Key result
Adriamycin-induced cardiomyopathy in rabbits significantly reduced the vasodilator response to acetylcholine by 41% (P<0.05) and to adenosine by 37% (P<0.05).
Why the study?
Does experimental left ventricular dysfunction impair endothelium-dependent vasodilation in the hindlimb circulation of rabbits?
Does experimental left ventricular dysfunction impair endothelium-dependent vasodilation in the hindlimb circulation of rabbits?
p-value: p=< 0.05
Experimental left ventricular dysfunction induced by adriamycin in rabbits attenuates the capacity of the hindlimb circulation to respond to endothelium-dependent vasodilators.
Experimental cardiomyopathy impairs hindlimb vasodilation in rabbits; hypothesis-generating for endothelial dysfunction in human HF.
The full range of vascular reactivity was investigated in the hindlimb circulation of conscious, autonomically blocked rabbits with experimental (adriamycin-induced) cardiomyopathy. 2. Adriamycin treatment caused a significant reduction in left ventricular systolic function, as assessed by echocardiography (left ventricular fractional shortening, controls vs adriamycin treatment; 36.7 +/- 1.7% vs 27.3 +/- 2.6%, P < 0.05). 3. Under pharmacological autonomic effector block, the range of the vasodilator response (resistance range, from resting to full vasodilatation) to acetylcholine was reduced by 41% (P < 0.05) and by 37% for adenosine (P < 0.05). Despite these changes the sensitivity (ED50) of the responses were unaltered. 4. The ED50 of constrictor responses to noradrenaline and angiotensin II were similarly unaltered, in conjunction with a non-significant attenuation of the constrictor-response range. 5. These results suggest that in this model of experimental left ventricular dysfunction, the capacity of the hindlimb circulation to respond to regionally infused endothelium dependent vasodilators is attenuated.
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Kaye et al. (1994) studied Experimental (adriamycin-induced) cardiomyopathy. Adriamycin treatment vs. Controls was evaluated on Vasodilator response (resistance range) to acetylcholine (p=< 0.05). Adriamycin-induced cardiomyopathy in rabbits significantly reduced the vasodilator response to acetylcholine by 41% (P<0.05) and to adenosine by 37% (P<0.05).
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