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September 30, 2003Circulation131 citations

Cardiac Angiotensin-(1-7) in Ischemic Cardiomyopathy

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DADavid B. AverillYIYuichiro IshiyamaMCMark C. Chappell

Key Result

Coronary artery ligation in rats led to elevated left ventricular end-diastolic pressures (25 vs 5 mm Hg; P<0.001) and increased expression of Ang-(1-7) restricted to cardiac myocytes.

Key Points

  • This research aims to assess the expression of angiotensin-(1-7) in the myocardium of normal rats and those with induced myocardial infarction.
  • 10-week-old Lewis rats underwent left coronary artery ligation for myocardial infarction (n=5) or sham procedure (n=5).
  • Measurements of left ventricular end-diastolic and systolic pressures were taken 4 weeks post-operation.
  • Ang-(1-7) immunoreactivity was assessed in ventricular tissue.
  • Left ventricular end-diastolic pressures were 25+/-1 mm Hg in ligated rats compared to 5+/-1 mm Hg in sham rats (P<0.001).
  • Left ventricular systolic pressures were significantly reduced in ligated rats at 86+/-4 mm Hg compared to 110+/-5 mm Hg in sham rats (P<0.01).
  • Ang-(1-7) expression was significantly increased in ventricular tissue surrounding the infarct area in myocardial infarction rats.

Structured PICO

Does myocardial infarction induced by coronary artery ligation alter the expression of Ang-(1-7) in the myocardium of rats?

P
Population
10-week-old Lewis rats (n=10 total; 5 ligated, 5 sham)
I
Intervention
Left coronary artery ligation to induce myocardial infarction
C
Comparator
Sham operation (left coronary artery exposed but not occluded)
O
Outcome
Expression and localization of Ang-(1-7) in the myocardiumsurrogate

In a rat model of ischemic cardiomyopathy, heart failure subsequent to coronary artery ligation leads to increased expression of Ang-(1-7) restricted to cardiac myocytes.

Main Result

Absolute Event Rate: 25% vs 5%

p-value: p=<0.001

Abstract

BACKGROUND: Accumulating evidence suggests that angiotensin-(1-7) (Ang-1-7) may play an important role in counteracting the pressor, proliferative, and profibrotic actions of angiotensin II in the heart. Thus, we evaluated whether Ang-(1-7) is expressed in the myocardium of normal rats and those in which myocardial infarction was produced 4 weeks beforehand. METHODS AND RESULTS: The left coronary artery in 10-week-old Lewis rats was either ligated (n=5) or exposed but not occluded in age-matched controls (sham; n=5). Left ventricular end-diastolic pressures were significantly elevated 4 weeks after myocardial infarction (25+/-1 versus 5+/-1 mm Hg for sham; P<0.001), whereas left ventricular systolic pressures were significantly reduced (ligated 86+/-4 versus sham 110+/-5 mm Hg; P<0.01). Hemodynamic effects of coronary artery ligation were accompanied by significant cardiac hypertrophy (heart weight to body weight: ligated 4.3+/-0.1 versus sham 2.9+/-0.1 mg/g; P<0.001). In both ligated and sham rats, Ang-(1-7) immunoreactivity was limited to cardiac myocytes and absent in interstitial cells and coronary vessels. Ang-(1-7) immunoreactivity was significantly augmented in ventricular tissue surrounding the infarct area in the heart of rats with myocardial infarction. CONCLUSIONS: Development of heart failure subsequent to coronary artery ligation leads to increased expression of Ang-(1-7),which was restricted to myocytes.

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Cite This Study

Averill et al. (2003) studied Ischemic Cardiomyopathy (n=10). Coronary artery ligation vs. Sham operation was evaluated on Left ventricular end-diastolic pressure (p=<0.001). Coronary artery ligation in rats led to elevated left ventricular end-diastolic pressures (25 vs 5 mm Hg; P<0.001) and increased expression of Ang-(1-7) restricted to cardiac myocytes.

synapsesocial.com/papers/6a1c7b0d0e2acd31eb2fcccchttps://doi.org/10.1161/01.cir.0000092888.63239.54
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