Evidence map›Paper›PMID 8680268›Full record

ArticleTexas Heart Institute journal1996

Localized administration of sodium nitroprusside enhances its protection against platelet aggregation in stenosed and injured coronary arteries.

J T Willerson, S R Igo, S K Yao, J C Ober, M P Macris, J J Ferguson

Open access · greenAbstract readComparative Study
In one paragraph

Article in Texas Heart Institute journal, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.4field-weighted citation impact, top 21% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

10 citing papers in PubMed, 30 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Intrapericardial therapy and diagnosis.Current cardiology reports · 2002
    Review
  8. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

J T WillersonCardiovascular Research Laboratory, Texas Heart Institute, Houston, USA.
S R Igo
S K Yao
J C Ober
M P Macris
J J Ferguson
Houston Methodist · US

Funding

SPECIALIZED CENTER OF RESEARCH, ISCHEMIC HEART DISEASEP50HL017669 · NHLBI · UNIVERSITY OF TEXAS SW MED CTR/DALLAS · PI SAMBROOK, JOSEPH · 1985 to 1994
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CORONARY ARTERY RESTENOSIS--A MAJOR CARDIOLOGY PROBLEMR01HL050179 · NHLBI · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI WILLERSON, JAMES T. · 1993 to 1996
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NHLBI NIH HHS HL-17669NHLBI NIH HHS R0-1-HL50179-01
6 · The paper itself

Abstract

Sodium nitroprusside, a potent vasodilator, was evaluated for its effect on platelet aggregation in stenosed and endothelium-injured coronary arteries in a canine model. Twenty-five anesthetized dogs were studied; coronary blood flow velocity was continuously monitored. Recurrent intracoronary platelet aggregation and dislodgment (indicated by cyclic variations in coronary blood flow) were induced by mechanically injuring and stenosing the left anterior descending coronary artery. Sodium nitroprusside was administered either intrapericardially or intravenously 30 min after cyclic flow variations were established. Intrapericardial administration of saline (control) did not affect cyclic flow variations in any of 6 tested dogs. Sodium nitroprusside abolished cyclic flow variations in all 7 dogs (100%) when given intrapericardially and in 5 to 7 dogs (71%) when given intravenously (compared to intrapericardial salines, p < 0.01). A smaller dose of sodium nitroprusside was required to abolish cyclic flow variations when given intrapericardially than when given intravenously (1.6 +/- 0.5 micrograms.kg-1.min-1 vs 4.8 +/- 0.8 micrograms.kg-1.min-1, p < 0.01). The mean aortic pressure was reduced by 10 to 20 mmHg after intrapericardial sodium nitroprusside administration and by 30 to 40 mmHg after intravenous sodium nitroprusside administration. To investigate the mechanism of protection by sodium nitroprusside, NG-monomethyl-L-arginine, an inhibitor of nitric oxide synthetase, was used to induce cyclic flow variations in mildly injured and stenosed left anterior descending coronary arteries in 5 dogs. Intrapericardial sodium nitroprusside abolished the cyclic flow variations in all 5 dogs. Then oxyhemoglobin, an inhibitor of nitric oxide, was administered into the left anterior descending coronary arteries of these dogs, and it restored the sodium nitroprusside-abolished cyclic flow variations in all 5 dogs. Thus, sodium nitroprusside protects against platelet aggregation and cyclic flow variations in stenosed and endothelium-injured canine coronary arteries, probably by the action of nitric oxide, and it is more effective and hemodynamically safer when administered intrapericardially than when administered intravenously.

Indexed as

Administration, TopicalAnimalsArginineCoronary CirculationCoronary DiseaseDogsEndothelium, VascularEnzyme InhibitorsHemodynamicsInjections, IntravenousNitric OxideNitric Oxide SynthaseNitroprussideomega-N-MethylargininePericardiumPlatelet AggregationArginineEnzyme InhibitorsNitric OxideNitric Oxide SynthaseNitroprussideomega-N-MethylargininePlatelet Aggregation InhibitorsVasodilator Agents

Identifiers

PMID8680268
PMCPMC325295
OpenAlexW75277290

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.