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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cerebrovascular autoregulation and CO2 reactivity were measured repeatedly in 3 patients with the multiple system atrophy type of autonomic insufficiency (Shy-Drager syndrome) by means of the 133Xe injection method. The degree of cerebral blood flow (CBF) dysautoregulation showed day-to-day variations in 2 of the 3 patients. The CO2 reactivity was normal or supernormal in the supine position in patients with impaired autoregulation. In the head-up position the response to CO2 was slightly suppressed in 2 of the patients, suggesting that chemical control may have tended to compensate for CBF dysautoregulation. It is concluded that the mechanism of chemical control of the cerebrovasculature is different from that which controls autoregulation and may have partially compensated for CBF dysautoregulation.
Stroke
PMID:Cerebral hemodynamics in Shy-Drager syndrome: variability of cerebral blood flow dysautoregulation and the compensatory role of chemical control in dysautoregulation. 70 33

The effect of chronic antiplatelet treatment on PAF--induced platelet aggregation, ATP--release, and cytoplasmic ionized calcium was studied in 20 acute ischemic stroke patients. Chronic antiplatelet treatment failed to suppress these PAF--induced platelet responses. We speculate that selective PAF antagonists may be useful in suppressing PAF--induced platelet activation, and thereby possibly improve the treatment of stroke.
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PMID:[Effect of chronic antiplatelet treatment on platelet activating factor-induced platelet activity in stroke]. 186 62

PAF-acether, a naturally occurring phospholipid, is a potent activator of various biological processes, including platelet aggregation. The mechanisms of action of PAF are largely unknown. We have found that the psychotropic triazolobenzodiazepine drugs, alprazolam and triazolam, potently (IC50 less than 1 microM) inhibit PAF-induced shape change, aggregation and secretion of human platelets. These effects are specific for PAF-activation, since the responses of human platelets to other agonists (ADP, thrombin, epinephrine, collagen, arachidonate and the Ca++ ionophore, A23187) are not inhibited by these triazolobenzodiazepines. The action of triazolobenzodiazepines on PAF-induced platelet function has clinical relevance, especially in diseases where enhanced platelet aggregability may lead to thrombosis and atherosclerosis. In addition, the ability of triazolobenzodiazepines to inhibit other PAF-mediated cellular-responses, such as anaphylactic shock or bronchoconstriction, suggests that these drugs may be useful in preventing several known pathophysiological effects of PAF. The specific antagonism of PAF action by psychotropic drugs also suggests that PAF or PAF-like phospholipids may play a role in neuronal function. This possibility was tested by examining the effects of PAF on neural cells of the clonal line NG108-15, grown in culture in a chemically defined, serum-free medium. Low concentrations of PAF (0.5-2.5 microM) induced neurite extension in NG108-15 cells, whereas higher concentrations (greater than 3 microM) were cytotoxic. Using NG108-15 cells preloaded with aequorin, it was found that PAF causes an increase in intracellular ionized calcium concentration, which is dependent on the presence of extracellular calcium. These results suggest that PAF-induced Ca++ uptake may play a role in neuronal development, and that circulating PAF may contribute to the neuronal degeneration caused by the exposure of neural tissues to blood in situations such as spinal cord injury, trauma, or stroke.
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PMID:Interactions of the alkyl-ether-phospholipid, platelet activating factor (PAF) with platelets, neural cells, and the psychotropic drugs triazolobenzodiazepines. 289 25

Previous investigations have demonstrated that the postural stimulation of arginine vasopressin (AVP) release is reduced in patients with Shy-Drager syndrome. We studied the effects of lypressin nasal spray on hemodynamic parameters in ten patients with chronic orthostatic hypotension. Heart rate, blood pressure, and stroke volume were measured at 0 degrees, 45 degrees and 70 degrees tilt before and one-half hour after two nasal sprays (four United States Pharmacopeia posterior pituitary pressor units, 7.4 micrograms) of lypressin. Lypressin did not significantly alter the effect of tilt on heart rate, stroke volume, and cardiac output but increased the blood pressure and total peripheral resistance. AVP analogues should be tested for treating chronic postural hypotension.
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PMID:Hemodynamic effects of lysine-vasopressin in orthostatic hypotension. 402 27

The effects of prenalterol, a selective beta 1-adrenoreceptor agonist, were studied in a patient with the Shy-Drager syndrome, presenting with incapacitating orthostatic hypotension. The main haemodynamic defect was an impressive postural fall in stroke volume and cardiac output pointing to denervation of the capacitance vessels. Prenalterol 4 X 30 mg orally produced a marked increase in supine and standing blood pressure, along with substantial symptomatic improvement. Notable positive chronotropic and inotropic effects were observed. Association of fludrocortisone 0.5 mg/day resulted in further haemodynamic and symptomatic improvement, presumably due to plasma volume expansion. Haemodynamically, prenalterol and fludrocortisone resulted in a substantial increase in standing cardiac output, primarily due to the chronotropic effects of prenalterol. In addition to the haemodynamic effects, prenalterol stimulated the renin-aldosterone system and restored the normal diurnal pattern of water and sodium excretion, the latter may have contributed to the improvement of orthostatic tolerance. Prenalterol could be a valuable adjunct to the existing treatment schedules of neurogenic orthostatic hypotension.
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PMID:Prenalterol in the treatment of orthostatic hypotension in Shy-Drager syndrome. 614 74

Hemodynamic studies were performed in a case of Shy-Drager syndrome with severe orthostatic hypotension. Marked depression of blood pressure was recognized immediately after the tilt-up, wherein decrease in cardiac output was detected (65 leads to 35 ml; stroke volume) during measurements by echocardiography. In association with the depression of blood pressure and decrease in cardiac output, Doppler sonograms showed the overall blood flow reduction in the brain-supplying arteries, suggesting some breakdown of autoregulation of the cerebral blood flow. Medication with indomethacin obviously limited the depression of blood pressure during the standing exercise. The pressor mechanism of indomethacin might be regarded as a result of increased vasoconstrictivity by inhibiting the synthesis of prostaglandins.
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PMID:Hemodynamics in Shy-Drager syndrome and treatment with indomethacin. 666 53

Study of the reflex heart rate response in humans to apneic facial immersion (simulated diving) and its modifications showed that bradycardia caused by simple application of cold compresses to the face (cold face test) correlated well with that produced by the simulated diving reflex. Bilateral application of cold stimulus to the individual divisions of the trigeminal nerve revealed the ophthalmic division to be the most sensitive pathway for this reflex. The cold face test was standardized in 50 normal individuals and further validated in 10 patients by comparison with the simulated diving reflex, the Valsalva maneuver, and administration of atropine. Patients with diabetes mellitus, brainstem stroke, multiple sclerosis, or Shy-Drager syndrome developed less than normal bradycardia or minimal tachycardia in response to the cold facial stimulus. The cold face test is a novel, simple, safe, and economical test of the integrity of trigeminal-brainstem-vagal reflex pathways, can be utilized practically to assess vagal and brainstem dysfunctions, and has the special advantage of being applicable even in an uncooperative or comatose patient.
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PMID:Cold face test in the assessment of trigeminal-brainstem-vagal function in humans. 736 21

1. In autonomic failure, supine exercise lowers blood pressure and worsens postural hypotension. The somatostatin analogue, octreotide, reduces post-prandial and postural hypotension, but its effects on exercise-induced hypotension and on postural hypotension post-exercise are unknown. 2. Eighteen subjects with chronic sympathetic denervation were studied; 12 had pure autonomic failure and six had additional neurological features of the Shy-Drager syndrome. Haemodynamic, hormonal and biochemical changes were measured before, during and after incremental supine leg exercise on two occasions: on no treatment and after subcutaneous octreotide. Exercise was performed 120 min after octreotide in eight subjects and 60 min after octreotide in ten subjects. 3. Octreotide did not improve exercise-induced hypotension; the blood pressure fall was greater during exercise, but the blood pressure level was no different than without treatment. Heart rate, stroke distance, cardiac index and systemic vascular resistance were similar at rest and changed to the same degree with exercise on and off octreotide. After octreotide, resting levels of serum growth hormone, plasma noradrenaline, adrenaline and renin were unchanged, but glucose was higher and insulin was lower. There was no change in biochemical and hormone levels during exercise either off or on octreotide. 4. After octreotide, although the rate of blood pressure recovery was similar post-exercise, the levels of blood pressure were higher than in the non-treatment phase and postural hypotension was improved before and after exercise. 5. In conclusion, in primary autonomic failure, octreotide did not improve exercise-induced hypotension in the supine position, suggesting that octreotide-sensitive vasodilatory peptides do not contribute to the blood pressure fall.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of the somatostatin analogue, octreotide, on exercise-induced hypotension in human subjects with chronic sympathetic failure. 749 36

Platelet-activating factor (1-O-hexadecyl-2-acetyl-sn-glycero-3-phosphocholine [PAF]) is a potent lipid autocoid produced by many cell types. PAF is produced by cultured rat cerebellar neurons and human fetal brain cells, and has been extracted from brain tissue. Multiple PAF receptors have been demonstrated in brain tissue. PAF stimulates intracellular Ca2+ mobilization and phosphatidylinositol (PI) metabolism in transformed neuronal cell lines via the PAF receptor, to which both pertussis toxin (PTX)-sensitive and -insensitive G protein appear to couple. PAF has potent actions on cerebral vessels and cerebral metabolism when administered in vivo. Direct neuronal effects of PAF, such as inhibition of acetylcholine release, are observed in vitro. Excessive PAF production in pathological states of the nervous system, such as neurotrauma and stroke, has been shown. In multiple studies in rodent and non-rodent models using highly specific and potent PAF antagonists, reversal or prevention of key consequences of brain injury, such as hypoperfusion following ischemia, reperfusion and edema, inflammatory cell accumulation, neurologic/motor deficits, and neuronal salvage, has been demonstrated. These studies taken together support a role for PAF as an important mediator in the pathophysiology of brain injury.
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PMID:Platelet-activating factor: a putative neuromodulator and mediator in the pathophysiology of brain injury. 790 80

Platelet-activating factor acetylhydrolase (PAF-AH), a plasma enzyme that hydrolyzes PAF and oxidized phospholipids, is thought to be involved in protecting cells against oxidative stress. A G(994) (M allele)-->T (m allele) mutation in the plasma PAF-AH gene, which results in a Val(279)-->Phe substitution in the mature protein, leads to a loss of catalytic activity. To elucidate the relationships among PAF-AH enzyme activity, genotype, age, and atherosclerosis, we assayed these parameters in a large Japanese population (n=3932) that consisted of three groups; a control group (healthy individuals; n=1684), a risk-factor group (individuals having at least one conventional risk factor for atherosclerosis; n=1398), and a diseased group (patients who had suffered a myocardial infarction or stroke; n=850). We observed a significantly increased frequency of the m allele in the diseased group as compared with the control or risk-factor groups. Plasma PAF-AH activity increased significantly with age in women in the control group with the MM and Mm genotypes, and in men in the control group with the MM genotype, but not in men with the Mm genotype. In both the risk-factor and diseased groups, however, no correlation was observed between plasma PAF-AH activity and age in subjects with either genotype. These results suggest that in individuals with the MM genotype, plasma PAF-AH activity may be increased in response to stresses induced by PAF and/or oxidized phospholipids that might accumulate with age, but that this response is not evident or reduced in healthy individuals with the m allele, or in subjects with atherosclerotic disease, or having risk factors. Together with our previous findings, the G(994)-->T mutation in the PAF-AH gene may be one of the genetic determinants for atherosclerotic disease in the Japanese population.
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PMID:Correlations between plasma platelet-activating factor acetylhydrolase (PAF-AH) activity and PAF-AH genotype, age, and atherosclerosis in a Japanese population. 1078 53


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