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Hemorrhagic cardiomyopathy and hemothorax in vitamin K deficient mice
A M Allen1, C T Hansen, T D Moore
1Microbiological Associates, Inc., Rockville, Maryland 20850.
Insights
Vitamin K deficiency caused a fatal condition in mice, leading to hemorrhagic cardiomyopathy and blood clotting issues. Supplementing vitamin K (menadione Na-bisulfite) resolved the outbreak, confirming the deficiency as the cause.
Area of Science:
- Veterinary Pathology
- Nutritional Science
- Hematology
Background:
- A fatal condition characterized by hemorrhagic cardiomyopathy, hemothorax, and coagulation defects was observed in hysterectomy-derived male mice.
- Microscopic examination revealed multifocal hemorrhage, necrosis, inflammation, and fibroplasia in the heart, particularly near the atrioventricular junction.
Purpose of the Study:
- To investigate the etiology of the fatal hemorrhagic condition in mice.
- To determine the role of vitamin K in the observed syndrome.
Main Methods:
- Investigated a spontaneous outbreak in mice.
- Administered a vitamin K-free diet to germ-free male mice.
- Administered Warfarin to conventional male and female mice.
- Assessed the effects of menadione Na-bisulfite (vitamin K) supplementation.
Main Results:
- The outbreak was halted by increasing dietary menadione Na-bisulfite (vitamin K) to 20 ppm.
- The syndrome, including hemorrhagic cardiomyopathy, was reproducible in mice on a vitamin K-free diet.
- Warfarin administration also induced the syndrome in conventional mice.
Conclusions:
- The primary cause of the observed fatal condition, including hemorrhagic cardiomyopathy and coagulation defects, was identified as vitamin K deficiency.
- Dietary vitamin K levels are critical for preventing this syndrome in mice.
Abstract:
The cause of a fatal condition characterized by hemorrhagic cardiomyopathy, hemothorax, and coagulation defects in hysterectomy-derived male mice was investigated. Microscopic heart alterations included multifocal hemorrhage and necrosis with variable degrees of acute inflammation and fibroplasia that were most severe in the region of the atrioventricular junction. A spontaneous outbreak was arrested by increasing menadione Na-bisulfite (vitamin K) in the feed to 20 ppm. The complete syndrome including hemorrhagic cardiomyopathy was readily reproduced in germ-free male mice given a vitamin K-free diet, and in conventional male and female mice given Warfarin in the diet. We concluded that the cause of this condition was vitamin K deficiency.