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Mechanical, biochemical, and structural effects of vitamin D deficiency on the chick heart
E Hochhauser1, J Barak, T Kushnir
1Department of Thoracic and Cardiovascular Surgery, Ichilov Hospital, Tel Aviv, Israel.
Insights
Vitamin D deficiency initially increases chick heart contractility but leads to faster decline and reduced energy compounds. Supplementation with 1,25(OH)2D3 improved cardiac performance, indicating vitamin D
Area of Science:
- Cardiology
- Endocrinology
- Nutritional Science
Background:
- Vitamin D plays a crucial role in calcium homeostasis and has extraskeletal effects.
- The impact of vitamin D on cardiac function is not fully understood.
- Investigating vitamin D's role in heart health is essential for understanding cardiovascular physiology.
Purpose of the Study:
- To investigate the effects of vitamin D deprivation on chick heart contractility, high-energy phosphorus compounds, and structure.
- To determine if 1,25(OH)2D3 supplementation can ameliorate cardiac dysfunction in vitamin D-deficient chicks.
Main Methods:
- Vitamin D-deficient chicks were used, with groups receiving cholecalciferol, different perfusion methods, or 1,25(OH)2D3.
- Isolated spontaneously beating hearts (modified Langendorff preparation) were perfused with Krebs-Henseleit solution.
- Cardiac contractility (+/- dP/dT) and intracellular high-energy phosphorus compounds were measured.
Main Results:
- Vitamin D-deficient chick hearts showed significantly increased contractility initially, followed by a significant decline.
- A faster rate of decline in intracellular high-energy phosphorus compounds was observed in vitamin D-deficient hearts.
- Presacrifice administration of 1,25(OH)2D3 improved cardiac performance in deficient chicks.
Conclusions:
- Vitamin D plays a significant role in maintaining normal cardiac function.
- Vitamin D deficiency negatively impacts myocardial contractility and energy metabolism.
- 1,25(OH)2D3 shows potential in improving cardiac performance under vitamin D deficiency.
Abstract:
The effects of vitamin D deprivation on the chick heart were investigated from three aspects: cardiac contractility (+/- dP/dT), intracellular high-energy phosphorus compounds, and structural differences. Four-week-old vitamin D-deficient chicks were divided into four groups: Group A served as the normal group and received subcutaneous injections of cholecalciferol; Groups B and C were vitamin D-deficient hearts but perfused differently; Group D received daily subcutaneous injections of 5 micrograms of 1,25(OH)2D3. When the isolated spontaneously beating hearts (modified Langendorff preparation) were perfused with Krebs-Henseleit (KH) solution containing a calcium concentration of 2.5mM, the myocardial contractility of the vitamin D-deficient hearts was significantly increased when compared with group A. After the isolated heart had beaten for one hour, the myocardial contractility in the vitamin D-deficient hearts was found to decline to significantly lower values. Presacrifice administration of 1,25(OH)2D3 improved cardiac performance. Vitamin D deficiency resulted in an enhanced rate of decline of the intracellular high-energy phosphorus compounds. No differences were found in the microscopic study. These observations suggest that vitamin D has a role in cardiac function.