Collagenase treatment reduces the anisotropy of ultrasonic backscatter in rat myocardium by reducing collagen crosslinks

Author:

Pittman Lindsay A.1,Whittaker Peter2,Milne Michelle L.3,Chung Charles S.1ORCID

Affiliation:

1. Department of Physiology Wayne State University Detroit Michigan USA

2. Green Templeton College University of Oxford Oxford UK

3. Department of Physics St Mary's College of Maryland St Mary's City Maryland USA

Abstract

AbstractDysregulation of collagen deposition, degradation, and crosslinking in the heart occur in response to increased physiological stress. Collagen content has been associated with ultrasonic backscatter (brightness), and we have shown that the anisotropy of backscatter can be used to measure myofiber alignment, that is, variation in the brightness of a left ventricular short‐axis ultrasound. This study investigated collagen's role in anisotropy of ultrasonic backscatter; female Sprague–Dawley rat hearts were treated with a collagenase‐containing solution, for either 10 or 30 min, or control solution for 30 min. Serial ultrasound images were acquired at 2.5‐min intervals throughout collagenase treatment. Ultrasonic backscatter was assessed from anterior and posterior walls, where collagen fibrils are predominately aligned perpendicular to the angle of insonification, and the lateral and septal walls, where collagen is predominately aligned parallel to the angle of insonification. Collagenase digestion reduced backscatter anisotropy within the myocardium. Collagen remains present in the myocardium throughout collagenase treatment, but crosslinking is altered within 10 min. These data suggest that crosslinking of collagen modulates the anisotropy of ultrasonic backscatter. An Anisotropy Index, derived from differences in backscatter from parallel and perpendicularly aligned fibers, may provide a noninvasive index to monitor the progression and state of myocardial fibrosis.

Funder

National Institute of Biomedical Imaging and Bioengineering

National Heart, Lung, and Blood Institute

Publisher

Wiley

Subject

Physiology (medical),Physiology

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