Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Interleukin-8 (IL-8) belongs to a family of small, structurally related cytokines similar to platelet factor 4. It is produced by phagocytes and mesenchymal cells exposed to inflammatory stimuli (e.g., interleukin-1 or tumor necrosis factor) and activates neutrophils inducing chemotaxis, exocytosis and the respiratory burst. In vivo, IL-8 elicits a massive neutrophil accumulation at the site of injection. Five neutrophil-activating cytokines similar to IL-8 in structure and function have been identified recently. IL-8 and the related cytokines are produced in several tissues upon infection, inflammation, ischemia, trauma etc., and are thought to be the main cause of local neutrophil accumulation.
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PMID:Interleukin-8, a chemotactic and inflammatory cytokine. 163 1

The effect of pacing-induced myocardial ischemia on platelet activation and fibrin formation was investigated in seven patients with severe proximal lesions of the left anterior descending coronary artery to determine if acute ischemia activates the coagulation system. Fibrin formation was assessed from plasma levels of fibrinopeptide A. Platelet activation was assessed by levels of platelet factor 4, beta-thromboglobulin and thromboxane B2. Plasma levels were measured before, during and after acute myocardial ischemia induced by rapid atrial pacing. Blood samples were collected from the ascending aorta and from the great cardiac vein through heparin-bonded catheters. The occurrence of anterior myocardial ischemia was established by electrocardiography and by myocardial lactate extraction. No significant transmyocardial gradients in the levels of fibrinopeptide A, platelet factor 4, beta-thromboglobulin or thromboxane B2 were found at rest, during ischemia or in the recovery period, and levels in the great cardiac vein did not change in response to ischemia. These data indicate that pacing-induced myocardial ischemia does not result in release of fibrinopeptide A, platelet factor 4, beta-thromboglobulin or thromboxane B2 into the coronary circulation, and imply that acute ischemia does not induce platelet activation or fibrin formation in the coronary circulation.
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PMID:Effect of pacing-induced myocardial ischemia on platelet activation and fibrin formation in the coronary circulation. 295 18

We investigated the behavior of beta-thromboglobulin (beta-TG) and platelet factor 4 (PF 4) during exercise--upright bicycle ergometry--in 30 patients (median age, 62.4 years) with arteriographically proven peripheral arterial occlusive disease (PAOD) in a chronic stable phase. In 15 patients the exercise study was done twice; the second time was concurrent with administration of acetylsalicylic acid (ASA) in a dosage of 1.0 g/day, while the first time was without ASA therapy. There were no significant differences in either the group of patients with or that without ASA with regard to the platelet-specific proteins at rest, immediately after, and 30 min after exercise. Blood collected simultaneously (n = 6) from an arm vein and from a femoral artery and femoral vein also revealed no significant differences. Our findings support the conclusion that exercise-induced peripheral ischemia with severe symptoms of claudication does not produce platelet alpha-granule release.
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PMID:Lack of elevation of beta-thromboglobulin and platelet factor 4 in plasma during exercise in patients with chronic peripheral arterial occlusive disease. 295 58

Unstable coronary artery disease (CAD) might be related to obstructions of coronary blood flow by platelet aggregates. In 121 men and 43 women admitted to the coronary care unit with suspected unstable CAD, blood samples for tests of platelet function were obtained within 24 hours after admission. Platelet reactivity was tested in vitro in platelet rich plasma as the aggregability towards ADP 1 microM and collagen 1 mg/ml and as the sensitivity to prostacyclin (PSP). The levels of beta-thromboglobulin and platelet factor 4 were determined ex vivo in platelet poor plasma. Patients who developed a nontransmural myocardial infarction (n = 39) or had signs of myocardial ischemia at an exercise test performed within a week (n = 39) were considered to have unstable CAD while patients without signs of ischemia constituted the control group. In the acute phase the PSP was reduced in patients with unstable CAD without any difference between genders. The aggregability towards ADP was higher in women than men but otherwise there were no differences between groups or sexes in any other test in the acute phase. After 12 months there were no differences in PSP between the groups but women had a lower PSP than men. Thus, in the acute phase of unstable CAD, the platelet sensitivity to the inhibitory effects of prostacyclin was reduced which might contribute to the risk for further platelet aggregation, coronary occlusion and myocardial infarction.
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PMID:Platelet reactivity in unstable coronary artery disease. 295 54

Platelet suppressive agents have been shown to improve the prognosis of coronary diseases such as myocardial infarction and unstable angina. Several markers of platelet activation during myocardial ischemia have been found to be increased. Platelet granule constituents (beta thromboglobulin or platelet factor 4) or thromboxane B2 have been reported to be enhanced and, in some studies, to be correlated with the ischemia. Molsidomine or its active metabolite SIN-1 have antithrombotic properties in experimental models. This effect seems to be at least partly related to their antiplatelet activities. SIN-1A inhibited platelet aggregation and release reaction. Specific investigations have demonstrated that SIN-1A acts at a early stage of platelet activation inhibiting calcium influx and phospholipase activity which lead to inhibition of thromboxane formation and fibrinogen binding. Antiplatelet properties were also observed after oral administration of molsidomine but the extent of inhibition appeared to vary with the subjects.
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PMID:[Role of molsidomine on platelet activation in coronary ischemia]. 296

Platelets are believed to play a role in the pathogenesis of atherosclerosis and of the vascular obstruction that causes the acute complications of coronary artery disease. Since specific behavioral patterns appear to be related to the development of coronary artery disease and since emotional stress may predispose an individual to acute cardiovascular ischemia, it was hypothesized that platelet activation by catecholamines might be involved in these events. To study emotional stress, plasma samples were obtained from 61 senior medical residents immediately before they were to speak in public. There were significant increases in the plasma concentrations of the platelet-secreted proteins platelet factor 4 and beta-thromboglobulin and epinephrine and norepinephrine immediately before speaking, which demonstrates that platelet activation and secretion occur in association with this type of emotional stress. Four trials were carried out to study the mechanism for this observed platelet secretion: (1) phenoxybenzamine, (2) propranolol, (3) 650 mg aspirin, and (4) 80 mg aspirin were given several hours before the public speaking engagement. Neither phenoxybenzamine nor propranolol in doses that blocked the hemodynamic effects of alpha 1- and beta 1-adrenergic stimulation modified platelet secretion. Aspirin also did not block platelet secretion, which suggests that platelets were not being stimulated through a cyclooxygenase-dependent pathway. This study provides direct evidence of platelet secretion in vivo in association with emotional stress, and underscores the potential importance of platelet activation and secretion in the acute events that occur in patients with vascular disease.
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PMID:Platelet activation and secretion associated with emotional stress. 298 76

It remains uncertain whether platelet activation in ischemic stroke is contributory or secondary to brain ischemia. The efficacy of aspirin (ASA) in stroke prevention suggests that platelet activation contributes to the occurrence of stroke. On the other hand, platelet activation may be simply a generalized consequence of cerebral ischemic damage. To examine this issue, plasma levels of the platelet specific proteins beta-thromboglobulin (beta-TG) and platelet factor 4 (PF4) were measured in fifty-eight patients with various defined types of acute ischemic strokes. beta-TG was a broader indicator of platelet activation than PF4. Compared with an age-matched control group, thromboembolic and cardioembolic stroke patients had significantly elevated beta-TG levels (p less than 0.001). Also, beta-TG levels in these stroke categories were significantly higher in samples drawn within the first week after the event than in those drawn later (p less than 0.001). In contrast, beta-TG levels in lacunar stroke patients and in most TIA patients were normal. beta-TG levels did not correlate with the volume of cerebral infarction as measured by planimetry from CT scans. Moreover, beta-TG levels in patients on chronic ASA therapy at the time of stroke did not differ from those in patients of the same diagnostic categories not taking aspirin. These data indicate that platelet activation may be important in some, but not all, subtypes of ischemic stroke and that platelet activation can occur in stroke even though the platelet cyclooxygenase pathway is suppressed.
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PMID:Enhanced in vivo platelet activation in subtypes of ischemic stroke. 316 Dec 20

Platelet factor 4, which has a potent affinity for heparin, has been shown to inhibit the binding of basic fibroblast growth factor to the cell surface receptor and to counteract the biological activities of basic fibroblast growth factor in certain peripheral tissues. In the present in vitro [125I]basic fibroblast growth factor binding experiments, platelet factor 4 consistently inhibited the binding of iodinated basic fibroblast growth factor to cell membranes of the gerbil hippocampus. To investigate the in vivo function of endogenous basic fibroblast growth factor and/or basic fibroblast growth factor receptor possibly activated in the ischemic gerbil brain, we infused platelet factor 4 continuously into the left lateral ventricle with an osmotic minipump. When platelet factor 4 infusion was started within three days after a 3-min ischemic insult, it significantly enhanced ischemia-induced learning disability and ischemic neuronal loss in the CA1 region of the hippocampus, as demonstrated by the results of the step-down passive avoidance task and by subsequent histological examinations. Infusion of platelet factor 4 into the cerebral ventricle of intact gerbils did not affect learning ability or CA1 neuron number. Basic fibroblast growth factor-neutralizing antibody, when infused continuously in the cerebral ventricle, also exhibited a neurotoxic effect in ischemic but not intact gerbils. Basic fibroblast growth factor co-infused with heparin, but not basic fibroblast growth factor alone, rescued a significant number of ischemic neurons which were destined to degenerate without the infusion of heparinized basic fibroblast growth factor, and it prevented ischemia-induced learning disability.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Protective effect of basic fibroblast growth factor-heparin and neurotoxic effect of platelet factor 4 on ischemic neuronal loss and learning disability in gerbils. 777 64

The purpose of this study was to investigate the effects of beraprost sodium, a stable prostacyclin analog, on the parameters of hemostasis, fibrinolysis, and myocardial ischemia in patients with exertional angina. Thirty-one patients with exertional angina who had significant organic coronary artery stenosis in at least one of the three major coronary arteries were selected. All patients underwent quantitative exercise thallium-201 emission computed tomography before and 1 month after 120 micrograms per day of beraprost sodium administration. Before exercise, blood samples were collected from 8:30 a.m. to 9:30 a.m. after the patients had been lying in bed undisturbed for at least 10 minutes. Plasma platelet factor 4 (PF4), fibrinopeptide A (FPA), tissue plasminogen activator antigen (t-PA), and plasminogen activator inhibitor-1 activity (PAI-1) were measured. There were no significant differences in exercise parameters on both exercise tests. However, both the extent and severity scores of ischemia were significantly aggravated (p < 0.05 for both) during beraprost sodium administration. Plasma FPA levels decreased significantly during beraprost sodium administration (p < 0.01). Likewise, plasma PF4 levels decreased significantly during beraprost sodium administration (p < 0.05). As for plasma t-PA antigen levels, there was no significant difference before versus during beraprost sodium administration. Plasma PAI-1 activity levels decreased significantly during beraprost sodium administration (p < 0.05). The results indicate that beraprost sodium has strong antithrombogenic properties. However, its aggravation of myocardial ischemia may limit clinical usage.
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PMID:Effects of beraprost sodium, a new prostaglandin I2 analog, on parameters of hemostasis, fibrinolysis, and myocardial ischemia in patients with exertional angina. 854 11

Mental stress can affect a range of variables relevant to hemostasis and thrombosis. However, research has not clarified whether these effects occur as part of a generalized sympathoadrenal response or whether stress-induced increases in catecholamines and blood pressure have selective and independent effects on hematologic variables. This study assessed the effects of mental and cold pressor stress on platelet activation, hematocrit, and total plasma protein and the relationship of these changes to sympathoadrenal and hemodynamic mechanisms. Platelet factor 4, beta-thromboglobulin, total plasma protein, hematocrit values, and hemoglobin were measured in 22 healthy men (32 +/- 7 years) during rest, mental arithmetic, and cold pressor task. A no-stress control group of five male subjects was used to rule out the possible effects of blood withdrawal in producing these changes. Significant increases to mental arithmetic and cold pressor (p < .001) were observed in platelet factor 4 and beta-thromboglobulin. Increases (p < .002) in hematocrit values and total plasma protein also occurred with mental arithmetic and cold pressor. Correlational analyses revealed that changes in hematocrit and total plasma protein concentrations were related to increased mean arterial pressure during stress, and platelet activation correlated positively with norepinephrine and negatively with epinephrine. The present results indicate that acute psychologic and cold stress cause concurrent changes in several hemostatic factors (increased platelet activation, hematocrit, and total plasma protein) that may play key roles in thrombosis and ischemia. The relationships of hematocrit and total plasma protein to blood pressure increases and the associations between platelet activation and catecholamines support the notion that stress-induced increases in catecholamines and blood pressure have selective effects on specific hemostatic variables.
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PMID:Prothrombotic effects of environmental stress: changes in platelet function, hematocrit, and total plasma protein. 860 Apr 86


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