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January 1, 1995Journal of Applied Physiology98 citations

Myocardial edema, left ventricular function, and pulmonary hypertension

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KDKaren L. DavisUMUwe MehlhornGLGlen A. Laine

Key Result

Acute pulmonary hypertension induced by pulmonary artery banding in dogs significantly increased left ventricular myocardial interstitial edema (wet-to-dry weight ratio 3.57 vs 3.41).

Structured PICO

Does acute pulmonary hypertension cause left ventricular myocardial interstitial edema and subsequent left ventricular dysfunction in a canine model?

P
Population
Dogs subjected to 3 hours of pulmonary artery banding or sham operation to evaluate left ventricular myocardial interstitial edema and function.
I
Intervention
Acute pulmonary hypertension induced by pulmonary artery banding for 3 hours
C
Comparator
Sham operation
O
Outcome
Left ventricular myocardial interstitial edema (wet-to-dry weight ratios) and left ventricular function (preload recruitable stroke work [PRSW] and rate of active relaxation [tau])surrogate

Acute pulmonary hypertension induces left ventricular myocardial interstitial edema, which contributes to both systolic and diastolic left ventricular dysfunction.

Main Result

Absolute Event Rate: 3.57% vs 3.41%

Abstract

Left ventricular dysfunction has been reported in both experimentally induced and clinical pulmonary hypertension. However, the mechanism by which pulmonary hypertension causes left ventricular dysfunction is unknown. We hypothesized that acute pulmonary hypertension causes left ventricular myocardial interstitial edema and that it is this edema that causes left ventricular dysfunction. In pulmonary artery-banded or sham-operated dogs, left ventricular diameter (septal-free wall axis) and pressure were measured using sonomicrometry crystals and a micromanometer, respectively. These measurements were used to calculate preload recruitable stroke work (PRSW), an index of contractility, and the rate of active relaxation (tau) to assess systolic and diastolic left ventricular function, respectively. After 3 h of pulmonary arterial hypertension or control, the dogs were killed and the left ventricles were excised to determine wet-to-dry weight ratios. The wet-to-dry weight ratios were significantly higher in the pulmonary artery-banded dogs (3.57 +/- 0.12) than in the sham-operated dogs (3.41 +/- 0.17). PRSW decreased to 56.8 +/- 30.3% of control after 3 h of pulmonary hypertension. tau Slowed significantly from 29.8 +/- 5.8 ms at baseline to 63.6 +/- 30.4 ms after 3 h of pulmonary arterial hypertension. There were no differences in PRSW or tau in the sham-operated dogs. We conclude that pulmonary hypertension causes left ventricular myocardial interstitial edema, which results in both systolic and diastolic left ventricular dysfunction.

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Cite This Study

Davis et al. (1995) studied Pulmonary hypertension. Acute pulmonary hypertension (pulmonary artery banding) vs. Sham operation was evaluated on Left ventricular wet-to-dry weight ratios. Acute pulmonary hypertension induced by pulmonary artery banding in dogs significantly increased left ventricular myocardial interstitial edema (wet-to-dry weight ratio 3.57 vs 3.41).

synapsesocial.com/papers/6a46fed4f81ec6c7245ed14chttps://doi.org/10.1152/jappl.1995.78.1.132
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