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

S. P. Didiom, Irving H Zucker, W. G. Maythan

Research output: Contribution to journalArticle

Abstract

Tha aim of this study was to datarmine whether chronic myocardial infarction (MI) atlers vascular reactivity of rat skeletal (spinotrapazius) muscle arterioles in vivo. The coronary artery ligation model of chronic MI. which produced -40% infarction of the MI ventricle, was used in this study. At 4 and 8 Weeks following chronic MI or sham surgery the splnotrapezius muscle was prepared for direct visualization of the microcirculation. Responses of third order artarioles (30-50 μm in diameter) to topical sulfusion of acetyicholine (ACh), substance P (SP), calcitonin gene-ralated peptide(CQRP), sodium nitroprusside SNP), and adanosine (ADO; 100μM) were measured on-line using an image shearing device. The response of arterocine to ADO were similar in control, 4 WK MI and 8 WK MI rats (p>0.05). Response of arteriocime to the other agonists were as follows: -4fy.h| fffgrti IP-<MCUIlnMl BWKMIfrwlSrlBl ACh 0.01μM 23±5% 4±11% 0±5%0.1μM 58±11% 19±10%16±4%1.0μM 34±10% 6.5±8% 47±8% CGRP 0.01μM 18±3% 11±3% 12±4%0.01μ± 40±0% 22±6 % 22±4% 23±4%1.0μM 77±7% 57±10%34±4% SP 0.01μM 24±0% 15±7% 18±4% 0.10μM 40±11% 32±9% 30±9% 1.0μM 47±4% 36±8% 31±7%SNP 10μM 45±12% 45±10% 21±4%10μM 71±10% 75±80% 48±56% All responses are expressed as a percent of maximal dlation to adenosine (100μM). Masns±SE.p<0.05 vs. controls. WK MI. # weeks of following Myocardial infarction These findings suggest that 4 weeks of chronic MI impairs the response of skeletal muscle arterioies to specific endothellum-dependent agonists, but not to endothelium-independent agonists. Whereaa, 8 weeks of chronic MI has a non-specific affect on responses of skeletal mucle arterioies to vasoactive agonists, suggesting that chronic MI of >4 weeks impairs andothellal function and impairs cGMP-mediated relazation of vascular smooth muscle. (S.P.D. is an American Heart Association/NE Affillate Pre-Doctoral Fellow: 9404011S and 9504027S).

Original languageEnglish (US)
Pages (from-to)A56
JournalFASEB Journal
Volume10
Issue number3
StatePublished - Dec 1 1996

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infarction
myocardial infarction
Arterioles
Infarction
Muscle
skeletal muscle
long term effects
Skeletal Muscle
Myocardial Infarction
Rats
Microcirculation
Calcitonin
Nitroprusside
Substance P
Shearing
blood vessels
Surgery
Visualization
Genes
Peptides

ASJC Scopus subject areas

  • Biotechnology
  • Biochemistry
  • Molecular Biology
  • Genetics

Cite this

Effect of chronic myocaroial infarction on in vivo reactivity of skeletal muscle arterioles. / Didiom, S. P.; Zucker, Irving H; Maythan, W. G.

In: FASEB Journal, Vol. 10, No. 3, 01.12.1996, p. A56.

Research output: Contribution to journalArticle

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abstract = "Tha aim of this study was to datarmine whether chronic myocardial infarction (MI) atlers vascular reactivity of rat skeletal (spinotrapazius) muscle arterioles in vivo. The coronary artery ligation model of chronic MI. which produced -40{\%} infarction of the MI ventricle, was used in this study. At 4 and 8 Weeks following chronic MI or sham surgery the splnotrapezius muscle was prepared for direct visualization of the microcirculation. Responses of third order artarioles (30-50 μm in diameter) to topical sulfusion of acetyicholine (ACh), substance P (SP), calcitonin gene-ralated peptide(CQRP), sodium nitroprusside SNP), and adanosine (ADO; 100μM) were measured on-line using an image shearing device. The response of arterocine to ADO were similar in control, 4 WK MI and 8 WK MI rats (p>0.05). Response of arteriocime to the other agonists were as follows: -4fy.h| fffgrti IP-<MCUIlnMl BWKMIfrwlSrlBl ACh 0.01μM 23±5{\%} 4±11{\%} 0±5{\%}0.1μM 58±11{\%} 19±10{\%}16±4{\%}1.0μM 34±10{\%} 6.5±8{\%} 47±8{\%} CGRP 0.01μM 18±3{\%} 11±3{\%} 12±4{\%}0.01μ± 40±0{\%} 22±6 {\%} 22±4{\%} 23±4{\%}1.0μM 77±7{\%} 57±10{\%}34±4{\%} SP 0.01μM 24±0{\%} 15±7{\%} 18±4{\%} 0.10μM 40±11{\%} 32±9{\%} 30±9{\%} 1.0μM 47±4{\%} 36±8{\%} 31±7{\%}SNP 10μM 45±12{\%} 45±10{\%} 21±4{\%}10μM 71±10{\%} 75±80{\%} 48±56{\%} All responses are expressed as a percent of maximal dlation to adenosine (100μM). Masns±SE.p<0.05 vs. controls. WK MI. # weeks of following Myocardial infarction These findings suggest that 4 weeks of chronic MI impairs the response of skeletal muscle arterioies to specific endothellum-dependent agonists, but not to endothelium-independent agonists. Whereaa, 8 weeks of chronic MI has a non-specific affect on responses of skeletal mucle arterioies to vasoactive agonists, suggesting that chronic MI of >4 weeks impairs andothellal function and impairs cGMP-mediated relazation of vascular smooth muscle. (S.P.D. is an American Heart Association/NE Affillate Pre-Doctoral Fellow: 9404011S and 9504027S).",
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