Antiplatelet monoclonal F(ab')2 antibody directed against the platelet GPIIb/IIIa receptor complex prevents coronary artery thrombosis in the canine heart
dc.contributor.author | Mickelson, Judith K. | en_US |
dc.contributor.author | Simpson, Paul J. | en_US |
dc.contributor.author | Lucchesi, Benedict Robert | en_US |
dc.date.accessioned | 2006-04-07T20:51:26Z | |
dc.date.available | 2006-04-07T20:51:26Z | |
dc.date.issued | 1989-04 | en_US |
dc.identifier.citation | Mickelson, Judith K., Simpson, Paul J., Lucchesi, Benedict R. (1989/04)."Antiplatelet monoclonal F(ab')2 antibody directed against the platelet GPIIb/IIIa receptor complex prevents coronary artery thrombosis in the canine heart." Journal of Molecular and Cellular Cardiology 21(4): 393-405. <http://hdl.handle.net/2027.42/27996> | en_US |
dc.identifier.uri | http://www.sciencedirect.com/science/article/B6WK6-4C547GX-GD/2/fafd2f710bf9acc40620d98897585720 | en_US |
dc.identifier.uri | https://hdl.handle.net/2027.42/27996 | |
dc.identifier.uri | http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=2746660&dopt=citation | en_US |
dc.description.abstract | Interactions between platelets with injured vascular endothelium contribute to thrombotic occlusion. A murine monoclonal antibody [7E3 F(ab')2] to the platelet GPIIb/IIIa receptor complex was used to inhibit platelet aggregation in an experimental model of coronary artery thrombosis. Prevention of thrombotic occlusion by 7E3 F(ab')2 (0.8 mg/kg bolus i.v.) was studied in dogs with direct current induced intimal injury (100 [mu]A for 5 h) and critical stenosis of the left circumflex coronary artery (LCCA). Baseline LCCA blood flow (CBF) was similar in 7E3 F(ab')2 and control groups, but decreased in the controls [24 +/- 2 ml/min to 0 +/- 0 ml/min, n = 13 (mean +/-)] due to thrombotic occlusion in each case (time to thrombosis 136 +/- 15 min). In the group treated with 7E3 F(ab')2, CBF did not change significantly (27 +/- 3 ml/min to 22 +/- 3 ml/min, n = 6) and thrombotic occlusion did not occur during the 5-h observation period in which intimal injury was produced in the LCCA (P 2 treatment (2.2 +/- 0.7 vs. 0 +/- 0, P 2 (P ex vivo, before the administration of the test agents, platelets from both groups of dogs aggregated in response to ADP and arachidonic acid. However, after treatment, the ex vivo aggregation of platelets from 7E3 F(ab')2 animals was inhibited whereas platelets from the control animals continued to aggregate ex vivo throughout the period of the experimental protocol (P 111indium showed accumulation of radio-activity within the thrombus and upon the vascular endothelium which was less in 7E3 F(ab')2 treated dogs as compared to the control group (P 2 did not affect hemodynamic values or the circulating platelet count during the experimental protocol. In conclusion, antibody to platelet GPIIb/IIIa receptors: (1) prevented thrombotic LCCA occlusion, (2) inhibited ex vivo platelet aggregation, (3) minimized platelet deposition on injured vascular endothelium and within formed thrombi, and (4) stabilized CBF during 5 h of continuous direct currrent induced intimal injury of the LCCA. | en_US |
dc.format.extent | 3066292 bytes | |
dc.format.extent | 3118 bytes | |
dc.format.mimetype | application/pdf | |
dc.format.mimetype | text/plain | |
dc.language.iso | en_US | |
dc.publisher | Elsevier | en_US |
dc.title | Antiplatelet monoclonal F(ab')2 antibody directed against the platelet GPIIb/IIIa receptor complex prevents coronary artery thrombosis in the canine heart | en_US |
dc.type | Article | en_US |
dc.rights.robots | IndexNoFollow | en_US |
dc.subject.hlbsecondlevel | Internal Medicine and Specialties | en_US |
dc.subject.hlbtoplevel | Health Sciences | en_US |
dc.description.peerreviewed | Peer Reviewed | en_US |
dc.contributor.affiliationum | Department of Internal Medicine (Cardiology), The University of Michigan Medical School, Ann Arbor, MI 48109-0626, USA; Department of Pharmacology, The University of Michigan Medical School, Ann Arbor, MI 48109-0626, USA. | en_US |
dc.contributor.affiliationum | Department of Internal Medicine (Cardiology), The University of Michigan Medical School, Ann Arbor, MI 48109-0626, USA; Department of Pharmacology, The University of Michigan Medical School, Ann Arbor, MI 48109-0626, USA. | en_US |
dc.contributor.affiliationum | Department of Pharmacology, The University of Michigan Medical School, Ann Arbor, MI 48109-0626, USA; Department of Internal Medicine (Cardiology), The University of Michigan Medical School, Ann Arbor, MI 48109-0626, USA. | en_US |
dc.identifier.pmid | 2746660 | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/27996/1/0000431.pdf | en_US |
dc.identifier.doi | http://dx.doi.org/10.1016/0022-2828(89)90650-0 | en_US |
dc.identifier.source | Journal of Molecular and Cellular Cardiology | en_US |
dc.owningcollname | Interdisciplinary and Peer-Reviewed |
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