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Biomedical subjects

J E Hardebo

Publications and source records attributed to J E Hardebo.

At least 73 records · Page 4Linked to original sources
PubMed1987

Retro-Gasserian glycerol injection in the treatment of chronic cluster headache.

Seven therapy-resistant patients with cluster headache (six of whom were chronic) were treated by percutaneous retro-Gasserian glycerol injections under general anesthesia. In four of the patients immediate and complete relief of attacks was obtained. There was a close correlation between pain relief and the degree of ophthalmic sensory loss. Quantitative estimation of thresholds for thermal perception and pain showed a good correlation to clinically evaluated sensory loss. As the analgesia waned, headaches returned, and the glycerol injections had to be repeated. Two patients were still considerably improved after 5 1/2 and nearly 3 years, respectively. In the other patients the results were less satisfactory at long-term follow-up study. Pure glycerol is highly hypertonic, and the damage of the trigeminal nerve root may be due to this property.

Adult↗
PubMed1987

Nerves containing serotonin, its interaction with noradrenaline, and characterization of serotonin receptors in cerebral arteries of monkey.

1 Immunohistochemistry was applied to study the presence of 5-hydroxytryptamine (5-HT) and dopamine-beta-hydroxylase (DBH) in cerebrovascular nerves of monkeys, and serotonergic receptors were characterized in the vessels by in vitro pharmacology. 2 A well-developed plexus of 5-HT immunoreactive fibres was found to supply the pial arteries at the base of the brain. The network closely resembled the distribution of neural DBH, used as an index for noradrenergic nerves. 3 5-HT contracted the basilar artery (BA) and middle cerebral artery (MCA) with equal potency and intrinsic activity. The effect was not antagonized by phentolamine or propranolol. 4 The 5-HT2 receptor antagonist, ketanserin, inhibited the response to 5-HT in a competitive manner in both vessels, with pA2 values obtained from Schild plots of 9.15 in BA and 9.40 in MCA. 5 Electrical field stimulation elicited a neurogenic contraction that was completely blocked by 3 X 10(-7) M tetrodotoxin, 3 X 10(-6) M guanethidine, and 10(-6) M phentolamine. The response was also antagonized by ketanserin, but only in concentrations higher than those inhibiting the response to 5-HT. 6 In accordance with the findings during nerve stimulation, noradrenaline (NA) contracted the pial arteries, particularly MCA where the intrinsic activity closely resembled the value obtained with 5-HT. Ketanserin antagonized the response, but less efficiently than that induced by 5-HT. 7 5-HT had no effect on the (noradrenergic) neurogenic contraction obtained during electrical stimulation. Nor did 5-HT affect the contraction induced by exogenous NA. 8 It is concluded that 5-HT and NA may be co-localized in perivascular nerves of the monkey brain. 5-HT contracts pial arteries through postjunctional 5-HT2 receptors, but does not seem to interfere prejunctionally with the noradrenergic nerves or with exogenous NA.

Animals↗
PubMed1987

Endothelium-dependent relaxation by uridine tri- and diphosphate in isolated human pial vessels.

Uridine triphosphate (UTP) and uridine diphosphate (UDP) are present in platelets, probably linked to storage organelles. In several animal species, UTP is a powerful constrictor of cerebral arteries, with no detectable dilatory component, which was confirmed in the present study. When testing the vasomotor effects of UTP and UDP in precontracted isolated segments of human pial arteries it was found that these nucleotides were powerful, transient dilators in the concentration range 10(-7)-10(-5) M in the majority of vessels studied. At higher doses a contractile response supervened. Uridine monophosphate and uridine were without effect. Removal of the vessel endothelium mechanically or by perfusion with Triton abolished the dilatory response, and now the contraction appeared already at 3 X 10(-6) M. The present findings add UTP and UDP among the group of endothelium-linked biogenic vasodilators. This may be of pathophysiological importance in the maintenance of an adequate brain circulation in disorders involving platelet dysfunction.

Blood Vessels↗
PubMed1986

Electrical field stimulation in cerebral and peripheral arteries: a critical evaluation of the contractile response.

Electrical field stimulation with recording of isometric contraction in vitro was carried out on small circular segments of pial arteries, in comparison with peripheral arteries from several regions of rat, rabbit, cow, cat, dog and man. It was found that tetrodotoxin (TTX)-resistant contractions were obtained more readily in pial arteries of various species, including man, than in peripheral arteries of similar size. In fact, it was not possible to obtain a purely neurogenic response -- without a TTX-resistant change in tone -- in any pial vessels tested. The stimulation parameters that induced TTX-resistant contraction in pial arteries were similar to those weak parameters that could reveal a purely neurogenic response in certain other arteries, such as rabbit central ear artery and rabbit and feline mesenteric arteries. In these arteries, release of noradrenaline (NA) onto postjunctional alpha-adrenoreceptors was found to be fully responsible for the contraction. The contractile response could be considerably potentiated by blockade of neuronal and extraneuronal uptake, prejunctional alpha-receptor blockade, and 4-aminopyridine (4-AP)-induced enhancement of transmitter release. Addition of compounds to prevent oxidation of released NA (EDTA by its ability to bind metal ions, and ascorbic acid-glutathione, which prevents formation of free radicals) did not enhance the neurogenic response. However, not even under any of these conditions was it possible to reveal a purely neurogenic response in cerebral arteries. Only TTX-resistant contractions, likely to be due to direct smooth muscle activation, were obtained. The explanation may be morphological differences related to myogenic propagation, probably together with poorly sensitive alpha-adrenoreceptors, in these pial arteries. The situation was further complicated by the fading of the TTX-resistant contraction which often occurred upon repeated stimulation. Therefore, acceptance of partial blockade by TTX as a criterion for a neurogenic response in cerebral vessels, as by several previous investigators, may lead to misinterpretation of the true nature of the response. Hence, when studying neurogenic mechanisms in vitro in these arteries, parameters other than vascular tone should be recorded in conjunction with electrical field stimulation, such as registration of junction potentials and measurements of released transmitter.

Animals↗
PubMed1986

Neuropeptide Y induces and modulates vasoconstriction in intracranial and peripheral vessels of animals and man.

Neuropeptide Y (NPY) has recently been reported to coexist with noradrenaline (NA) in central as well as peripheral noradrenergic nerves. NPY-containing nerve fibres are particularly numerous around blood vessels. Studies were performed on isolated pial arteries as well as on arteries and veins from several peripheral vascular beds from rabbit, cat and man. NPY induced a varying degree of direct contraction of the vessels with an EAm up to 15 mN. Pial arteries were more sensitive than peripheral arteries to NPY (mean EC50 = 7.6 X 10(-9) M). The presence of NPY did not cause any consistent or significant potentiation of the contractile response to NA in any of the vessels tested. Transmural electrical stimulation of the perivascular nerves (including blockade with tetrodotoxin) was performed mainly with auricular artery from the rabbit. Blocking experiments confirmed that the neurogenic contraction was mediated by noradrenergic-type fibres. NPY caused a concentration-related potentiation of the neurally evoked contractile response. The peptide also potentiated the tetrodotoxin-resistant probably non-neurogenic contractions obtained during enhanced electrical field stimulation. It is concluded that NPY interacts with NA during sympathetic nerve activation primarily through a presynaptic effect.

Animals↗
PubMed1986

Does sympathectomy or antihypertensive treatment affect the morphometry of basal cerebral arteries in spontaneously hypertensive rats?

Spontaneously hypertensive rats (SHR) and stroke-prone spontaneously hypertensive rats (SHRSP) were treated with a combination of a beta 1-blocker (Metoprolol) and a calcium antagonist (Felodipine) from 1 to 4 or from 4 to 6 months of age. Cross sections of plastic embedded basal cerebral arteries were measured with a digitizer. The ratio between media thickness and luminal radius (m/r ratio) could then be calculated for a standardized condition assuming a smooth, circular internal elastic membrane. The treatment caused a significant decrease of the m/r ratio in various basal cerebral arteries of young and adult SHR and SHRSP, i.e. the therapy may prevent as well as reverse hypertensive structural changes. Unilateral superior cervical ganglionectomy or preganglionic denervation did not affect the structure of basal cerebral arteries in young SHRSP or normotensive controls. A slight decrease of m/r ratio was indicated in the smallest pial arteries on the sympathectomized side, but the results did not allow any conclusion as to differences in effect between preganglionic denervation and ganglionectomy.

Age Factors↗
PubMed1985

Calcitonin gene-related peptide is present in mammalian cerebrovascular nerve fibres and dilates pial and peripheral arteries.

Calcitonin gene-related peptide (CGRP) is a novel 37-amino acid peptide occurring in neurones within sensory ganglia, in brain stem, as well as in the walls of blood vessels of peripheral organs. Pial arteries of cat showed a well-developed supply of CGRP-positive nerve fibres. The peptide was found to be a potent dilator of both pial and peripheral vessels of rabbit and cat, and of pial vessels from man. The dilatory effect was independent of the vascular endothelium and was not mediated through adrenergic, cholinergic or histaminergic smooth muscle receptors. The neurogenic vasoconstriction induced by electrical field stimulation was temporarily inhibited by CGRP, as studied in central ear arteries from rabbits. The results suggest that CGRP is a transmitter or modulator playing a role in the regulation of vascular tone.

Animals↗
PubMed1985

Folic acid responsive postmenopausal homocysteinemia.

Homocysteinemia is associated with juvenile arteriosclerosis, recurrent thromboembolic complications and osteoporosis. Plasma homocysteine, measured as homocysteine-cysteine mixed disulfide (MDS), has in other than homocysteinemics been reported to be higher in patients with coronary heart or cerebrovascular disease than in controls, and higher in men than in premenopausal women. Here, in groups of normal men and normal premenopausal and postmenopausal women, we measured plasma MDS in the fasting state and four hours after a methionine load (100 mg/kg body weight), before and after four weeks of folic acid therapy at 5 mg daily. In their fasting plasma, postmenopausal women (n = 5) had significantly (P less than 0.05) higher MDS concentrations than premenopausal women (n = 5) and younger men (n = 5). After the methionine load MDS concentrations in postmenopausal women rose markedly, reaching levels significantly higher than those in younger men (P less than 0.05), and with no overlap with values in premenopausal women (P less than 0.01), or in older men (n = 5, P less than 0.01). Folic acid therapy resulted in substantial reductions (n = 15, P less than 0.01) of MDS concentrations both before the methionine load (-31%) and after (-28%), though subjects had initially had normal concentrations of serum and erythrocyte folates. We speculate that moderate homocysteinemia might contribute to postmenopausal arteriosclerosis and osteoporosis. Should this prove to be the case, folic acid might be a useful prophylactic.

Adult↗
PubMed1985

Endothelial negative surface charge areas and blood-brain barrier function.

Recent evidence points to the negative surface charge of the luminal endothelial membrane of brain vessels as one determinant for morphologic blood-brain barrier function. The present study evaluates, in awake rats, how barrier function is affected by the polycation protamine to neutralize the negatively charged groups. High local doses of protamine, as infused intracarotideally, are able to substantially impair barrier capacity against albumin and inulin, which normally do not pass the blood-brain barrier. Evidence is presented that it is the positive charge of protamine that is a major factor underlying the barrier opening. However, when comparing the barrier opening obtained by corresponding concentration of the polycation lysine, it was obvious that another property of protamine contributed. This property was not linked to hyperosmolar, hypertensive or vasodilatory barrier opening, but may be a direct, cytotoxic effect of protamine. It is discussed whether barrier opening through transendothelial vesicular or channel transport occurs only at locations on the cell membrane deprived of negative surface charge areas.

Animals↗
PubMed1984

Influence of blood pressure on blood-brain barrier function in brain ischemia.

The influence of systemic blood pressure on blood-brain barrier leakage and hemorrhage in brain ischemia was evaluated in Sprague-Dawley rats with blood pressures at the lower and upper limit normally found in these animals when anesthetized on 70% N2O:30% O2. 24 h after unilateral cerebral microembolization - when significant increases in water content and barrier permeability and decrease in blood flow is present - the extravasation of Evans Blue-albumin and inulin as well as hemorrhage in the infarcted brain area was considerably more prominent in animals with the higher blood pressure. The findings imply that attempts to elevate pressure, as well as subacute surgical circulatory reconstruction to increase perfusion of an ischemic area, may be potentially harmful.

Animals↗
PubMed1984

Perivascular cholinesterase and morphological blood-brain barrier function.

Little is known about the function of cholinesterase activity present in the walls of cerebral microvessels. It has been shown that systemically administered physostigmine, a cholinesterase inhibitor that penetrates the blood-brain barrier, causes barrier opening. This has led to suggestions that perivascular cholinesterase is involved in the maintenance of morphological blood-brain barrier function. The present study demonstrates that the physostigmine-induced barrier opening is fully attributable to the acute hypertension and hypercapnia the agent gives rise to. Thus, it is discussed whether the enzyme activity may function as an enzymatic barrier to cholinergic agents.

Animals↗