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https://hdl.handle.net/2440/8734
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DC Field | Value | Language |
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dc.contributor.author | Chirkov, Y. | - |
dc.contributor.author | Holmes, A. | - |
dc.contributor.author | Chirkova, L. | - |
dc.contributor.author | Horowitz, J. | - |
dc.date.issued | 1999 | - |
dc.identifier.citation | Circulation, 1999; 100(2):129-134 | - |
dc.identifier.issn | 0009-7322 | - |
dc.identifier.issn | 1524-4539 | - |
dc.identifier.uri | http://hdl.handle.net/2440/8734 | - |
dc.description.abstract | <h4>Background</h4>Hemodynamic resistance to nitrates has been previously documented in congestive heart failure. In patients with stable angina pectoris (SAP), we have observed a similar phenomenon: decreased platelet response to disaggregating effects of nitroglycerin (NTG) and sodium nitroprusside (SNP).<h4>Methods and results</h4>In blood samples from normal subjects (n=32) and patients with SAP (n=56), we studied effects of NO donors (NTG and SNP) on ADP-induced platelet aggregation and on intraplatelet cGMP. NTG and SNP inhibited platelet aggregation in patients to lesser extents than in normal subjects (P<0.01). The cGMP-elevating efficacy of NTG and SNP was diminished in platelets from patients in comparison with those from normals (P<0.001). Inhibition of the anti-aggregatory effects of NTG and SNP by ODQ, a selective inhibitor of NO-stimulated guanylate cyclase, was significantly less pronounced in patients than in normal subjects. Content of O2- was higher in blood samples from patients than in those from normal subjects (P<0. 01). In blood samples from patients with SAP, but not in normal subjects, the O2- scavenger superoxide dismutase (combined with catalase) suppressed platelet aggregation (P<0.01) and increased the extent of anti-aggregatory effect of SNP (P<0.01).<h4>Conclusions</h4>In patients with SAP, platelets are less responsive to the anti-aggregating and cGMP-stimulating effects of NO donors; this may reflect both reduction in guanylate cyclase sensitivity to NO and inactivation of the released NO by O2-. The implied impairment of anti-platelet efficacy of endogenous NO (in the form of EDRF) may contribute to platelet hyperaggregability associated with angina pectoris. | - |
dc.language.iso | en | - |
dc.publisher | Highwire Press | - |
dc.source.uri | http://dx.doi.org/10.1161/01.cir.100.2.129 | - |
dc.subject | Blood Platelets | - |
dc.subject | Humans | - |
dc.subject | Angina Pectoris | - |
dc.subject | Nitroprusside | - |
dc.subject | Nitrates | - |
dc.subject | Nitroglycerin | - |
dc.subject | Adenosine Diphosphate | - |
dc.subject | Nitric Oxide Donors | - |
dc.subject | Platelet Aggregation Inhibitors | - |
dc.subject | Platelet Aggregation | - |
dc.subject | Drug Resistance | - |
dc.subject | Reference Values | - |
dc.subject | Adult | - |
dc.subject | Aged | - |
dc.subject | Middle Aged | - |
dc.subject | Female | - |
dc.subject | Male | - |
dc.title | Nitrate Resistance in platelets from patients with stable angina pectoris | - |
dc.type | Journal article | - |
dc.identifier.doi | 10.1161/01.CIR.100.2.129 | - |
pubs.publication-status | Published | - |
dc.identifier.orcid | Horowitz, J. [0000-0001-6883-0703] | - |
Appears in Collections: | Aurora harvest 4 Medicine publications |
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