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Biomedical subjects

B Hindfelt

Publications and source records attributed to B Hindfelt.

At least 55 records · Page 3Linked to original sources
PubMed1983

Prostaglandin metabolism and prostacyclin in cerebral vasospasm.

1. Contractions of isolated human pial arteries, induced either by exposition to hemorrhagic cerebrospinal fluid (CSF) from patients with subarachnoid hemorrhage and cerebral vasospasm or by exposition to noradrenaline, were markedly augmented after preincubation of the vessel segments with the cyclooxygenase inhibitor indomethacin, while serotonin-induced contractions were unaffected. 2. Prostacyclin relaxed human pial arteries contracted by either PGF2 alpha, noradrenaline, serotonin or hemorrhagic CSF. The same though less marked effects were obtained with 6-keto-PGE1. 3. The results support the contention that an intact vascular prostacyclin synthesis is important for the maintenance of a normal cerebrovascular tone, and that disturbances of the prostaglandin metabolism may be a prerequisite for the development of arterial spasm after aneurysmal subarachnoid hemorrhage. Tentatively. 4. a prostacyclin deficiency may be involved in the pathogenesis of delayed cerebral vasospasm after subarachnoid hemorrhage.

Alprostadil↗
PubMed1983

Are the vascular effects of naloxone attributable to the preservatives methyl- and propylparaben?

In vitro, the Nalonee preparation of naloxone caused a concentration-dependent relaxation of human pial cortical arteries contracted by potassium, noradrenaline, serotonin, prostaglandin F2 alpha (PGF2 alpha), and haemorrhagic cerebrospinal fluid, or inhibited contractions elicited by these agents. However, the preservatives in the Nalonee preparation, methyl- and propylparaben, had similar effects. Pure naloxone alone had no effect on potassium or PGF2 alpha-induced contractions. It is suggested that the relaxant effects on vascular smooth muscle of Nalonee can be attributed to the alkylparabens rather than to naloxone. The pronounced relaxations induced by the alkylparabens had a rapid onset, and they were stable and could easily be cleared after rinsing.

Arteries↗
PubMed1983

Visually evoked slow eye movements, visual-vestibular interaction, and infratentorial lesions.

The maximum velocity gain of smooth pursuit and optokinetic, vestibular, and optovestibular slow phases was examined in 15 patients with pontine, 10 with medullary, 10 with cerebellar, and 5 with combined cerebello-brain stem disorders. Marked dissociations were observed between smooth pursuit and optokinetic slow phases, especially in medullary disease. A cerebellar deficit enhanced slow phase velocity gain during rotation in darkness, whereas the corresponding gain during rotation in light was normal.

Adolescent↗
PubMed1982

Brachial neuropathy--a vascular cause? Two case reports.

The pathogenesis of brachial neuropathy remains unknown though an infectious or allergic disorder has been postulated. The causes are probably diverse. Two patients are presented suffering from brachial neuropathy of presumed vascular origin.

Brachial Plexus↗
PubMed1982

Clinical and cerebrospinal fluid findings in lymphocytic meningo-radiculitis (Bannwarth's syndrome).

11 patients with lymphocytic meningo-radiculitis (Bannwarth's syndrome) are described. The disease is characterized by intensive pain, often radiating and migrating, and neurological deficits, i.e. peripheral facial palsies, as well as disseminated radiculopathies. In 4 patients the onset was preceded by an arthropod bite, close to which 3 patients exhibited an erythema chronicum migrans. In the cerebrospinal fluid there was a mononuclear pleocytosis, predominantely by lymphocytes. In the early stages, a plasma cell reaction was frequently encountered. Protein analysis indicated a defect in the blood brain barrier and an intrathecal synthesis of IgG. All patients recovered almost completely from their neurological symptoms within 1-2 months, irrespective of treatment.

Adult↗
PubMed1982

Carotid fibromuscular dysplasia and paresis of lower cranial nerves (Collect-Sicard syndrome). Case report.

A patient suffered the acute onset of unilateral pareses of the ninth through 12th cranial nerves (Collet-Sicard syndrome). Ipsilateral retrograde jugular phlebography and carotid angiography revealed irregular aneurysmal changes of the internal carotid artery at the base of the skull, causing compression of the internal jugular vein below the jugular foramen. This finding is discussed in relation to the clinical symptoms and signs, and possible mechanisms are examined. Family history as well as the clinical and roentgenological findings were compatible with a diagnosis of fibromuscular dysplasia.

Adult↗
PubMed1981

Rapid eye movements reflecting neurological disorders.

The accuracy and velocity of voluntary saccades together with the velocity of fact phases of nystagmus were studied in 26 patients belonging to 4 groups with defined neurological disorders. Patients with speech disorders of the dyspraxia type, indicating the lesion in the left frontal cortex, showed a pronounced decrease in saccadic accuracy in combination with normal saccadic and quick phase velocity. Patients with pontine disorders showed a significant decrease in the peak velocity of saccades and quick phases of nystagmus while the accuracy of the saccades ranged from normal to severely disturbed. Patients with acute meningo-encephalitis showed increases in peak velocity of saccades and of quick phases of nystagmus and the accuracy was somewhat reduced. Patients with a labyrinthine disease showed normal velocity of saccades and of quick phases as well as normal accuracy of saccades.

Acute Disease↗
PubMed1981

The effect of temperature elevation on the cerebrovascular response to noradrenaline and 5-hydroxytryptamine.

Fever frequently complicates stroke and subarachnoid haemorrhage. A transient rise in transmitter monoamine levels of plasma and cerebrospinal fluid occurs in these diseases. The present study demonstrates an enhanced vasoconstrictor response of cerebral vessels to noradrenaline-but not 5-hydroxytryptamine-following a rise in temperature. The augmented response is more likely due to an impaired inactivation (re-uptake) of the amine than to an altered sensitivity of the post-synaptic alpha-adrenergic receptor, since it could be reproduced by pretreatment with cocaine. The finding indicates that it may be important to combat fever in these patients.

Animals↗
PubMed1981

Cerebrovascular effects of ammonia in vitro.

The effect of ammonia (ammonium salts) upon human and rabbit cerebral arteries was studied in vitro. Ammonia (NH3/NH4+) caused relaxation of cerebrovascular smooth muscle which was transient and occurred irrespective of how the vessels were preconstricted (potassium-Krebs solution, noradrenaline, serotonin, prostaglandin F2 alpha). The effect was independent of ammonia-induced extracellular changes in pH. It is concluded that ammonia may contribute to the vasodilatation and increase in cerebral blood flow which occurs under certain pathophysiological conditions.

Ammonia↗
PubMed1981

Vasoconstrictive effects of human post-hemorrhagic cerebrospinal fluid on cat pial arterioles in situ.

Cat cortical arterioles were exposed in vivo to cerebrospinal fluid (CSF) from four patients with subarachnoid hemorrhage (SAH) due to a ruptured intracranial aneurysm. Pial arteriolar caliber was measured by the television image-splitting technique. There was a consistent vasoconstrictive response to CSF. This effect could be ascribed neither to the pH of the CSF nor to the potassium concentration. The vasoconstriction, which was more pronounced with decreasing arteriolar caliber, could be resolved by the perivascular application of nifedipine.

Adult↗
PubMed1981

Effects of indomethacin and prostacyclin on isolated human pial arteries contracted by CSF from patients with aneurysmal SAH.

In small human cerebral arteries preincubated with indomethacin, contractions induced by cerebrospinal fluid (CSF), from patients with subarachnoid hemorrhage were markedly increased. Also contractions induced by noradrenaline, but not 5-hydroxytryptamine, were augmented. Prostacyclin and its metabolite 6-keto-prostaglandin (PG)E1 reversed the contractions induced by CSF, as well as by noradrenaline, 5-hydroxytryptamine, and PGF2 alpha. The findings suggest that these substances are able to counteract the influence of vasoconstrictor material in hemorrhagic CSF. If the capacity to synthesize these "protective" arachidonic acid metabolites is reduced, the resulting imbalance between contractile and relaxant forces acting on the vessel wall may lead to sustained cerebral vasoconstriction.

Adult↗
PubMed1980

Experimental porta-caval anastomosis and motor nerve conduction velocity in the rat.

The influence of portal-systemic shunting on maximal motor nerve conduction velocity (MCV) was analyzed in rats with portacaval shunts. At 3 and 8 weeks after the shunting there was a marked but transient fall in MCV. This was not prevented by colectomy. At 16 weeks the MCV had almost normalized, despite sustained portal-systemic shunting. When examined at 3 weeks postoperatively, MCV was less affected by ischaemia than in control animals. The results favour hepatocellular failure as the more important pathophysiological mechanism in hepatic neuropathy.

Animals↗
PubMed1980

Soluble brain proteins in dialysis encephalopathy.

Soluble brain proteins were analyzed regionally in a case of dialysis encephalopathy and compared to the findings in patients dying from uncomplicated uremia and acute myocardial infarction. Sixteen individual proteins were quantitated and the results may indicate that dialysis encephalopathy is accompanied by defects in the blood-brain barrier. However, such a postulated does not explain why certain proteins (gamma-trace protein) occur at very low concentrations in dialysis encephalopathy.

Blood-Brain Barrier↗
PubMed1979

Brain proteins in experimental portal-systemic shunting.

Experimental portal-systemic shunting is accompanied by a reduction of the soluble brain proteins. Isoelectric focusing does not indicate any selective decrease of one particular protein or group of proteins. The reduction persists with sustained shunting. The interference with brain protein metabolism is compatible with a grossly normal behavior, alterness and locomotion.

Albumins↗
PubMed1979

Benign brainstem hematoma.

Brainstem hematoma is generally considered a very rare condition with a grave prognosis. This report presents two patients with extensive brainstem hematomas who both recovered without major sequele. A brainstem hematoma is often impossible to differentiate from an infarction despite angiographic and cerebrospinal fluid examinations, but is readily disclosed by computerized tomography. It is suggested that the seriousness of the prognosis in brainstem hematoma may earlier have been exaggerated as there may have been a tendency to classify cases exhibiting a good recovery as infarcts, while the diagnosis hematoma was reserved for cases verified at autopsy.

Adult↗
PubMed1978

HLA--determination in families with hereditary ataxia.

In three families with hereditary ataxia, where the inheritance pattern was autosomal and dominant, HLA antigens were determined in 25 members. In two of the families, HLA linkage of disease was suggested, whereas in the third family, the data did not directly support this concept, since two recombinational events between the postulated locus for disease and the HLA region had to be assumed. However, with this assumption, our data are compatible with those of one family described recently (Jackson et al. 1977) implying the presence on the sixth chromosome, outside the HLA region, of a locus that determines the development of spino cerebellar ataxia (SCA). Further tests with definition of enzyme markers will have to be performed before conclusions as to HLA linkage of a postulated SCA gene can be made.

Adolescent↗