Platelets, Drugs and Longevity in a Geriatric Population

101

SUMMARYThe capacity of intracarotid Infusion of urokinase to salvage neurologic function in a baboon model of acute thrombotk stroke has been studied. The model consists of reversible eccentric balloon compression (3 hours) of the right middle cerebral artery (MCA) proximal to the take-off of the lentlculostriate arteries (LSA), resulting in in situ thrombosis of perforating branches supplying the right corpus striatum. Neurologic endpoints included quantitative assessment of neurologic function (NE), estimation of cerebral infarction volume by computerized tomographic (CT) scan, and carotid angiography. In untreated acute stroke control animals (n = 6), a persistent decrease in functional score (from 100 to 36 ± 11) at 14 days and a defined region of cerebral infarction (volume = 3.2 ± 1.5) were detected at 10 days. Intracarotid urokinase administered to five animals (1.2 x 10* II) over 60 min) following the 3 hour period of MCA occlusion improved neurologic function (NE = 50, 55, 85,100,100) and reduced infarction size (0.3, 0.5, 0.8,0.7,1.1 cm 3 , respectively) without evidence of intracranial hemorrhage. Systemk fibrinogenolysis was produced in all five treated animals. We conclude that thrombolytic therapy given within 3 hours of experimental thrombotic ocdusion may salvage neurologic function and reduce cerebral Infarction volume without CT scan detectable intracranial bleeding.

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confidence: 99%

The beneficial effect of intracarotid urokinase on acute stroke in a baboon model.

Zoppo¹,

Copeland²,

Waltz³

et al. 1986

101

“…So, platelet activation was abnormal in acute cerebral ischemia but usually returned to normal with or without anti-platelet therapy. It has been observed that Sulfinpyrazone was effective in the patients with stroke, 6 and Amaurosis fugax. 5,17 Recently, Ticlopidine has been reported to be a potent, long-lasting inhibitor of platelet aggregation and to exert a potent anti-thrombotic action.…”

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confidence: 99%

Usefulness of the measurement of plasma beta-thromboglobulin (beta-TG) in cerebrovascular disease.

Taomoto¹,

Asada²,

Kanazawa³

et al. 1983

The plasma concentration of the platelet-specific protein beta-thromboglobulin (beta-TG) was measured in 39 normal subjects and 568 patients of neurological diseases. The beta-TG RIA commercially available KIT was also evaluated. Abnormally high plasma levels of beta-TG were demonstrated in groups of ischemic or obstructive cerebrovascular diseases as compared with that of normal subjects. The highest concentrations were found in 8 patients with Moya-Moya disease, (mean concentration of beta-TG was 204.4 ng/ml), completed stroke at an acute stage was next (mean beta-TG level was 194.8 +/- 70.8 ng/ml). On the other hand, many hemorrhagic cerebro-vascular diseases or other neurological diseases such as brain tumors, hydrocephalus, etc. do not show elevated beta-TG levels. In many patients with ischemic or obstructive cerebro-vascular diseases treated with anti-platelet drugs such as Aspirin, Dipyridamole, Bencyclane or Ticlopidine, a significant fall in plasma concentration of beta-TG was chronologically demonstrated. The measurement of plasma beta-TG concentration may be useful not only in the diagnosis of ischemic or obstructive cerebro-vascular disorders but also in judging the efficacy of anti-platelet therapies and prognosis.

“…Blakely and Gent randomly allocated 291 older men to sulfinpyrazone or placebo and observed a significant reduction in death from apparent vascular causes in the sulfinpyrazone treated group. 10 Thus, there is some evidence that sulfinpyrazone is therapeutically effective in patients with cerebrovascular disease.…”

Section: Discussionmentioning

confidence: 99%

Effect of sulfinpyrazone on platelet survival time in patients with transient cerebral ischemic attacks.

Steele¹,

Carroll²,

Overfield³

et al. 1977

Platelet suppressant drugs have been suggested as beneficial for patients with transient cerebral ischemic attacks and these drugs have been shown to lengthen shortened platelet survival time. In the present study platelet survival time (autologous labeling with 51Chromium) was measured in 25 patients with transient cerebral ischemia involving a carotid distribution. Platelet survival was shortened in all patients (2.5 +/- 0.10 days; AVE t 1/2 +/- SEM; Normal 3.7 +/- 0.04 days P less than 0.001). Sulfinpyrazone increased platelet survival in 9 of 19 (47%) of patients (2.4 +/- 0.10 to 2.8 +/- 0.16 days; P less than 0.01). Of the 19 treated with sulfinpyrazone, 10 had a marked reduction in the frequency of transient ischemic episodes and an increased in platelet survival (2.6 +/- 0.16 to 3.1 +/- 0.22 days; P less than 0.01) was observed in all patients. Three patients had no benefit from sulfinpyrazone and alteration of platelet survival did not occur. Results suggest that platelet survival is shortened in patients with transient cerebral ischemia, that sulfinpyrazone increases platelet curvival and may decrease the frequency of ischemic episodes, and that there may be a relationship between clinical benefit and alteration of platelet survival time.