Heterogeneous effects of chronic myocardial infarction on skeletal muscle arteriole functional dilation

Chronic myocardial infarction (MI) is known to diminish arteriolar responses to nitric oxide (NO)‐dependent vasodilators. We investigated whether 1) MI leads to impaired arteriolar responses to muscle contraction, 2) MI affects different branching orders differently, and 3) NO is responsible for MI‐related impairments. MI was induced by coronary artery ligation in female rats (n = 22; MI = 13, SHAM = 9). Intravital microscopy was used to measure the diameter and velocity responses of feed and arcade arterioles in the spinotrapezius muscle to electrically stimulated contraction before and after NOS blockade with L‐NAME (30 mg/kg IV). Resting diameter and calculated flow through the feed arterioles was the same for the MI and SHAM groups. Post‐contraction flow through the feed arterioles was diminished in the MI group compared to the SHAM group (p = 0.046), which was caused by a trend toward smaller post‐contraction diameters in these arterioles. L‐NAME had no effect on feed arterioles. In the arcade arterioles, resting and post‐contraction diameter and flow were similar between MI and SHAM groups. L‐NAME tended to reduce resting diameter (p = 0.054), and significantly reduced post‐contraction diameter in arcade arterioles (p = 0.033). These results demonstrate that feed arterioles are a primary site of MI‐induced derangements of microvascular function, while NO primarily affects the arcade arterioles. Support NHLBI HL18292, AHA‐VA‐0315362U, Jeffress Trust J‐710