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Related Experiment Video

Updated: Jun 6, 2026

Induction of Right Ventricular Failure by Pulmonary Artery Constriction and Evaluation of Right Ventricular Function in Mice
09:40

Induction of Right Ventricular Failure by Pulmonary Artery Constriction and Evaluation of Right Ventricular Function in Mice

Published on: May 13, 2019

Exposure Pattern Determines Methamphetamine-Induced Right Ventricular Dysfunction and Vascular Remodeling.

Ashok Kumar1, Aatish Mahajan1, Balaji Krishnamachary1

  • 1Division of Pulmonary, Critical Care and Sleep Medicine, Department of Internal Medicine, University of Kansas Medical Center, Kansas City, Kansas, USA.

Comprehensive Physiology
|June 5, 2026
PubMed
Summary
This summary is machine-generated.

Binge-and-crash methamphetamine exposure in rats created a pulmonary arterial hypertension (PAH) model. This model highlights HMGB1 as a key factor in methamphetamine-associated PAH (MA-PAH) development.

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Evaluation of Right Ventricular Function in Experimental Models of Pulmonary Arterial Hypertension
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Last Updated: Jun 6, 2026

Induction of Right Ventricular Failure by Pulmonary Artery Constriction and Evaluation of Right Ventricular Function in Mice
09:40

Induction of Right Ventricular Failure by Pulmonary Artery Constriction and Evaluation of Right Ventricular Function in Mice

Published on: May 13, 2019

Evaluation of Right Ventricular Function in Experimental Models of Pulmonary Arterial Hypertension
10:03

Evaluation of Right Ventricular Function in Experimental Models of Pulmonary Arterial Hypertension

Published on: June 27, 2025

Area of Science:

  • Cardiovascular Research
  • Pharmacology
  • Toxicology

Background:

  • Methamphetamine (MA) use is linked to pulmonary arterial hypertension (PAH).
  • Mechanisms of MA-associated PAH (MA-PAH) are not fully understood.
  • Reproducible animal models for MA-PAH are lacking.

Purpose of the Study:

  • To develop a rat model of MA-PAH mirroring human MA abuse patterns.
  • To investigate the hemodynamic and vascular changes associated with MA exposure.
  • To identify potential molecular mechanisms driving MA-PAH.

Main Methods:

  • Male Wistar rats received MA (5 mg/kg, i.p.) for 8 weeks via chronic daily or binge-and-crash regimens.
  • Hemodynamic parameters, right ventricular (RV) function, and cardiac indices were assessed.
  • Pulmonary arterial remodeling, HMGB1 levels, and in vitro endothelial and smooth muscle cell responses were analyzed.

Main Results:

  • Binge-crash MA exposure induced significant RV dilation, reduced ejection fraction, elevated RV systolic pressure, and hypertrophy.
  • Both MA regimens caused pulmonary arterial medial thickening; binge-crash showed more severe remodeling.
  • Elevated HMGB1 in plasma and pulmonary endothelial cells was observed in binge-crash rats.
  • MA-induced endothelial HMGB1 release via sigma-1 receptor signaling stimulated smooth muscle cell proliferation, blocked by HMGB1 neutralization.

Conclusions:

  • Binge-crash MA exposure in rats generates a clinically relevant PAH phenotype.
  • HMGB1 is identified as a potential mechanistic link between MA exposure patterns and MA-PAH pathogenesis.
  • This model provides a platform for further investigating MA-PAH and potential therapeutic targets.