Indium-111 labeled platelets: Studies on preparation and evaluation of in vitro and in vivo functions

Thakur, Mathew L.; Welch, Michael J.; Joist, J. Heinrich; Coleman, RE

doi:10.1016/0049-3848(76)90135-3

Cited by 449 publications

(121 citation statements)

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“…In other models in which in situ perfusion fixation was reportedly employed following MCA interruption or occlusion by several different methods, the effect of MCA occlusion on the dependent vascular bed was not examined. 26 - 21 The failure to observe occlusive material in perforating vessels in the regions of a lenticulostriate artery-dependent cerebral infarction in various primate models when specimens were prepared remotely after stroke induction may be explained by active endogenous fibrinolysis of occlusive thrombi within these small vessels within hours of thrombus formation as recently demonstrated for acute thrombotic occlusion during myocardial infarction. 34 Previous morphologic studies employing in situ perfusion fixation have been inconclusive.…”

Section: Discussionmentioning

confidence: 99%

“…A score was determined for each corpus striatum (maximum = 40 arbitrary units), representing the summation of individual scores from each 10 (M section (maximum = 1 unit = presence of complete thrombotic occlusion; minimum = 0 units = absence of occlusions in any In ten animals (including the eight animals used for occlusion scoring), autologous baboon platelets were labeled with '"in-oxine (Amersham Corp., Arlington Heights, IL) according to the following protocol. 21 Whole blood (100 ml) was collected directly into plastic bags (TA-3, Fenwal Labs, Deerfield, IL) containing 20 ml acid-citrate-dextrose anticoagulant (NIH formula A). The blood was centriftiged in the bag at 300 X g for 10 minutes.…”

Section: Histologic Neuropathologymentioning

confidence: 99%

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Experimental acute thrombotic stroke in baboons.

Zoppo¹,

Copeland²,

Harker³

et al. 1986

Stroke

157

138

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SUMMARY To study the effects of antithrombotic therapy in experimental stroke, we have characterized a baboon model of acute cerebrovascular thrombosis. In this model an inflatable silastic balloon cuff has been implanted by transorbital approach around the right middle cerebral artery (MCA), proximal to the take-off of the lentlculostriate arteries (LSA). Inflation of the balloon for 3 hours in six animals produced a stereotypic sustained stroke syndrome characterized by contralateral hemiparesis. An Infarction volume of 3.2 ± 1 . 5 cm 3 in the ipsilateral corpus striatum was documented by computerized tomographic (CT) scanning at 10 days following stroke induction and 3.9 ± 1 . 9 cm 3 (n = 4) at 14 days by morphometric Deuropathotogic determinations of brain specimens fixed in situ by pressure-perfusion with 10% buffered formalin.Immediate pressure-perfusion fixation following deflation of the balloon was performed in 16 additional animals given Evans blue dye intravenously prior to the 3 hour MCA balloon occlusion. Light microscopy and transmission electron microscopy consistently confirmed the presence of thrombotic material occluding microcirculatory branches of the right LSA in the region of Evans blue stain, but not those of the contralateral corpus striatum.When autologous '"in-platelets were infused intravenously in four animals from the above group prior to the transient 3 hour occlusion of the right MCA, gamma scintillation camera imaging of each perfused-flxed whole brain demonstrated the presence of a single residual focus of '"in-platelet activity involving only the Evans blue-stained right corpus striatum. Focal right hemispheric activity was equivalent to 0.55 ± 0.49 ml of whole blood, and the occlusion score derived from histologic examination of the microcirculatton of the Evans blue-stained corpus striatum averaged 34.8 ± 2.8. Similar "'in-platelct imaging and histologic scoring experiments carried out hi four animals pretreated with the antithrombotic combination heparin and tidopidine showed marked reduction of both "'in-platelet activity (0.01 ± 0.03 ml vs. 0.55 ± 0.49 ml; p < 0.01) and thrombotic occlusion of the microcirculation (10.8 ± 7.4 units vs. 34.8 ± 2.8 units; p < 0.01) in the right corpus striatum following 3 hours of MCA occlusion. In separate control experiments "'inlabeled autologous platelets were infused after the 3 hour period of right MCA occlusion and subsequent balloon deflation hi two animals; no focus of '"in-platelet activity was demonstrated in fixed whole brain.We conclude that thrombi form in situ In the microcirculation of perforating branches of the LSA located in the ipsilateral corpus striatum following a 3 hour period of MCA occlusion and that these thrombi may be prevented when antithrombotic therapy is administered prior to MCA balloon occlusion. This model of acute thrombotic stroke may be useful to assess the safety and efficacy of thrombolytic therapies.

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Section: Discussionmentioning

confidence: 99%

Section: Histologic Neuropathologymentioning

confidence: 99%

Experimental acute thrombotic stroke in baboons.

Zoppo¹,

Copeland²,

Harker³

et al. 1986

Stroke

157

138

View full text Add to dashboard Cite

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“…l'Indium-labelling ofplatelets Rabbit platelets were labelled in vitro with "'In-oxine (Thakur et al, 1976). Details of this procedure have been previously described (Page et al, 1982;Oyekan & Botting, 1986) and validated for the rabbit (May et al, 1989).…”

Section: Animal Selection and Exclusion Criteriamentioning

confidence: 99%

Endothelin‐1 inhibits platelet aggregation in vivo: a study with ¹¹¹indium‐labelled platelets

Thiemermann

May

Page

et al. 1990

British J Pharmacology

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A non‐invasive technique for the scintigraphic determination of 111indium‐labelled platelet aggregation stimulated with submaximal doses of adenosine diphosphate (ADP, 56 μg kg−1 i.v.), collagen (100 μg kg−1 i.v.), platelet‐activating factor (PAF, 0.1 μg kg−1 i.v.) or thrombin (18 iu kg−1 i.v.) was used to investigate the platelet‐inhibitory effects of endothelin 1 (ET‐1) in anaesthetized rabbits in vivo. ET‐1 (1 nmol kg−1 i.v.) inhibited ADP‐stimulated platelet aggregation in vivo; a maximum inhibition of 78% of the control value was reached at 3 min, with 45% inhibition at 15 min, and a return to control values at 30 min after injection of the peptide. ET‐1 (1 nmol kg−1 i.v.) inhibited in vivo platelet aggregation in response to collagen or PAF by 86% and 52%, respectively, but had no effect on thrombin‐induced platelet aggregation. Indomethacin (5 mg kg−1 i.v.) abolished the ET‐1‐induced inhibition of ADP‐stimulated platelet aggregation and significantly potentiated and prolonged the pressor response brought about by ET‐1. In conclusion, the data demonstrate that ET‐1 potently inhibits platelet aggregation in the anaesthetized rabbit in vivo by releasing a hypotensive and anti‐aggregatory cyclo‐oxygenase product, presumably prostacyclin, into the circulation.

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“…The details of platelet labeling technique have been 6,14,15,18,[24][25][26][27][28][29] extensively explored in different species.…”

Section: Discussionmentioning

confidence: 99%

“…The indium-1Il oxine complex was formed by a modification of the method of Thakur et al 6 One to 3 mCi of 'In Cl3 solution in a volume of 1.5 ml were added to 1.5 ml of distilled water. The pH was adjusted to 5.5 by addition of 0.2 ml of 0.3 M sodium acetate; 0.2 ml of an oxine-ethanol solution was added and the solution was mixed.…”

Section: Methods Preparation Of Indium-111 Oxinementioning

confidence: 99%

Indium-111-labeled platelets: effects of heparin on uptake by venous thrombi and relationship to the activated partial thromboplastin time.

Fedullo¹,

Moser²,

Moser³

et al. 1982

Circulation

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SUMMARY The goal of heparin therapy in deep vein thrombosis is to prevent thrombus extension. The relationship between thrombus extension and the results of coagulation tests used to monitor heparin therapy is unclear. To explore this relationship, we studied the effect of several heparin regimens on the accretion of indium-111-labeled platelets on fresh venous thrombi, as detected by gamma imaging, and monitored the activated partial thromboplastin time (APTT). Six dogs were treated with a 300-U/kg bolus of heparin followed by a 90-U/kg/hour heparin infusion, a dose of heparin sufficient to increase the APTT to levels greater than eight times baseline (APTT ratio); platelet accretion (thrombus imaging) occurred only after the heparin effect was reversed with protamine sulfate. Nineteen dogs were treated with a 150-U/kg bolus of heparin followed by a 4-hour, 45-U/kg/hour heparin infusion; a thrombus was demonstrated only after protamine injection in 12 (mean APTT ratio 1.3 0.19) and before protamine injection in seven. In thirteen of these 19 dogs, 30 minutes separated the platelet injection from heparin therapy, while in six this duration was less than 30 minutes. In four of these six dogs, thrombi were demonstrated before protamine therapy and at APTT ratios greater than 3.0. Finally, 10 dogs were treated with a 100-UIkg bolus followed by a 3-hour, 50-U/kg/hour heparin infusion, after which the APTT was allowed to return to baseline values spontaneously. In all 10 dogs, a thrombus was demonstrated only after cessation of the heparin infusion, and at a mean APTT ratio of 1.4 ± 0.15 times baseline. These results suggest that, except with very early platelet injection, platelet accretion by thrombi is consistently inhibited by heparin at APTT ratios greater than 2.5. fine the relationship between such regimens and the behavior of selected coagulation assays.In the present study, we explored this thesis by intravenously injecting indium-1 1 -labeled platelets in dogs after formation of venous thrombi. Platelet accretion on thrombi was continuously monitored by gamma camera. We sought to determine (1) The indium-1Il oxine complex was formed by a modification of the method of Thakur et al.6 One to 3 mCi of 'In Cl3 solution in a volume of 1.5 ml were added to 1.5 ml of distilled water. The pH was adjusted to 5.5 by addition of 0.2 ml of 0.3 M sodium acetate; 0.2 ml of an oxine-ethanol solution was added and the solution was mixed. After 15 minutes, the solution was removed and added to 3 ml of dichloromethane. After a 1-minute vortex mix, the dichloromethane-oxine layer was removed and evaporated to dryness. The complex was resuspended in 0.1 ml of DMSO, and 0.1 ml of 0.9% NaCl was added just before use. Platelet Preparation and LabelingForty-three milliliters of venous blood were drawn into a clean, dry syringe that contained 7 ml of ACD solution.

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Indium-111 labeled platelets: Studies on preparation and evaluation of in vitro and in vivo functions

Cited by 449 publications

References 10 publications

Experimental acute thrombotic stroke in baboons.

Experimental acute thrombotic stroke in baboons.

Endothelin‐1 inhibits platelet aggregation in vivo: a study with ¹¹¹indium‐labelled platelets

Indium-111-labeled platelets: effects of heparin on uptake by venous thrombi and relationship to the activated partial thromboplastin time.

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Indium-111 labeled platelets: Studies on preparation and evaluation of in vitro and in vivo functions

Cited by 449 publications

References 10 publications

Experimental acute thrombotic stroke in baboons.

Experimental acute thrombotic stroke in baboons.

Endothelin‐1 inhibits platelet aggregation in vivo: a study with 111indium‐labelled platelets

Indium-111-labeled platelets: effects of heparin on uptake by venous thrombi and relationship to the activated partial thromboplastin time.

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Endothelin‐1 inhibits platelet aggregation in vivo: a study with ¹¹¹indium‐labelled platelets