Key result
In a dog model of pacing-induced heart failure, skeletal muscle underperfusion was driven by a reduced mean arteriovenous pressure gradient (91 vs 119 mmHg, P<0.001) rather than impaired vasodilation.
In a dog model of pacing-induced heart failure, skeletal muscle underperfusion during exercise is driven by a reduced arteriovenous pressure gradient rather than impaired skeletal muscle arteriolar vasodilation.
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Questions impaired vasodilation as cause of HF underperfusion; extends animal insights but leaves open human relevance.
To investigate the mechanism responsible for underperfusion of working skeletal muscle in heart failure, we measured systemic and femoral bed hemodynamics during treadmill exercise and gracilis muscle resistance during contraction frequencies of 1-9 Hz in 8 dogs ventricularly paced at 260 beats/min for 3 wk to induce heart failure (HF) and in 9 control dogs. At peak treadmill exercise (4 mph, 10%), HF dogs had reduced cardiac outputs (control: 297 +/- 42 vs. HF: 212 +/- 16 ml X min-1 X kg-1) and femoral bed flows (control: 352 +/- 112 vs. HF: 229 +/- 95 ml/min) and elevated arterial lactates [control: 1.7 +/- 0.7 vs. HF: 4.1 +/- 0.7 mM (all P less than 0.04)], consistent with skeletal muscle underperfusion. This muscle underperfusion was associated with reduced mean arteriovenous pressure gradients [control: 119 +/- 12 vs. HF: 91 +/- 9 mmHg (P less than 0.001)] but with normal systemic vascular [control: 21 +/- 6 vs. HF: 23 +/- 5 U (P = NS)] and femoral bed resistances [control: 3.5 +/- 1.6 vs. HF: 4.4 +/- 2.3 X 10(2) U (P = NS)]. Both groups also had similar gracilis muscle minimal resistance during exercise (control: 2.0 +/- 1.1 vs. HF: 1.9 +/- 0.9 X 10(3) U/100 g) and following maximal vasodilation (control: 2.0 +/- 1.0 vs. HF: 2.1 +/- 1.0 X 10(3) U/100 g). These results suggest that 1) short-term rapid ventricular pacing in the dog produces a model of low output HF resembling HF in humans, and 2) skeletal muscle underperfusion in this model is due to a reduced muscle arteriovenous pressure gradient and not to impaired skeletal muscle arteriolar vasodilation.
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Wilson et al. (1986) studied Heart failure (n=17). Ventricular pacing-induced heart failure vs. Control was evaluated on Mean arteriovenous pressure gradients at peak treadmill exercise (mmHg) (p=<0.001). In a dog model of pacing-induced heart failure, skeletal muscle underperfusion was driven by a reduced mean arteriovenous pressure gradient (91 vs 119 mmHg, P<0.001) rather than impaired vasodilation.
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