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 m yocardial infarction alters reactivity of rat skeletal muscle arteriol es in vivo. At 4, 8, and 16 wk after induction of chronic myocardial i nfarction or sham (control) surgery, the spinotrapezius muscle was pre pared for direct visualization of the microcirculation. Responses of t hird-order arterioles (37.9 +/- 0.9 mu m) were measured after topical suffusion of acetylcholine (ACh; 0.1, 1.0, and 10 mu M), calcitonin ge ne-related peptide (CGRP; 0.01, 0.1, and 1.0 nM), substance P (SP; 0.0 1, 0.1, and 1.0 mu M), and sodium nitroprusside (SNP; 1.0, 10, and 100 mu M). Arteriolar reactivity was impaired after chronic myocardial in farction 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 rea ctivity during chronic myocardial infarction may be related to an alte red availability of L-arginine (L-Arg). Suffusion of L-Arg (1.0 mM) pa rtially restored impaired ACh- and CGRP-induced responses in myocardia l-infarcted animals toward that observed in controls. Thus the present study demonstrates that impaired reactivity of skeletal muscle arteri oles during chronic myocardial infarction appears to be partially rela ted to an alteration in L-Arg availability.