found in cortical areas, whereas pons had the lowest flow (48 ml/100 g/min). Intravenous infusion of noradrenaline or adrenaline markedly reduced rCBF (by 22-48% of control levels) in all regions except thalamus, mesencephalon, and pons. The noradrenaline-induced reduction was blocked, and the effect of adrenaline reversed, after pretreatment with the alpha-receptor antagonist, phentolamine. Isoprenaline infusion markedly augmented rCBF in thalamus, mesencephalon, pons, and also in the caudate nucleus. The response was reduced by the beta-receptor antagonist, propranolol. The experiments show the presence and heterogenous distribution in the cerebrovascular bed of slpha- and beta-adrenoceptors that can be activated by sympathomimetics given systematically. If noradrenaline was allowed to pass the blood-brain barrier after osmotic opening with urea, an increased regional flow was obtained, probably due to a mechanism where the vasodilator effect secondary to activation of cerebral metabolism predominated over the direct vasoconstrictor effect of the amine.

Adrenergic alpha-Agonists↗
PubMed1979

Effect of a calcium antagonist on experimental constriction of human brain vessels.

In search for a potent dilatator or deactivator of constriction of cerebrovascular smooth muscle, the effects of a specific antagonist of the calcium influx necessary for the excitation-contraction coupling process was studied on isolated human pial arteries. The arteries were constricted by addition of noradrenaline, 5-hydroxytryptamine, human plasma or blood. All these agents induced a strong contraction which could effectively be reduced by addition of the Ca++-antagonist, nifedipine, to the organ bath. It is suggested that calcium antagonists might be of value in the treatment of cerebrovascular spasm following a subarachnoid hemorrhage.

Calcium↗
PubMed1979

Effects of nifedipine of pial arteriolar calibre: an in vivo study.

In cats the response of individual pial arterioles to perivascular microapplication of the Ca++-antagonistic drug nifedipine was studied using the image-splitting technique developed by Baez. It has previously been shown that the coefficient of variation for repeated measurements of pial vessel diameter using this system is 1%, under conditions of steady arterial pressure and blood gas tensions. All investigated pial arterioles invariably responded with a dilatation at an injected nifedipine concentration of 10 microM. The dilatatory response was inversely proportional to the resting vessel calibre, i.e., arterioles less tham 70 microns responded with a significantly stronger dilatation as compared with arterioles greater than 100 microns in diameter. In experiments where a minor subarachnoid hemorrhage was made by the injection micropipette injuring capillaries just before the perivascular microapplication of nifedipine, a dilatatory response invariably ensued in spite of the perivascular blood which in itself constricted the arterioles under examination.

Animals↗
PubMed1978

Sympathetic nervous control of cerebrospinal fluid production from the choroid plexus.

The rabbit choroid plexus, responsible for the bulk production of cerebrospinal fluid, is well supplied by sympathetic nerves emanating in the superior cervical ganglia. Electrical stimulation of these nerves markedly reduces production of cerebrospinal fluid, measured by [14C] inulin dilution during ventricular perfusion, whereas sympathetic denervation enhances the rate of formation.

Adrenergic Fibers↗
PubMed1978

Influence of the cerebrovascular sympathetic innervation on regional flow, autoregulation, and blood-brain barrier function.

Experiments have been done on rats, rabbits and baboons to elucidate the role of the cranial sympathetic nerves originating in the superior cervical ganglia in the regulation of local cerebral blood flow, including its autoregulation, and in blood-brain barrier functions. Flow was measured by the [14C] ethanol technique, thermoclearance, and xenon-133 clearance. Blood-brain barrier functions were studied by the extravasation of an Evan's blue-albumin complex and by calculation of brain uptake index for two compounds (noradrenaline and inulin). Electrical stimulation of the sympathetic nerves reduces regional flow to a degree that is related to the amount of local perivascular innervation. The breakthrough of autoregulation during induced systemic hypertension is prevented by bilateral stimulation of the superior cervical ganglia. Acute sympathectomy markedly enhances the vascular penetration both at normotension (tested by brain uptake index for noradrenaline and inulin) and rapidly induced hypertension (evidenced by extravasation of Evans' blue). This extravasation of Evans' blud during acute hypertension can be counteracted by sympathetic nerve stimulation. The results give further support for the view that the cranial sympathetic nerves afford an efficient control of the cerebrovascular bed.

Animals↗
PubMed1978

Demonstration of 5-hydroxytryptamine receptors through inhibition by methergoline in cat pial arteries in vitro.

1 In an attempt to characterize further the nature of the 5-hydroxytryptamine (5-HT)-induced contraction of intracranial vessels, cat's middle cerebral artery was exposed to this amine and the specific 5-HT receptor antagonist, methergoline, under standardized conditions in vitro. Methergoline, in increasing concentrations, produced a parallel shift of the log dose-response curve for 5-HT. 2 The Arunlakshana-Schild plot gave a straight line with a slope of -0.85. The figure corresponding to the pA2 value was 8.80. 3 The findings offer further support for the assumption that the 5-HT-induced intracranial vasoconstriction is mediated by specific 5-HT receptors.

Animals↗
PubMed1978

Effects of dopaminergic agonists and antagonists on isolated cerebral blood vessels.

The vasomotor response of dopamine and dopaminergic agonists was studied in vitro on middle cerebral arteries from cat and pial arteries from humans. The action of various inhibitors was tested in order to define the receptors involved. A contractile response could be obtained by epinine, apomorphine and dopamine in the mentioned order of potency. The effect was blocked by alpha-receptor as well as serotonin receptor antagonists. The mode of inhibition suggested that serotonin receptors rather than alpha-adrenoceptors mediated the dopamine-induced contraction. A dose-dependent dilatation could be evoked by the dopaminergic agonists on actively contracted pial arteries. The relative potency was epinine greater than dopamine greater than apomorphine. The order of potency for the agonists, together with blocking experiments (including a parallel shift in the log dose-response curve induced by bulbocapnine), indicated that the vasodilatation is mediated by specific dopamine receptors.

Animals↗
PubMed1978

Effect of exogenous noradrenaline on local cerebral blood flow after osmotic opening of the blood-brain barrier in the rat.

1. The regional penetration into the brain of exogenous labelled noradrenaline (following unilateral injection into the internal carotid artery) was correlated with the effect of this amine on regional cerebral blood flow as measured by the [14C]ethanol technique in anaesthetized rats. 2. A hyperosmolar solution of urea was injected into the ipsilateral internal carotid artery to induce osmotic opening of the blood-brain barrier. 3. The extent of the blood-brain barrier damage was followed by macroscopic and fluorescence microscopic visualization of systemically injected Evans blue, and by the determination of the brain uptake index for noradrenaline. 4. The extravasation of Evans blue was restricted to the brain areas nourished by the internal carotid artery on the same side as the injection. 5. The normally low penetration of noradrenaline into the brain was enhanced fourfold in those brain regions that showed Evans blue extravasation following the administration of hypertonic urea. 6. In the same regions, the systemic administration of noradrenaline markedly increased local cerebral blood flow, compared to the contralateral hemisphere that was unaffected by the injection of urea. This effect on regional cerebral blood flow was blocked by the beta-receptor antagonist, propranolol.

Animals↗
PubMed1978

Pharmacological in vitro analysis of amine-mediated vasomotor functions in the intracranial and extracranial vascular beds.

The cerebrovascular system (the extra- as well as intracerebral vessels) receives a well-developed innervation by the adrenergic (originating in the superior cervical sympathetic ganglia) and cholinergic nerves. In addition, recent immunohistochemical studies have shown the presence of vasodilatory peptidergic nerve fibres. There may be an association of cerebral blood vessels also with various aminergic nerve systems of intracerebral origin. Besides the nerves, amine-containing mast cells are often located in close relation to the brain vessels. The specific receptors mediating the contractile and dilatory response of the various vasoactive amines--noradrenaline, dopamine, 5-hydroxytryptamine, histamine, acetylcholine--have been characterized in detail in pharmacological experiments. There is a number of major differences in the reactivity of cerebral vessels as compared to vasomotor functions in the peripheral circulation. The observations and results provide a basis for a better understanding of physiological neurogenic control mechanisms in the cerebral circulation, and they may also have implications for the interpretation of pathophysiological phenomena related to, for example, migraine and the vasospasm following subarachnoid hemorrhage.

Cerebral Arteries↗
PubMed1978

Potentiation and antagonism of serotonin effects on intracranial and extracranial vessels. Possible implications in migraine.

The vasoconstrictor action of serotonin and its interaction with drugs (methysergide, pizotifen, cyproheptadine, ergotamine, dihydroergotamine) that have serotonin-antagonistic properties and that are used in the treatment of migraine were studied on isolated feline and human intracranial and extracranial arteries in vitro. The intracranial vessels were more sensitive to serotonin than the extracranial ones. The serotonin antagonists caused the expected impairment of the serotonin-induced contraction. In minute doses, the various compounds potentiated the contraction produced by serotonin. There is reason to believe that the mechanism responsible for this interaction is selective for tryptaminergic agents. This dual action of the serotonin antagonists may contribute to a beneficial effect in migraine by an interference during both the vasoconstrictory and vasodilatory phase.

Animals↗
PubMed1978

Peptidergic (VIP) innervation of the esophagus.

Nerves displaying vasoactive intestinal polypeptide (VIP) immunoreactivity were demonstrated in the esophagus of rats, cats, and pigs. Furthermore, electron microscopy revealed the presence of nerve terminals displaying the features of peptidergic nerves. VIP nerves were abundant within the smooth muscle layer of the lower esophagus of cat and pig. Immunoreactive nerve fibers and nerve cell bodies were found in the plexuses of the esophageal wall. In pig fetuses VIP immunoreactive nerve cell bodies were observed already at crown-rump length of 4 cm. VIP nerves were also observed in human fetal esophagus. For recording of the motor effects of VIP, segments were taken from cat esophagus close to the esophagogastric junction. VIP induced a dose-dependent relaxation upon contraction by carbamylcholine.

Animals↗