Publications by authors named "D Wallerson"

To determine the effect of the angiotensin II AT1 receptor antagonist losartan (DuP753) on echocardiographic left ventricular (LV) anatomy in Dahl rats on high sodium diet, 27 Dahl salt-sensitive (Dahl-S, 13 on drug and 14 receiving tap water) and 27 Dahl salt-resistant rats (Dahl-R, 13 on drug and 14 receiving tap water) were studied by M-mode echocardiography during 8 weeks of 8% NaCl diet. At the endpoint (after 8 weeks or the last echocardiogram for animals who died earlier), Dahl-S receiving losartan had lower LV mass (1.6 +/- 0.

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Supranormal left ventricular (LV) function has been reported in one-kidney, one-clip (1K,1C) and two-kidney, one-clip (2K,1C) Goldblatt hypertension. However, this finding might be at least partially due to mismatching endocardial rather than midwall fractional shortening to mean end-systolic stress. Accordingly, relations of echocardiographic endocardial and midwall shortening to circumferential end-systolic stress were calculated in 40 Wistar rats on 0.

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Objective: The relationship between left ventricular midwall shortening and circumferential end-systolic stress was studied in Dahl salt-sensitive (Dahl S) and salt-resistant (Dahl R) rats after 6-8 weeks of an 8% Na+ diet with or without losartan, an AT1 angiotensin II receptor antagonist.

Materials And Methods: Losartan was given in drinking water to 13 Dahl S and 13 Dahl R rats, while 14 control Dahl S and 14 control Dahl R rats were given tap water, for 8 weeks. The endpoint was the last blood pressure and echocardiographic examination after 8 weeks or before death for rats which did not survive the entire period.

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In validation studies, M-mode echocardiography has been shown to measure left ventricular (LV) mass with reasonable accuracy (r > or = .90 v necropsy measurements) in species ranging in body size from humans to rats. The sensitivity of antemortem echocardiography for the detection of necropsy LV hypertrophy as a qualitative abnormality has also been high (85% to 100%).

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Previously reported experimental models of aortic regurgitation generally have manifested normal systolic performance and have not developed heart failure [Magid et al. Am. J.

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