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Distribution of LDH-1 in normal, ischemic, and necrotic myocardium. An immunoperoxidase study
Insights
Lactate dehydrogenase (LDH-1) staining is positive in normal heart muscle. LDH-1 loss is detectable in necrotic myocardium within 3 hours of coronary artery occlusion, but not in ischemic tissue without necrosis.
Area of Science:
- Cardiovascular Pathology
- Biochemistry
- Immunohistochemistry
Background:
- Lactate dehydrogenase (LDH-1) is an enzyme crucial for cellular energy metabolism.
- Understanding LDH-1 distribution aids in diagnosing myocardial damage.
- Immunohistochemical techniques offer precise localization of enzymes in tissue.
Purpose of the Study:
- To investigate the distribution of LDH-1 (H4) in normal, ischemic, and necrotic myocardium.
- To assess the utility of LDH-1 staining for early detection of myocardial infarction.
- To differentiate between ischemic and necrotic myocardial tissue using LDH-1 expression.
Main Methods:
- Studied formalin-fixed, paraffin-embedded human (n=11) and canine (n=28) myocardium.
- Employed the peroxidase-antiperoxidase (PAP) technique for LDH-1 immunostaining.
- Utilized triphenyl tetrazolium chloride (TTC) staining and microscopy to confirm necrosis and ischemia.
Main Results:
- Normal myocardium showed positive LDH-1 immunostaining.
- Necrotic myocardium (infarcts ≥10 hours old) exhibited markedly diminished LDH-1 staining.
- In canine models, necrotic myocardium (≥3 hours occlusion) showed reduced LDH-1, while ischemic but not necrotic myocardium stained intensely.
- LDH-1 loss was detectable in necrotic myocardium as early as 3 hours post-occlusion.
Conclusions:
- Immunoperoxidase staining effectively demonstrates LDH-1 in normal human and canine myocardium.
- LDH-1 expression remains intact in ischemic myocardium without necrosis.
- LDH-1 loss is a sensitive marker for myocardial necrosis, detectable early after coronary artery occlusion.
Abstract:
To study the distribution of lactate dehydrogenase (LDH-1) (H4) in normal, ischemic, and necrotic myocardium using the peroxidase-antiperoxidase technic, the authors studied formalin-fixed paraffin-embedded sections of human (n = 11) and canine (n = 28) myocardium. All normal control myocardium showed positive immunostaining for LDH-1 (H4). In infarcts 10 hours or more old, the histologically necrotic myocardium (by triphenyl tetrazolium chloride staining) (TTC) showed markedly diminished immunostaining. In 24-dogs ischemia was induced in a closed-chest model using a balloon-tipped catheter inflated in the left anterior descending coronary artery. In dogs with 3 hours or more of occlusion, myocardium that was necrotic by TTC staining, light and/or electron microscopy, showed diminished staining for LDH-1, while normal, control myocardium stained intensely. In four dogs, ischemia was induced by a controlled perfusion apparatus by which left main coronary flow was reduced by 50%. Ischemia without necrosis was documented by demonstration of glycogen loss with no light or electron microscopic evidence of necrosis. These ischemic fibers stained intensely for LDH-1, as did controls. Thus, by immunoperoxidase staining, LDH-1 can be demonstrated in normal human and canine myocardium. In experimental models of ischemia in dogs, tissue that was ischemic but not necrotic showed no diminished staining. LDH-1 loss can be detected in necrotic myocardium as early as 3 hours after coronary artery occlusion.