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Significant and Sustained Impairment of Distal Limb Perfusion in Wistar Kyoto (WKY), Lean (LZR) and Obese (OZR) Zucker and Spontaneously Hypertensive Rat (SHR) Models of Hindlimb Ischemia Is Revealed by Femoral Vein Outflow During Functional Hyperemia

Following femoral artery ligation/excision, hindlimb perfusion at rest and during contraction‐induced hyperemia was assessed by venous outflow (VO). After 2 wks, a sustained impairment at rest was observed only in WKY rats (72 ± 9.2% of control). The maximal VO increase during muscle contraction induced by electrical stimulation was greatly reduced in the ligated vs control limb (505±37% vs 119±36% in WKY). In Zucker rats, the maximal VO increase in the chronically occluded limb during muscle contraction was greater in the lean than in the obese rats (112 ± 23 vs 22 ± 10%). Administration of ramipril for 2 weeks, initiated 2 weeks after femoral artery excision, greatly improved the perfusion during muscle contraction in SHR (206 ± 14% vs 82 ± 36%). These results indicate that 1) a sustained perfusion deficit exists even at rest in WKY and skeletal muscle contraction unmasks a much greater perfusion deficit, 2) the presence of vascular disease risk factors can exacerbate the insufficiency as seen between LZR and OZR, and 3) rodent models might be useful in predicting clinical outcomes, as observed in SHR receiving ramipril therapy post‐occlusion. Contrary to the common perception, the data obtained during rest and contraction‐induced hyperemia by venous outflow demonstrate that some rodent models of hindlimb ischemia can mimic the human condition of subcritical arterial insufficiency. Supported by HL42898.