Platelet Aggregation and Fibrinolytic Activity in Transient Cerebral Ischemia

Andersen, Leif Agerskov; Gormsen, J

doi:10.1111/j.1600-0404.1977.tb05628.x

Cited by 60 publications

(23 citation statements)

References 16 publications

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“…16 - 17 This hemostatic condition may cause or contribute to thromboembolic processes responsible for cerebral vascular occlusion and ischemia. To examine the potential contribution of platelet hyperaggregability in the high dose/low flow response to ET-1, we evaluated ex vivo ADP-induced platelet aggregation.…”

Section: Resultsmentioning

confidence: 99%

Effect of endothelin on cortical microvascular perfusion in rats.

Willette¹,

Sauermelch²,

Ezekiel³

et al. 1990

Stroke

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We used laser-Doppler flowmetry to study the effects of endothelin-1 on local cortical microvascular perfusion and resistance in 29 pentobarbital-anesthetized rats. Intravenous administration of 10-300 pmol endothelin-1 reduced arterial blood pressure and microvascular resistance and increased microvascular perfusion. However, intracarotid administration of low doses of endothelin-1 increased microvascular perfusion and reduced microvascular resistance and arterial blood pressure, whereas high doses (^300 pmol) reduced microvascular perfusion and increased microvascular resistance and arterial blood pressure. Only the high dose/low flow response was associated with attenuation of the electrocorticogram. The low dose/high flow and high dose/low flow responses to endothelin-1 were not altered by blockade of muscarinic and adrenergic receptors. In addition, systemic metabolic changes (arterial pH, PacO}, PaO], and plasma glucose concentration) did not account for the cerebrovascular effects of endothelin-1. Platelet hyperaggregability also did not appear to be a causative factor in the high dose/low flow response to endothelin-1. In fact, ex vivo rat platelet aggregation was inhibited by intracarotid administration of 300 pmol endothelin-1. In conclusion, the cerebral vasculature exhibits extreme sensitivity to the vasodilator properties of endothelin-1 at low doses. The ischemic vasoconstrictor effects observed at high doses implicate endothelin-1 as an important mediator of cerebral vasospasm and/or postlschemic hypoperfusion. (Stroke 1990^1:451-458) E ndothelin (ET-1), a 21-amino acid peptide originally characterized from cultures of porcine aortic endothelial cells, is one in a family of recently described vasoactive isopeptides (ET-1, ET-2, and ET-3).1 -3 The most extensively studied member of this family, ET-1 is an extremely potent vasoconstrictor in a variety of in vitro vascular preparations, with veins being more sensitive than arteries. 4 In pithed or chemically denervated rats, the systemic administration of ET-1 elicits a slowly developing, prolonged pressor response. 1 -4 In contrast, in conscious and anesthetized rats the systemic administration of ET-1 produces an immediate hypotensive response, 4 which is associated, to varying degrees, with reductions in carotid, hind limb, renal, and mesenteric vascular resistance but little or no effect on heart rate (HR). 5 The decrease in vascular resistance may be related to the release of endotheliumderived relaxing factor (EDRF) and prostacyclin (PGI 2 ). Received June 27, 1989; accepted October 18, 1989. pmol/kg i.v.) to conscious or anesthetized rats often results in a biphasic arterial blood pressure response, that is, hypotension followed by hypertension. 4Little is known about the cerebrovascular effects of ET-1. However, the localization of specific, highaffinity ET-1 binding sites in small arteries and paravascular nerves, 7 together with the recent demonstration of prolonged basilar artery vasospasm following intracisternal administration of [8][...

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Section: Resultsmentioning

confidence: 99%

Effect of endothelin on cortical microvascular perfusion in rats.

Willette¹,

Sauermelch²,

Ezekiel³

et al. 1990

Stroke

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“…Activated fibrinolysis in patients with stroke has been indicated by an increase of fragment E, 27 an increase of fibrin monomer 1 -5 or its soluble complex, 28 and a decreased half-life of fibrinogen. 29 The degradation of cross-linked fibrin is catalyzed by plasmin.…”

Section: Discussionmentioning

confidence: 99%

Coagulation-fibrinolysis abnormalities in acute and chronic phases of cerebral thrombosis and embolism.

Tohgi

Kawashima

Tamura

et al. 1990

Stroke

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We assayed plasma concentrations of fibrinogen, fibrinopeptide A, plasmin-os plasmin inhibitor complex, D dimer, and antithrombin III activity in 40 patients with cerebral thrombosis and nine patients with cerebral embolism during the acute (<7 days), subacute (7-27 days), and chronic (>28 days) periods and compared these with 69 controls. In cerebral thrombosis, fibrinogen and fibrinopeptide A levels were elevated significantly in all stages (/7<0.001), whereas plasmin-a, plasmin inhibitor complex and D dimer levels were elevated significantly in the subacute and chronic periods. The antithrombin III activity was significantly decreased in the acute stage. The elevation of fibrinogen and plasmin-tt 2 plasmin inhibitor complex levels in the acute stage was significantly greater in patients with an infarct size greater than 10 mm 2 compared to patients with an infarct size less than 10 mm 2 . We observed similar changes in patients with cerebral embolism. These results suggest that enhanced coagulation exists at all stages and endogenous fibrinolysis is activated in the subacute and chronic periods in a large proportion of patients with cerebral thrombosis and embolism.

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“…The thrombocythemia was not the result of splenectomy, since the platelet number was initially brought to normal values. These hemostasis anomalies are very different from those observed after ischemic vascular stroke, where an excessive response to aggregating substances is seen, 9 " 15 transitory in certain cases 16 ' " and perhaps induced by the ischemia. 18 An excess of circulating platelet aggregates (method of Wu and Hoak) or a spontaneous pathologic aggregation of platelets (Born method) have also been observed after transitory or constituted ischemic stroke, in the absence of a perfect correlation with responses to aggregating substances.…”

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confidence: 68%