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34 MYOCARDIAL ISCHEMIA CAUSES HIGHER CREATINE KINASE RELEASE IN CALCITONIN GENE-RELATED PEPTIDE KNOCKOUT MALE MOUSE HEARTS.
  1. H. Ma,
  2. R Huang,
  3. A. Carve,
  4. I. Shah,
  5. S. C. Supowit*,
  6. D. J. DiPette*,
  7. G. S. Abela
  1. Department of Medicine, Michigan State University, East Lansing, MI; *Texas A & M University, Scott and White Hospital, Temple, TX

Abstract

Background Calcitonin gene-related peptide (CGRP) influences vasoregulatory activities. We determined the gender-specific effects of CGRP knockout (KO) on creatine kinase (CK) activity following ischemia.

Methods Ninety-six mice were studied in a Langendorff preparation using 50 mm Hg perfusion pressure. Myocardial ischemia was induced by stopping flow to the coronary arteries for 20 minutes. The perfusion buffer was collected from a small chamber that housed the heart. Perfusion buffer was collected over 2 hours and CK activity was measured.

Results CK activity was significantly greater in CGRP-KO mouse hearts compared to wild-type (see graphs). Male CGRP-KO hearts released 1.5 times more CK than female CGRP-KO hearts 15 minutes after ischemia (130.4 vs 90.2 unit/mL, p < .003). Conclusions: CGRP contributes significantly to CK release during ischemia. This effect is more prominent in the male compared to the female mouse heart.

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