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Cell injury off the Heart Muscle
Question for discussion
Mr. Smith was lifting a heavy piece of furniture when he experienced crushing pain in his chest, began sweating heavily, and was nauseated. His wife drove him to the hospital, where he was diagnosed with a myocardial infarction (MI, also called a heart attack) and given intravenous drugs to dissolve a clot that was obstructing a major coronary artery. After his hospitalization, Mr. Smith?s doctor told him that some of his heart muscle had died.
Pathological processes associated with the death of the heart muscle
The function of heart relies on a complex network of cells’ ‘the cardiomyocytes for its appropriate function. These cells are the contracting cells in the heart, that exist in a three dimensional network of endothelial cells, vascular smooth muscle, an abundant fibroblasts and transient populations of immune cells. Gap junctions electrochemically coordinate the contraction of the individual cardiomyocytes, and their contraction to the extracellular matrix that transduces force and coordinates the overall contraction of the heart. In the cells, the repeating units of actin, as well as the myosin form the sarcomere structure, the basic functional unit of the cardiomyocyte.
The sarcomere has more than 20 proteins form connections between extracellular matrix and myocytes that regulate muscle contraction. The dysfunction occurs due to the disruption in the interaction in the complex activity that exist between multimeric complexes and many proteins. The heart can tolerate a variety of pathological insults, even then if the adoptive responses that aim to maintain functions eventually fail, they result in a range of functional deficits of cardiomyopathy. (Pamela and Leslie,2011).
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Patho-physiological processes of cell injury
Tissue injury and cell death occur due to ischemic insult, is determined by the magnitude and duration of the blood supply and the changer induced due to reperfusion. Prolonged ischemia, reduces the ATP levels and intracellular PHdue to anaerobic metabolism and accumulation of lactate. This results in the dysfunction of ATPase dependent ion transport mechanisms, that contribute to increasing intracellular mitochondrial calcium levels, swelling of the cell and the rupture of the cell, ultimately resulting in the death of the cell by necrotic, necroptotic. Apoptopic and autophagic mechanisms. (Theodore et.al,2012).
Reversible and irreversible cell injury
Reversible cell injury
Reversible cell injury denotes pathological changes that can be reversed, provided the stimulus is removed and the cellular injury is mild. Cellular injury can be recovered only to a certain point.(Farber et.al,1981)
Irreversible cell injury
Irreversible cell injury is a pathological change that is permanent and can cause cell death and cannot be reversed to normal state.(Farber et.al,1981)
Sustaining heart attack
The cell injury causes loss of phosphorylation in mitochondria, increase in anaerobic glycolysis, slowing down of the pumping of sodium, failure of active transport. The morphological changes that include swelling of the cell, loss of microvilli and blebs. All these abnormalities can be reversible if the oxygenation is restored.
References
- Pamela A. Harvey and Leslie A. Leinwand (2011) Cellular mechanisms of cardiomyopathy, Journal of cell Biologyh, vol. 194 no. 3 355-365
2. Theodore Kalogeris, Christopher P. Baines, Maike Krenz, and Ronald J. Korthuis(2012). Cell Biology of Ischemia/Reperfusion Injury, Int Rev Cell Mol Biol. 2012; 298: 229–317.
- J. L. Farber, K. R. Chien, S. Mittnacht, Jr(1981) Myocardial ischemia: the pathogenesis of irreversible cell injury in ischemia. Am J Pathol. 1981 February; 102(2): 271–281.
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