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Related Experiment Videos

Histamine decreases left ventricular contractility in normal human subjects.

D J Cooper1, C R Thompson, K R Walley

  • 1University of British Columbia, Division of Cardiology, St. Paul's Hospital, Vancouver, Canada.

Journal of Applied Physiology (Bethesda, Md. : 1985)
|December 1, 1992
PubMed
Summary

Histamine reduces human heart contractility by affecting left ventricular function. This effect is mediated, in part, by H1 receptors, as shown by studies on healthy volunteers.

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Area of Science:

  • Cardiology
  • Pharmacology
  • Physiology

Background:

  • Histamine is a key mediator in allergic reactions and inflammation.
  • Its direct effects on human cardiac contractility remain incompletely understood.
  • Understanding histamine's cardiac impact is crucial for managing cardiovascular conditions.

Purpose of the Study:

  • To investigate the impact of histamine on human left ventricular contractility.
  • To determine the role of H1 receptors in histamine's cardiac effects.

Main Methods:

  • Healthy volunteers underwent measurements of heart rate, arterial pressure, and left ventricular dimensions via echocardiogram.
  • Baseline contractility was assessed using pressure-dimension and wall stress-velocity relationships.
  • Histamine infusions were administered before and after H1 receptor antagonist (diphenhydramine) pretreatment.

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Main Results:

  • Histamine decreased end-systolic pressure but not end-systolic dimension or fractional shortening.
  • Histamine reduced velocity of circumferential fiber shortening at consistent end-systolic wall stress.
  • H1 receptor antagonist pretreatment inhibited these observed effects of histamine.

Conclusions:

  • Histamine's primary effect on the human heart is a reduction in left ventricular contractility.
  • This negative inotropic effect is significantly mediated by H1 receptor activation.