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Reassessment of changes in leucocyte and serum ascorbic acid after acute myocardial infarction
Insights
Following myocardial infarction, white blood cells deplete ascorbic acid, indicating tissue damage. Supplementation can correct this depletion, highlighting the need for targeted treatment after heart attacks.
Area of Science:
- Biochemistry
- Cardiology
- Hematology
Background:
- Acute myocardial infarction (AMI) is associated with significant physiological changes, including alterations in white blood cell count and serum cortisol.
- Leukocyte ascorbic acid levels appear to decrease following AMI, coinciding with an increase in white blood cells.
Purpose of the Study:
- To investigate the relationship between myocardial infarction, white blood cell changes, and ascorbic acid levels.
- To differentiate between stress-induced changes and tissue-specific depletion of ascorbic acid post-myocardial infarction.
Main Methods:
- Measurement of leukocyte and serum ascorbic acid levels in patients post-myocardial infarction.
- Comparison of these levels with those in normal subjects and subjects undergoing adrenal stimulation (tetracosactrin infusion).
- Analysis of ascorbic acid content in different white blood cell types (granulocytes and lymphocytes).
Main Results:
- An acute fall in leukocyte ascorbic acid post-AMI is primarily due to granulocytosis, as granulocytes have lower ascorbic acid content than lymphocytes.
- Following granulocytosis resolution, white blood cells remain depleted of ascorbic acid for at least 56 days, indicating persistent tissue desaturation.
- Adrenal stimulation mimics the rise in white blood cells and apparent fall in leukocyte ascorbic acid but does not alter serum ascorbic acid levels, unlike AMI.
Conclusions:
- The observed tissue depletion of ascorbic acid post-myocardial infarction, reflected in both leukocytes and serum, is linked to damaged tissue and is distinct from generalized stress responses.
- Ascorbic acid supplementation can correct the persistent tissue desaturation and subnormal serum levels observed after AMI.
- Understanding this specific depletion mechanism is crucial for managing post-myocardial infarction recovery.
Abstract:
After an acute myocardial infarction, there is an apparent acute fall in leucocyte ascorbic acid associated with an acute rise in white blood cells and serum cortisol. The apparent fall in leucocyte ascorbic acid is the result of the granulocytosis which occurs after the infarction. Estimations of ascorbic acid disclose that the granulocyte contains approximately half the ascorbic acid of the lymphocyte. When the granulocytosis subsides, the new population of white blood cells is depleted of ascorbic acid for at least 56 days, reflecting tissue desaturation which can be corrected by ascorbic acid supplements. Tissue desaturation is also reflected in subnormal serum ascorbic acid levels which persist also unless ascorbic acid supplements are given. Observations on normal subjects given infusions of tetracosactrin (Synacthen) show that adrenal stimulation can produce a similar rise in white blood cells and an apparent fall in leucocyte ascorbic acid concentration with the exception that the serum ascorbic acid remains unaltered. Therefore, while adrenal stimulation can mimic 'stress' with regard to the changes in the white blood cells, tissue depletion of ascorbic acid as reflected in the white blood cells and serum after a myocardial infarction requires a focus of damaged tissue.