ArticleExperimental and therapeutic medicine2018
The effect of nitric oxide inhalation on heart and pulmonary circulation in rabbits with acute massive pulmonary embolism.
Article in Experimental and therapeutic medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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.
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.
Who cites it
2 citing papers in PubMed, 3 citations in OpenAlex.
- Non-mechanical haemodynamic support in acute pulmonary thromboembolism: a scoping review.Intensive care medicine experimental · 2025Review
- Pulmonary vasodilation in acute pulmonary embolism - a systematic review.Pulmonary circulationReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of the present study was to investigate the effect of nitric oxide inhalation (NOI) on cardiac troponin I (CTnI) levels and mean pulmonary arterial pressure (mPAP) in rabbits with acute massive pulmonary embolism (AMPE). Thirty rabbits were used as animal models for AMPE and received different treatments. A total of 4 h after successful modeling, the control group (CON, n=10) received conventional thrombolysis, whereas the treatment group (TRE, n=10) received conventional thrombolysis plus NOI. The experimental group (EXP, n=10) did not receive any treatments. Myocardial necrosis was pathologically confirmed in all 30 rabbits. In group EXP, the post-AMPE CTnI peak level was 0.42±0.12 µg/l, was achieved in 18.8±4.5 h and remained positive for 38.6±5.2 h (≥0.1 µg/l). These values were lower in group TRE when compared with those in groups CON and EXP (P<0.05). Group TRE exhibited significantly reduced mPAP at 24, 28, 32, and 34 h (P<0.05) when compared with group CON. AMPE-induced cardiac impairment was more severe in group EXP when compared with groups CON and TRE. The present findings indicated that the CTnI peak was significantly correlated with the corresponding mPAP. Furthermore, the results suggested NOI may reduce mPAP and CTnI peak levels, with protective effects against AMPE-induced myocardial damage in rabbits.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.