Effect of chronic myocardial infarction on in vivo reactivity of skeletal muscle arterioles.

The first goal of this study was to test the hypothesis that chronic myocardial infarction alters reactivity of rat skeletal muscle arterioles in vivo. At 4, 8, and 16 wk after induction of chronic myocardial infarction or sham (control) surgery, the spinotrapezius muscle was prepared for direct visualization of the microcirculation. Responses of third-order arterioles (37.9 +/- 0.9 microns) were measured after topical suffusion of acetylcholine (ACh; 0.1, 1.0, and 10 microM), calcitonin gene-related peptide (CGRP; 0.01, 0.1, and 1.0 nM), substance P (SP; 0.01, 0.1, and 1.0 microM), and sodium nitroprusside (SNP; 1.0, 10, and 100 microM). Arteriolar reactivity was impaired after chronic myocardial infarction in response to ACh and CGRP at all time periods examined. In contrast, vasodilatation in response to SP and SNP was preserved after 4, 8, and 16-wk of chronic myocardial infarction. The second goal of this study was to explore the possibility that impaired arteriolar reactivity during chronic myocardial infarction may be related to an altered availability of L-arginine (L-Arg). Suffusion of L-Arg (1.0 mM) partially restored impaired ACh- and CGRP-induced responses in myocardial-infarcted animals toward that observed in controls. Thus the present study demonstrates that impaired reactivity of skeletal muscle arterioles during chronic myocardial infarction appears to be partially related to an alteration in L-Arg availability.