Why the study?
Does myocardial structural adaptation in spontaneously hypertensive rats reduce left ventricular compliance and alter the Frank-Starling relationship compared to normotensive controls?
Does myocardial structural adaptation in spontaneously hypertensive rats reduce left ventricular compliance and alter the Frank-Starling relationship compared to normotensive controls?
Myocardial structural adaptation in hypertension leads to reduced left ventricular diastolic compliance and a rightward shift of the Frank-Starling relationship, contributing to the progression of hypertensive disease.
Answers are grounded in this paper and cite their sources.
Supports reduced LV compliance in hypertensive hypertrophy; leaves open translation to human diastolic dysfunction.
The Frank-Starling relationship of hearts from adult spontaneously hypertensive rats (SHR, Okamoto 1969), representing the established phase of hypertension, and of young SHR, representing the initial phase of hypertension, was investigated by using the isolated working heart preparation. In the "normal" diastolic pressure range (5 to 10 cm H2O), the left ventricle of both SHR groups displayed significantly reduced stroke volumes compared with hearts of normotensive controls (NCR); the degree of reduction being proportional to the left ventricular hypertrophy. This is suggested to be due to a reduced left ventricular diastolic compliance in SHR, as indicated by direct measurements of ventricular wall thickness and end-diastolic volumes in arrested hearts exposed to different end-diastolic filling pressures. Such a progressive shift of the Frank-Starling relationship to the right with duration of hypertension could, in combination with the gradual development of "structural autoregulation" of the precapillary resistance vessels, constitute dominating factors in shifting the hemodynamic situation in labile hypertension into that characterizing the established, or "fixed", state of hypertension.
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Hallbäck et al. (1975) studied this question.
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