Related Experiment Videos
[Metabolism of histamine in patients with coronary atherosclerosis]
Insights
Histamine metabolism is altered in coronary atherosclerosis. Treatments targeting histamine pathways improve outcomes and reduce angina attacks in patients with this condition.
Area of Science:
- Biochemistry
- Cardiology
- Pharmacology
Context:
- Coronary atherosclerosis involves complex physiological changes.
- Histamine and its metabolic pathways play a role in cardiovascular function.
- Understanding these roles is crucial for effective treatment.
Purpose:
- To investigate histamine metabolism in patients with coronary atherosclerosis stages I and III.
- To correlate histamine levels and enzyme activities with disease severity and angina attacks.
- To evaluate the efficacy of antihistamine and desensitizing agents.
Summary:
- In stage I coronary atherosclerosis, histamine levels and diaminooxidase activity increase during angina, while histidine decarboxylase and antihistamine factors remain normal.
- In stage III, increased degranulated basophils and histidine decarboxylase activity, alongside decreased histaminopexy and antihistamine factors, are observed during angina.
- A lack of correlation between blood histamine and diaminooxidase activity may lead to hyperhistaminaemia and increased urinary histamine excretion.
Impact:
- Findings highlight the dysregulation of histamine metabolism in coronary atherosclerosis.
- Antihistamine and desensitizing drugs, combined with vasodilators, enhance therapeutic effects.
- These treatments reduce angina frequency, accelerate clinical improvement, and normalize histamine metabolism.
Abstract:
In patients with coronary atherosclerosis in I and III stages content of histamine in blood, excretion of free histamine with urine, activities of serum histidine decarboxylase and diaminooxidase, histaminopexy of blood serum and content of antihistamine factor were studied. In patients with the disease of the I stage during the attacks of stenocardia content of histamine in blood, the activity of diaminooxidase and content of degranulated basophils were increased, but the histidine decarboxylase activity, histaminopexy, content of antihistamine factor and excretion of free histamine with urine were normal. During the stenocardia attacks in patients with coronary atherosclerosis of the III stage content of degranulated basophils, the histidine decarboxylase activity were increased, histaminopexy and titres of antihistamine factor were decreased. Between the content of histamine in blood and the diaminooxidase activity no correlation was observed. This lack of correlation could cause development of hyperhistaminaemia and increased excretion of free histamine with urine. Antihistamine and desensitizing preparations (pipolphen, heparin, amidopyrine and ascorbic acid) increased the therapeutic efficiency of vasodilating drugs, decreased stenocardia attacks, accelerated both clinical improvement and normalization of histamine metabolism.