A pressure overload model of congestive heart failure in rats

Approximately 32% of the rats used as animal models showed an elevated heart weight/body weight ratio (0.432[SEM 0.022] g·100 g−1 compared to 0.293[0.009] g·100 g−1 for sham-operated rats), a hydrothorax, pulmonary and liver congestion, and specific histological changes 82-93 weeks after surgically...

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Veröffentlicht in:Cardiovascular research 1988-10, Vol.22 (10), p.696-702
Hauptverfasser: DESJARDINS, SUZANNE, MUELLER, RUDOLF W, CAUCHY, MICHAEL J
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Sprache:eng
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Zusammenfassung:Approximately 32% of the rats used as animal models showed an elevated heart weight/body weight ratio (0.432[SEM 0.022] g·100 g−1 compared to 0.293[0.009] g·100 g−1 for sham-operated rats), a hydrothorax, pulmonary and liver congestion, and specific histological changes 82-93 weeks after surgically induced aortic constriction. The histological changes were comparable to those observed in hearts of people suffering from long term hypertension. Cardiac failure was also confirmed by depressed contractility as measured by maximum and minimum dP/dt (first derivative of left ventricular pressure), which were 4604(346) and 3627(526) mm Hg·sec−1, respectively, compared with 9165(745) and 5835(268) mm Hg·sec−1 respectively in rats that did not develop left ventricular hypertrophy and failure (CLIP rats). Systolic and left ventricular blood pressures measured under anaesthesia were also decreased: 71.6(5.0) and 88.1(6.3) mm Hg respectively in rats with congestive heart failure, compared with 83.6(2.4) and 109.5(3.6) mm Hg in CLIP rats. Except for a prolonged mean PQ interval associated with a lower heart rate and for a slightly shorter QRS interval in the conscious state, the electrocardiograms of rats with congestive heart failure did not show any major abnormalities specific to ventricular hypertrophy and/or failure. This model could be useful for studying the pathology and adaptative mechanisms in compensated pressure overload induced congestive heart failure as well as in studies comparing pathological changes and means of treatment of congestive heart failure with different aetiologies encountered in the human population.
ISSN:0008-6363
1755-3245
DOI:10.1093/cvr/22.10.696