Nitroglycerin inhibits experimental thrombosis and reocclusion after thrombolysis
dc.contributor.author | Werns, Steven W. | en_US |
dc.contributor.author | Rote, William E. | en_US |
dc.contributor.author | Davis, James H. | en_US |
dc.contributor.author | Guevara, Tristan | en_US |
dc.contributor.author | Lucchesi, Benedict Robert | en_US |
dc.date.accessioned | 2006-04-10T18:15:59Z | |
dc.date.available | 2006-04-10T18:15:59Z | |
dc.date.issued | 1994-04 | en_US |
dc.identifier.citation | Werns, Steven W., Rote, William E., Davis, James H., Guevara, Tristan, Lucchesi, Benedict R. (1994/04)."Nitroglycerin inhibits experimental thrombosis and reocclusion after thrombolysis." American Heart Journal 127(4, Part 1): 727-737. <http://hdl.handle.net/2027.42/31690> | en_US |
dc.identifier.uri | http://www.sciencedirect.com/science/article/B6W9H-4DCTMVX-13/2/c2d9208105b8db9454a3a723f159f6b4 | en_US |
dc.identifier.uri | https://hdl.handle.net/2027.42/31690 | |
dc.identifier.uri | http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=8154409&dopt=citation | en_US |
dc.description.abstract | Nitroglycerin inhibits platelet aggregation in vitro, but its effect on thrombosis and platelet function in vivo is controversial. This study assessed the effect of nitroglycerin on primary thrombus formation in response to vessel wall injury and secondary thrombus formation, or rethrombosis, after lysis of an existing thrombus. In the first protocol the right carotid artery was instrumented with a flow probe, stenosis, an anodal electrode, and a proximal infusion line. A 300 [mu]A anodal current was used to induce endothelial injury and subsequent thrombotic occlusion of the vessel. Anisoylated plasminogen streptokinase activator complex (APSAC; 0.05 U/kg intraarterially) was injected proximal to the thrombus 30 minutes after occlusion. After APSAC, nitroglycerin (1 [mu]g/kg/min intraarterially, n = 7) or vehicle (n = 6) was infused proximal to the thrombus for 3 hours. Reocclusion occurred in two of seven nitroglycerin-treated dogs and six of six vehicle-treated dogs (p n = 12) artery to determine control times to occlusion. The left carotid artery served as the test vessel, receiving either nitroglycerin (1 [mu]g/kg/min intraarterially, n = 6) or trimethaphan (0.05 mg/kg/hr intraarterially, n = 6). Trimethaphan was used to produce controlled hypotension to match the approximately 10% decrease in mean arterial blood pressure that was observed during nitroglycerin infusion. Control arteries and those treated with trimethaphan formed occlusive thrombi in all instances. Nitroglycerin infusion resulted in a lower incidence of occlusion (1 of 6; p p < 0.05). Local infusion of nitroglycerin reduced the formation of primary thrombi, independent of the hypotensive effect of the drug, and exerted systemic effects on platelet aggregation. Furthermore, platelet inhibition with nitroglycerin reduced the incidence of secondary thrombus formation (rethrombosis) after thrombolysis. The results suggest that a potential benefit of nitroglycerin therapy may be derived from its ability to inhibit thrombotic events in patients with unstable angina or myocardial infarction. | en_US |
dc.format.extent | 1559203 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 | Nitroglycerin inhibits experimental thrombosis and reocclusion after thrombolysis | 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 | Division of Cardiology, University of Michigan Medical Center, Ann Arbor, Mich., USA.; Department of Pharmacology, University of Michigan Medical Center, Ann Arbor, Mich., USA. | en_US |
dc.contributor.affiliationum | Department of Pharmacology, University of Michigan Medical Center, Ann Arbor, Mich., USA.; Division of Cardiology, University of Michigan Medical Center, Ann Arbor, Mich., USA. | en_US |
dc.contributor.affiliationum | Department of Pharmacology, University of Michigan Medical Center, Ann Arbor, Mich., USA.; Division of Cardiology, University of Michigan Medical Center, Ann Arbor, Mich., USA. | en_US |
dc.contributor.affiliationum | Department of Pharmacology, University of Michigan Medical Center, Ann Arbor, Mich., USA.; Division of Cardiology, University of Michigan Medical Center, Ann Arbor, Mich., USA. | en_US |
dc.contributor.affiliationum | Department of Pharmacology, University of Michigan Medical Center, Ann Arbor, Mich., USA.; Division of Cardiology, University of Michigan Medical Center, Ann Arbor, Mich., USA. | en_US |
dc.identifier.pmid | 8154409 | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/31690/1/0000626.pdf | en_US |
dc.identifier.doi | http://dx.doi.org/10.1016/0002-8703(94)90538-X | en_US |
dc.identifier.source | American Heart Journal | en_US |
dc.owningcollname | Interdisciplinary and Peer-Reviewed |
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