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

Sean P. Didion, William G. Mayhan

Research output: Contribution to journalArticlepeer-review

25 Scopus citations


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 μm) were measured after topical suffusion of acetylcholine (ACh; 0.1, 1.0, and 19 μM), calcitonin gene-related peptide (CGRP; 0.01, 0.1, and 1.0 nM), substance P (SP; 0.01, 0.1, and 1.0 μM), and sodium nitroprusside (SNP; 1.0, 10, and 100 μM). 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.

Original languageEnglish (US)
Pages (from-to)H2403-H2408
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Issue number5 41-5
StatePublished - 1997


  • L-arginine
  • acetylcholine
  • calcitonin gene-related peptide
  • rats
  • substance P

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

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