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Biomedical subjects

L Hasselmark

Publications and source records attributed to L Hasselmark.

13 recordsLinked to original sources
PubMed1998

Serotonergic 'vulnerability' in affective disorder: a study of the tryptophan depletion test and relationships between peripheral and central serotonin indexes in citalopram-responders.

A double-blind study of the tryptophan depletion (TD) challenge was performed on a sample consisting of 20 patients with a major depressive disorder in clinical remission after citalopram treatment. TD was induced by the intake of 43 g of an amino acid mixture containing the five large neutral amino acids. The control group received the same mixture, to which 2.3 g tryptophan had been added. Five of the 12 challenged patients showed a worsening of depressive symptoms during the day of the test. In contrast, there was no mood alteration in the eight control patients. Baseline cortisol levels were significantly higher in responders to TD compared to those in non-responders and controls. Platelet serotonin-receptor function and plasma prolactin levels were correlated. There was a significant positive correlation in the baseline data between rated mood state and plasma cortisol and a significant inverse correlation between related mood state and plasma tryptophan concentration. Thus low mood appeared to be associated with low serotonin precursor availability as well as with high cortisol levels.

Adult↗
PubMed1995

Platelet models and their possible usefulness in the study of migraine pathogenesis.

Platelets may be linked to migraine. On the one hand they are activated during the migraine attack and thus may participate in the pathogenesis of the disorder (the nature of this activation is still unknown). In order to understand this platelet anomaly, we discuss the data available in the literature. In particular, we review recent in vitro studies of alpha-granules and dense bodies secretion, and aggregation induced by collagen and PAF. On the other hand, platelets share many metabolic characteristics with serotonergic neurons and endothelial cells. Accordingly, platelets have been used to investigate the possible role of serotonin turnover and nitric oxide function in migraine. In both cases, the data obtained have shown peculiar abnormalities that may explain pathogenetic and clinical aspects of primary headache.

Blood Platelets↗
PubMed1995

Metabolism and menstrual cycle rhythmicity of serotonin in primary headaches.

We investigated the platelet and plasma levels of serotonin and its metabolite, 5-hydroxyindoleacetic acid, in patients suffering from episodic tension-type headache and migraine with and without aura, during a headache-free period. In female subjects, blood samples were drawn during the follicular, ovulatory, and late luteal phases of the menstrual cycle. In tension headache and migraine with aura, the group mean values of serotonin and 5-hydroxyindoleacetic acid in platelets and plasma were significantly increased, but migraine without aura patients' levels were normal. The pattern of menstrual cycle-related fluctuations in platelet serotonin levels were similar in female patients with tension headache and in controls, with a maximum value in the follicular phase. In both migraine groups, in contrast, the peak occurred in the ovulatory phase. The results are discussed in view of whether these aberrations in peripheral markers of the metabolism and menstrual cycle-related rhythmicity of serotonin may reflect similar alterations in the central nervous system.

Adolescent↗
PubMed1994

Decreased collagen-induced platelet aggregation and increased platelet arginine levels in migraine: a possible link with the NO pathway.

We studied whole blood platelet aggregation induced by collagen, platelet activating factor (PAF) and measured basal platelet L-arginine (L-arg) levels, as an indirect index of the nitric oxide (NO) pathway in migraine. Migraine, both with and without aura groups, showed a reduced aggregation to collagen, but not to PAF, compared with control subjects. Platelet L-arg levels were significantly increased in migraine with aura sufferers, whereas the plasma levels were in the same range in migraineurs and controls. Platelet hyperesponsiveness to collagen stimulation in migraine may be linked to an increased availability of the amino acid precursor and an abnormal NO synthesis.

Adolescent↗
PubMed1994

Platelet secretion from dense and alpha-granules in vitro in migraine with or without aura.

Several studies in vivo indicate platelet activation in migraine, as reflected by increased plasma concentrations of platelet secretory products. In vitro data on platelet secretion are scant, which prompted an investigation into agonist-induced platelet aggregation and secretion in platelets from patients with migraine. Sixty two patients with migraine with aura (MA) and 41 with migraine without aura (MwA) were studied during a headache-free phase, together with 26 healthy controls. Platelet aggregation and secretion in platelet-rich plasma were induced by collagen and platelet activating factor (PAF). Serotonin was measured by high performance liquid chromatography and platelet factor 4 (PF4) with an enzyme immunoassay kit. There were no significant aberrations in platelet aggregation in those with migraine compared with healthy controls. The platelet PF4 secretion induced by PAF (1.0 and 0.1 microM) was increased in MwA (p < 0.05, p < 0.0001) compared with controls, and there was a similar trend in MA (NS, p < 0.01). By contrast, the PF4 secretion induced by collagen (0.5 and 2.0 micrograms/ml) was reduced in MA (p < 0.01 and p < 0.05). Further, the MA group exhibited increased basal intraplatelet serotonin concentrations (p < 0.0001) and increased serotonin secretion induced by both concentrations of collagen (p < 0.0001) and PAF (p < 0.001). The data indicate an abnormal platelet a-granule secretion in those with migraine, and focus attention on PAF as a possible factor contributing to the platelet activation associated with migraine. The increased platelet content and secretion of serotonin was specific to MA, and may reflect different serotonin turnover in the two clinical migraine types.

Adolescent↗
PubMed1993

Increased platelet serotonin content and hypersecretion from dense and alpha-granules in vitro in tension-type headache.

We investigated platelet aggregation and secretion from dense and alpha-granules in vitro in 28 tension-type headache (TH) patients and 26 healthy controls. We also measured basal platelet serotonin levels. Platelet aggregation was normal in TH, but the secretion of serotonin and platelet factor 4 (PF4) was significantly increased in response to 0.5 and 2.0 micrograms/ml collagen and to 1.0 mumol/l PAF. The basal platelet serotonin levels were also higher in patients than in controls. The mechanisms of platelet hypersecretion remain to be determined, but the increased secretion of serotonin is probably in part related to the increased basal levels. The increased platelet serotonin in TH patients may reflect an enhanced serotonin turnover.

Adolescent↗
PubMed1993

Selenium supplementation in intrinsic asthma.

The accumulated data indicate that asthma is associated with reduced circulatory selenium (Se) status and lowered activity of the Se-dependent enzyme glutathione peroxidase (GSH-Px), which may have etiological implications, considering the important role of GSH-Px in the cellular elimination of hydroperoxides. The aim of the present double-blind study was to investigate whether Se supplementation in asthmatic patients may increase GSH-Px activity and possibly bring about clinical improvement. Twenty-four patients suffering from intrinsic asthma were selected and randomized into two groups, and after a preintervention period of 4 weeks, one group received a daily supplement of 100 micrograms sodium selenite for 14 weeks, whereas the other group received placebo. In the Se-supplemented group there were significant increases in serum Se and platelet GSH-Px activity after intervention, accompanied by a significant reduction in the irreversible platelet aggregation induced by 5 mumol/l ADP, while no significant changes in these parameters could be observed in the placebo group. Further, there was a significant clinical improvement in the Se-supplemented group, as compared with the placebo group, with regard to the assembled clinical evaluation made of each patient. This improvement could, however, not be validated by significant changes in the separate clinical parameters of lung function and airway hyperresponsiveness. The results are discussed in view of the role of GSH-Px in the cellular enzymatic oxidant defense system and as a modulator of arachidonic acid metabolism.

Adolescent↗
PubMed1992

Inhaled budesonide regimen enhances serotonin- and arachidonic acid-induced platelet aggregation.

The influence of inhaled budesonide regimen (400 micrograms x 2 for 7 days), on agonist-induced platelet aggregation and secretion, was investigated in 18 volunteers. Platelet activation induced by serotonin and arachidonic acid was significantly enhanced after budesonide, as demonstrated by an increase in aggregation velocity (Vmax) and amplitude (Amax), and in arachidonic acid-induced ATP-secretion. We found no change in platelet aggregation induced by ADP, epinephrine, and A23187. With the exception of epinephrine-induced platelet aggregation, which was inhibited by 10(-5)-10(-4) M budesonide, in vitro studies revealed no influence of 10 min budesonide preincubation (10(-9)-10(-4) M) on agonist-induced platelet activation, suggesting that the ex vivo enhancement of platelet function was mediated by secondary corticosteroid mechanisms. A tentative explanation of the increased arachidonic acid-induced platelet activation, may be a budesonide-induced stimulation of cyclooxygenase. The enhanced serotonin-induced platelet aggregation may be a reflection of exogenous corticosteroid stimulation of the 5-HT2-receptor.

Adenosine Triphosphate↗
PubMed1990

Lowered platelet glutathione peroxidase activity in patients with intrinsic asthma.

Platelet glutathione peroxidase (GSH-Px) activity and serum selenium (Se) levels were determined in 20 patients with intrinsic asthma. Nine of the patients had NSAID-intolerance. The mean value of GSH-Px activity in the patients was 47.0 +/- 7.1 U/10(11) platelets, which is significantly lower than that of 56.4 +/- 12 U/10(11) platelets in the controls (P less than 0.01). There was also a tendency towards lowered Se levels in the patients compared with controls. The results are discussed in view of the protective role of GSH-Px against oxidative stress and the tentative regulatory function of GSH-Px in arachidonic acid metabolism.

Adult↗
PubMed1988

The platelet and the neuron: two cells in focus in migraine.

Reports of platelet abnormalities in migraine are abundant, and the present paper discusses the role of platelets in the migraine aetiology. Platelets are considered good models for pre- and post-synaptic functions in serotonergic neurons. We propose that migraine is associated with a lowered threshold for stimulus response in both platelets and serotonergic neurons and that the alterations in platelet function reflect central serotonergic disturbances. The platelet abnormalities in migraine approach those found in depression, and there are several links between the two disorders. The clinical significance of platelet hyperactivity in migraineurs for the occurrence of thrombotic disorders is also discussed. Studies of platelet functions in migraine, using platelets as models for serotonergic neurons, may broaden our understanding of the neuronal processes that take place during a migraine attack. The platelet can also be an investigative tool for better understanding of the modes of action of anti-migraine drugs.

Blood Platelets↗
PubMed1987

Effect of a carbohydrate-rich diet, low in protein-tryptophan, in classic and common migraine.

Because serotonin, released from platelets, has been suggested to initiate migraine, a decreased platelet serotonin content, attained by a reduced intake of serotonin and the serotonin precursor tryptophan, might be beneficial. In the brain, however, increased serotonin levels, achieved by a high carbohydrate intake, are probably favourable. Seven migraine patients (four with classic, three with common migraine) were placed on a carbohydrate-rich diet, low in protein-tryptophan. Three of the four classic migraineurs, but none of the common migraineurs, noted improvement in their migraine. Platelet serotonin uptake was within the normal range both before and at the end of the diet period. The apparent positive effect in the classic migraineurs could be due to a reduced intake of migraine-precipitating foods and/or increased brain serotonin levels.

Adult↗
PubMedDate not supplied

Effect of picotamide and aspirin, combined or alone, on platelet aggregation in patients with cerebral infarction.

After 7 and 90 days of treatment, we studied the effect of picotamide, a thromboxane synthase inhibitor (450 and 900 mg/day), aspirin (150 mg/day), and aspirin plus picotamide (150 and 450 mg/day respectively) on platelet aggregation, evaluated in platelet rich plasma of 48 patients affected by ischemic stroke. Platelet aggregation, induced by collagen (1.0 and 2.0 micrograms/ml) and adenosine diphosphate (1.0 and 10 micrograms/L), was significantly increased in patients in comparison with healthy controls. Aspirin (150 mg/day) reduced collagen-induced platelet aggregation (1.0 microgram/ml) after 7 days of treatment. Picotamide (450 mg/day) reduced platelet aggregation induced by both concentrations of collagen, while the higher dose (900 mg/day) had no significant effect. Aspirin plus picotamide reduced the aggregation induced by 1.0 microgram/ml collagen and by 10 mumol/L adenosine diphosphate after 90 days of therapy. This study has shown that patients during the acute phase of stroke are characterized by an increased in vitro platelet aggregation. Aspirin may be beneficial in the acute phase of the cerebral ischemic event. Picotamide and picotamide plus aspirin could be useful for reducing platelet aggregation in long term treatment.

Acute Disease↗