Evidence map›Paper›PMID 28314763›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2017

Endothelial dysfunction inhibits the ability of haptoglobin to prevent hemoglobin-induced hypertension.

Jan A Graw, Binglan Yu, Emanuele Rezoagli, H Shaw Warren, Emmanuel S Buys, Donald B Bloch, Warren M Zapol

Abstract readComparative Study
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing 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

20 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
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  11. Nitric oxide: Clinical applications in critically ill patients.Nitric oxide : biology and chemistry · 2022
    Review
  12. Article
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  18. Review
  19. Statistical considerations in reporting cardiovascular research.American journal of physiology. Heart and circulatory physiology · 2018
    Article
  20. Review
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

7 authors at 2 institutions in 1 country.

Jan A GrawAnesthesia Center for Critical Care Research, Department of Anesthesia, Critical Care, and Pain Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts.
Binglan YuAnesthesia Center for Critical Care Research, Department of Anesthesia, Critical Care, and Pain Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts.
Emanuele RezoagliAnesthesia Center for Critical Care Research, Department of Anesthesia, Critical Care, and Pain Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts.
H Shaw WarrenInfectious Disease Unit, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts; and.
Emmanuel S BuysAnesthesia Center for Critical Care Research, Department of Anesthesia, Critical Care, and Pain Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts.
Donald B BlochAnesthesia Center for Critical Care Research, Department of Anesthesia, Critical Care, and Pain Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts.
Warren M ZapolAnesthesia Center for Critical Care Research, Department of Anesthesia, Critical Care, and Pain Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts; wzapol@mgh.harvard.edu.
Massachusetts General Hospital · USHarvard University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Intravascular hemolysis produces injury in a variety of human diseases including hemoglobinopathies, malaria, and sepsis. The adverse effects of increased plasma hemoglobin are partly mediated by depletion of nitric oxide (NO) and result in vasoconstriction. Circulating plasma proteins haptoglobin and hemopexin scavenge extracellular hemoglobin and cell-free heme, respectively. The ability of human haptoglobin or hemopexin to inhibit the adverse effects of NO scavenging by circulating murine hemoglobin was tested in C57Bl/6 mice. In healthy awake mice, the systemic hemodynamic effects of intravenous coinfusion of cell-free hemoglobin and exogenous haptoglobin or of cell-free hemoglobin and hemopexin were compared with the hemodynamic effects of infusion of cell-free hemoglobin or control protein (albumin) alone. We also studied the hemodynamic effects of infusing hemoglobin and haptoglobin as well as injecting either hemoglobin or albumin alone in mice fed a high-fat diet (HFD) and in diabetic (

Indexed as

HemoglobinsAnimalsAntihypertensive AgentsDiabetes MellitusDiet, High-FatEndothelium, VascularHaptoglobinsHemopexinHypertensionInfusions, IntravenousKidneyMaleMice, Inbred C57BLNitric OxideTime FactorsVasoconstrictionAntihypertensive AgentsHaptoglobinsHemoglobinsHemopexinNitric Oxidecell-free hemoglobinendothelial dysfunctionhaptoglobinhemopexinnitric oxide

Identifiers

PMID28314763
PMCPMC5495929
OpenAlexW2597283431

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.