34 MYOCARDIAL ISCHEMIA CAUSES HIGHER CREATINE KINASE RELEASE IN CALCITONIN GENE-RELATED PEPTIDE KNOCKOUT MALE MOUSE HEARTS.
Hongbao Ma, Rao Huang, A. Carve, Ibrahim Shah, Scott C. Supowit, D DIPETTE, George S. Abela
Abstract
Hongbao Ma, Rao Huang, A. Carve, Ibrahim Shah, Scott C. Supowit, D DIPETTE, George S. Abela
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.
A significance statement is not available in the OpenAlex record.
A contribution statement is not available in the OpenAlex record.
Method details are not available in the OpenAlex metadata.
Findings are not separately available in the OpenAlex metadata.
Limitations are not available in the OpenAlex metadata.
Application details are not available in the OpenAlex metadata.
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.
Key concepts: Calcitonin gene-related peptide, Calcitonin, Internal medicine, Perfusion, Ischemia, Creatine kinase, Endocrinology, Knockout mouse