Enhancement of contractility with sustained afterload in the intact murine heart blunting of length - Dependent activation

Maricela Reyes, Gregory L. Freeman, Daniel Escobedo, Shuko Lee, Mark E. Steinhelper, Marc D Feldman

Research output: Contribution to journalArticle

15 Citations (Scopus)

Abstract

Background - It has been hypothesized that because of its rapid heart rate, the intact murine heart functions near maximal contractility in the basal state. If this hypothesis is correct, then the fast and slow components of myocardial length-dependent activation should be blunted compared with larger mammals. Methods and Results - Mice (n=24) were anesthetized, and via an open chest, LV pressure-volume relationships were determined by a dual-frequency conductance catheter system. Baseline pressure-volume relationships were determined during transient occlusion of the inferior vena cava, and repeat measurements were made after 1 (n=10) and 7 (n=21) minutes of sustained aortic occlusion. Control experiments were performed in a subset of mice (n=3). For baseline to 1 minute, an increase in afterload (maximal pressure 95±9 to 126±7 mm Hg; P<0.001) and effective arterial elastance (5.9±3.1 to 9.2±3.9 mm Hg/μ1; P<0.001) resulted in an increase in end-diastolic volume (31±8 to 35±9 μL; P<0.001). The result was maintenance of stroke volume (17±6 to 15±6; P=NS) owing to an increase in contractility (leftward shift in V100 [the volume of end-systolic elastance at 100 mm Hg], 24±9 to 16±5 μL; P<0.001). No additional augmentation of systolic function was found at 7 minutes. Conclusions - This study demonstrates that the fast phase of length-dependent activation is intact but not the slow phase, consistent with murine myocardium functioning near maximal contractility in the basal state.

Original languageEnglish (US)
Pages (from-to)2962-2968
Number of pages7
JournalCirculation
Volume107
Issue number23
DOIs
StatePublished - Jun 17 2003

Fingerprint

Pressure
Inferior Vena Cava
Stroke Volume
Mammals
Myocardium
Thorax
Catheters
Heart Rate
Maintenance

Keywords

  • Afterload
  • Contractility
  • Diastole
  • Hemodynamics
  • Pressure

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine

Cite this

Enhancement of contractility with sustained afterload in the intact murine heart blunting of length - Dependent activation. / Reyes, Maricela; Freeman, Gregory L.; Escobedo, Daniel; Lee, Shuko; Steinhelper, Mark E.; Feldman, Marc D.

In: Circulation, Vol. 107, No. 23, 17.06.2003, p. 2962-2968.

Research output: Contribution to journalArticle

Reyes, Maricela ; Freeman, Gregory L. ; Escobedo, Daniel ; Lee, Shuko ; Steinhelper, Mark E. ; Feldman, Marc D. / Enhancement of contractility with sustained afterload in the intact murine heart blunting of length - Dependent activation. In: Circulation. 2003 ; Vol. 107, No. 23. pp. 2962-2968.
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AB - Background - It has been hypothesized that because of its rapid heart rate, the intact murine heart functions near maximal contractility in the basal state. If this hypothesis is correct, then the fast and slow components of myocardial length-dependent activation should be blunted compared with larger mammals. Methods and Results - Mice (n=24) were anesthetized, and via an open chest, LV pressure-volume relationships were determined by a dual-frequency conductance catheter system. Baseline pressure-volume relationships were determined during transient occlusion of the inferior vena cava, and repeat measurements were made after 1 (n=10) and 7 (n=21) minutes of sustained aortic occlusion. Control experiments were performed in a subset of mice (n=3). For baseline to 1 minute, an increase in afterload (maximal pressure 95±9 to 126±7 mm Hg; P<0.001) and effective arterial elastance (5.9±3.1 to 9.2±3.9 mm Hg/μ1; P<0.001) resulted in an increase in end-diastolic volume (31±8 to 35±9 μL; P<0.001). The result was maintenance of stroke volume (17±6 to 15±6; P=NS) owing to an increase in contractility (leftward shift in V100 [the volume of end-systolic elastance at 100 mm Hg], 24±9 to 16±5 μL; P<0.001). No additional augmentation of systolic function was found at 7 minutes. Conclusions - This study demonstrates that the fast phase of length-dependent activation is intact but not the slow phase, consistent with murine myocardium functioning near maximal contractility in the basal state.

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